The DOI matches its Crossref record; 27 of the 30 references it cites were found in a registry or an index; none of the 30 sources its claims cite is checked for support yet.
Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohydrate intolerance in Mild Diabetes Mellitus*
Open accessAbstract
Insulin secretory responses to paired intravenous and oral glucose loads were determined in 38 nonobese individuals classified as normal (nondiabetic) subjects, "mild" diabetics (fasting blood glucose below 105 mg per 100 ml), or "moderate" diabetics (fasting glucose below 192 mg per 100 ml). Studies were also performed in 29 obese persons who were similarly grouped. The intravenous load was given to assess the alacrity of hormonal release after glycemic stimulus, and the oral glucose to determine how the speed of initial insulinogenesis modifies the disposition of ingested carbohydrate. In the nonobese group, normal subjects responded to massive hyperglycemia after rapid injection of glucose with immediate and maximal outpouring of insulin, in contrast to a desultory insulinogenic response in patients with mild diabetes, and no initial response at all in moderate diabetics. During oral glucose tolerance tests, the much faster clearance of blood sugar in nondiabetic subjects was actually associated with lower absolute insulin output than was found in mildly diabetic patients, since the latter exhibited delayed hyperinsulinemia in concert with prolonged hyperglycemia. Moderate diabetics never showed excessive insulin release despite even greater hyperglycemia. An empirical "insulinogenic index," the ratio relating enhancement of circulating insulin to magnitude of corresponding glycemic stimulus, was used to compare the secretory capacities of respective groups. Despite the higher absolute hormonal output after oral glucose in mild diabetics, the index revealed that insulin release in normal subjects was proportionally more than twice as great. This relatively greater normal secretory response declared itself shortly after the administration of glucose by either route, and was maintained throughout both tests. In the 29 obese individuals, differences among groups were essentially the same as in persons of normal weight. Obese nondiabetics did show much larger absolute insulinogenic responses during both tests than did nonobese controls. Since corresponding glucose tolerance curves were also higher, the mean insulinogenic indexes for obese subjects were not statistically greater. Moreover, when comparable glucose curves of obese and nonobese controls
Overview
AI snapshot
Written from the paper’s full text.
TL;DR
In paired intravenous and oral glucose tests, mild diabetics showed delayed and blunted initial insulin release relative to normal subjects, despite later absolute hyperinsulinemia after oral glucose. The paper argues that early diabetes involves a defect in the speed and proportionality of insulin secretion per glycemic stimulus, not simply a reduced total amount.
Key findings
- After intravenous glucose, nonobese normal subjects had immediate maximal insulin release: blood glucose rose from 72 ± 1 to 296 ± 7 mg/100 ml and plasma insulin from 10 ± 1 to 142 ± 14 µU/ml (p < 0.001). Mild diabetics reached a similar 5-minute glucose level (294 ± 17 mg/100 ml) but insulin rose only from 12 ± 2 to 45 ± 9 µU/ml and plateaued at 47 ± 8 µU/ml; moderate diabetics showed no initial insulin rise.
- During oral glucose testing, mild diabetics had delayed hyperinsulinemia: glucose rose from 80 ± 3 to 201 ± 11 mg/100 ml at 60 minutes, while insulin rose from 9 ± 2 µU/ml to a delayed peak of 233 ± 42 µU/ml at 90 minutes. Normal subjects cleared glucose faster with a lower absolute insulin peak (129 ± 10 µU/ml at 45 minutes).
- The “insulinogenic index” (insulin increment area divided by glucose increment area) was lower in diabetics. For the total intravenous test, nonobese values were 0.66 ± 0.07 (100%) in normals, 0.31 ± 0.06 (47%) in mild diabetics, and 0.12 ± 0.04 (18%) in moderate diabetics; total oral values were 4.93 ± 0.54 (100%), 2.43 ± 0.39 (49%), and 0.47 ± 0.13 (10%), respectively.
- Obese subjects showed the same group patterns. Obese normals had larger absolute insulin responses, but their insulinogenic indexes were not statistically greater than nonobese normals because their glucose curves were also higher. Total intravenous indexes in obese subjects were 1.12 ± 0.25 (100%) in normals, 0.67 ± 0.08 (60%) in mild diabetics, and 0.19 ± 0.07 (17%) in moderate diabetics; oral indexes were 5.45 ± 0.69 (100%), 2.17 ± 0.21 (40%), and 0.58 ± 0.23 (11%).
Methods
- Paired intravenous and oral glucose loads were given to 38 nonobese individuals (21 normal, 10 mild diabetics, 7 moderate diabetics) and 29 obese individuals (11 normal, 11 mild diabetics, 7 moderate diabetics). Mild diabetes was defined as fasting blood glucose below 105 mg/100 ml; moderate diabetes as fasting glucose between 106 and 192 mg/100 ml.
- Intravenous glucose was 0.5 g/kg actual body weight injected over exactly 5 minutes; oral glucose was 1.75 g/kg desirable body weight consumed within 5 minutes. Blood glucose was measured by the Somogyi-Nelson method, and plasma insulin by a modification of the Yalow-Berson radioimmunoassay.
- Secretory responses were compared using plasma insulin and blood glucose patterns, insulin:glucose ratios, and an empirical “insulinogenic index” calculated as the area under the insulin increment curve divided by the area under the glucose increment curve over cumulative intervals.
Limitations
- The paper states that its interpretations depend on “unprovable but reasonable assumptions”: that immunoassayable insulin equals biological activity, that antecubital venous glucose reflects pancreatic arterial glucose, and that antecubital venous plasma insulin reflects pancreatic venous plasma insulin.
- The paper states that different dosage schedules for intravenous and oral tests “prevented strict comparison of the two secretory patterns for each person.” It also states that the precise nature of the lesion making diabetic islets hyporesponsive to rising glucose remains unknown.
- Evident from the text: the moderate diabetic groups were small (7 nonobese and 7 obese), and the study population was almost entirely men (only 3 nonobese normal women and 1 nonobese woman with mild diabetes).
Model-written summary. Check it against the paper before relying on it.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
0 of 30 cited sources checked · 0 supported · 0 flagged
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Moderate dia- betics never showed excessive insulin release despite even greater hypergly- cemia.”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Abstract
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“whereas in moderate diabetics it was virtually absent.”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Results
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“When the latter presumed determinant of insulino- genesis was eliminated by matching the highest glucose curves in normal weight controls with the lowest ones in obese subjects (Figure 6), the substantial difference that persisted between mean insulin patterns on both tests was again insig- nificant.”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Discussion
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“It was gratifying that values obtained from antecubital venous blood indicated that at least the early insulinogenic response seemed directly re- lated to glucose concentration, irrespective of pool size and other kinetics of glucose and insulin turnover.”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Discussion
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- The authors state this as an assumption: Events in the peripheral circulation of man reflect those occurring in the pancreas.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“At the end of the 5-min- ute injection into normal subjects, the rise in blood glucose from 72 + 1 mg per 100 ml (mean ± SEM) to 296 + 7 mg per 100 ml was paralleled by an increase in plasma insulin from 10 ± 1 ,uU per ml to 142 ± 14 puU per ml (p < 0.001).”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Results
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In none of the three groups did age significantly modify the insulinogenic response to intravenous or oral glucose loads.”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Results
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Similarly, among mild diabetics essentially parallel patterns of hormonal release were found in 6 patients 24 to 41 years of age (mean age 35 years) and in 10 patients between 47 and 69 years (average 58 years).”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Results
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesThe paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“In the 29 obese individuals, differences among groups were essentially the same as in persons of normal weight.”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Abstract
Strength:plain· not yet calibratedn = 29Tests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“in contrast to a desultory insulinogenic response in patients with mild diabetes”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In the nonobese group, normal subjects responded to massive hyperglycemia after rapid injection of glucose with immediate and maximal outpouring of insulin”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes
- It may state two separate claims as one. 28
- The quote only partly states this claim. 2
- Probably not a substantial claim. 12
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“since the latter exhibited delayed hyperinsulinemia in concert with prolonged hyperglycemia.”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The findings in Table V in- dicate that whether blood glucose descended from an acutely imposed hyperglycemic apex, or first rose and then fell postprandially, the insulin se- cretory response was always much greater in nor- mal subjects than in mild diabetics, and was even lower in moderate diabetics.”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Results
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“We found that both the speed of insulin release and the quantity of insulin secreted per unit of gly- cemic stimulus are much greater in normal sub- jects than in the mildest diabetic patients, in both nonobese and obese individuals.”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Introduction
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“In general, although obese nondiabetics and mild diabetics tended to produce higher plasma insulin concentrations after both glucose loads, they otherwise exhibited the same patterns of in- sulinogenic response as their nonobese counter- parts.”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Obese subjects and patients
Strength:hedged· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“For example, during the oral glucose tolerance test in nonobese individuals the index (Table V) for the first 30 minutes was 3.07 + 0.34 in normal controls and 1.14 ± 0.21 in mild diabetics (p < 0.001), and respective indexes for the entire test were 4.93 ± 0.54 and 2.43 ± 0.39 (p < 0.001).”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Discussion
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Even including them, however, when individual secretory response was expressed per unit of glycemic stimulus, the much greater absolute hyperinsulinemia of obesity lost statistical meaning (Table V) because glucose tolerance of overweight subjects, albeit still normal, was sufficiently higher than in nonobese controls.”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Discussion
Tests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Normal subjects responded immediately and max- imally to the massive glycemic stimulus, in con- trast to progressively blunted secretory responses in the diabetic groups.”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Results
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“For the initial 30 min- utes after oral glucose, the mean ratio for control subjects was 3.37 + 0.32, and the corresponding value for mild diabetics was 1.28 + 0.14 (p < 0.001).”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Results
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Since corresponding glucose tolerance curves were also higher, the mean insulinogenic indexes for obese subjects were not statistically greater.”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Abstract
Strength:plain· not yet calibratedn = 29Tests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In moderate dia- betics, mean fasting glucose of 126 + 8 mg per 100 ml rose to 342 + 17 mg per 100 ml in 5 min- utes with no increase above the fasting plasma in- sulin level of 24 5 ,uU per ml”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Results
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In the mild diabetics, fasting blood glucose was below 100 mg per 100 ml in 15 patients and less than 105 mg per 100 ml in the other 6; in all individuals blood glucose exceeded 160 mg per 100 ml at 1 hour and was well above 120 mg per 100 ml at 2 hours.”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Methods
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“100 ml elicited only a modest rise of plasma insulin from a fasting value of 12 + 2 ,uU per ml to 45 + 9 ,uU per ml (p < 0.001 compared to the 5-minute value in normal subjects), and plasma insulin plateaued at a maximum of 47 + 8 fLU per ml as circulating glucose slowly receded to the normal fasting range by 120 minutes.”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Results
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one. The quote only partly states this claim.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“In the moderate diabetics, since fasting glucose was always higher than 105 mg per 100 ml, blood levels 1 and 2 hours after the oral glu- cose load greatly exceeded 160 mg per 100 ml and 120 mg per 100 ml, respectively.”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Methods
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“During the first 10 minutes after intravenous glucose, the mean ratio for normal subjects was 0.56 + 0.03, and the corresponding ratio in mild diabetics was 0.22 + 0.06 (p < 0.001).”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Results
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thereafter, blood glucose dropped rapidly to a normal fasting level by 60 minutes, accompanied by a similar swift decline in circulating insulin concentration.”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Results
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“For the intravenous test, the”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Results
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“100 ml in 60 minutes, then fell slowly to 155 + 12 mg per 100 ml at 120 minutes and to 108 + 14 mg per 100 ml at 180 minutes.”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Results
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one. The quote only partly states this claim.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Corresponding over-all indexes after oral glucose were 4.93 + 0.54 (100o), 2.43 ± 0.39 (49%o), and 0.47 +0.13 (10%o).”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Results
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“This relatively greater normal secretory response de- clared itself shortly after the administration of glucose by either route, and was maintained throughout both tests.”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Despite the higher absolute hormonal output after oral glucose in mild diabetics, the index revealed that insulin release in normal subjects was proportionally more than twice as great.”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In the moderate diabetics, as fasting blood glucose of 137 ± 11 mg per 100 ml rose to a peak value of 295 ± 27 mg per 100 ml at 90 minutes and then declined to 211 ± 42 mg per 100 ml at 240 minutes, plasma insulin rose sluggishly from a control value of 19 ± 5 ,uU per ml to 103 + 29 ptU per ml at 120 minutes.”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Results
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Nevertheless, the present findings did show much greater insulin release after oral glucose loads in all three clinical groups, and regardless of body weight.”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Discussion
Strength:boosted· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“each patient was given intravenous and oral glucose, in random order and at intervals of a few days.”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Methods
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“Current work has narrowed the active substance down to glucagon (22), secretin (23-25), or pancreozymin (26).”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Discussion
What the sources say
- Not matchedcites [22]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [23]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [24]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [25]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [26]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
- Not matched
In the paper
“the interpretation in- voked by Seltzer, Fajans, and Conn (3), that the occurrence of symptomatic postprandial hypogly- cemia in patients with mild diabetes mellitus might be due to delayed initial release of insulin followed by subsequent excessive hormonal secretion”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Introduction
What the sources say
- Not matchedcites Seltzer, Fajans, and Conn (3)
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Tests✗ Asserted: fails✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim. The authors may not put it forward as true.
- Not matched
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“An acute rise or fall of blood glucose level directly induces an increase or decrease, respec- tively, of insulin release (1, 2, 8, 9).”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Methods
What the sources say
- Not matchedcites [1]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [2]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [8]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [9]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Not matched
In the paper
“In a carefully controlled study of comparably mild diabetics, Perley and Kipnis (16) also concluded that the diabetic state is associated with reduced insulin secretory capacity, regardless of body weight.”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Discussion
What the sources say
- Not matchedcites [16]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
- Not matched
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“which finding again sug- gested an anti-insulin effect of obesity.”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Discussion
Strength:hedged· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“At the same time, the general phenome- non of greater hormonal response to glucose loads in overweight normal subjects did suggest that the obese state somehow engenders peripheral in- sulin resistance (14, 15).”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Discussion
What the sources say
- Not matchedcites [14]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [15]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
- Not matched
In the paper
“previous work (2) having established that glucose-induced insulinogenesis does not alter pancreatic venous blood flow.”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Discussion
What the sources say
- Not matchedcites [2]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Strength:boosted· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
- Not matched
None of the sources cited for this claim have been checked yet.
In the paper
“Three of these groups suggested that assimilation of carbohydrate in the upper intestine stimulates release of a humoral agent that enhances the insulin-releasing potency of blood glucose level per se.”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Discussion
Strength:hedged· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Yalow and Berson (4) found subnormal plasma insulin concentrations at 30 minutes during glucose toler- ance testing of mild diabetics but supernormal levels at 2 hours.”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Introduction
What the sources say
- Not matchedcites Yalow and Berson (4)
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim. It may state two separate claims as one.
- Not matched
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“The dose-response curve, the reproducibility of values when the same plasma samples were repeatedly assayed, and the range of values obtained in normal and diabetic patients all duplicated the performance of the original technic.”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Methods
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“During continuous changes in circulating glucose concentrations after carbohydrate loads, the rate of insulin secretion is di- rectly (but not necessarily linearly) proportional to the simultaneous blood glucose level.”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Methods
What the sources say
- Not matchedcites Metz (1)
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
- Not matched
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In this respect diabetes melli- tus remains fundamentally a disease of deficient insulin secretion, but one of rate rather than mag- nitude in the initial stage of the disease.”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Discussion
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Conversely, the blunted capability of mildly diabetic islets to re- lease insulin after the same intravenous bolus of glucose implied an obtunded islet response to oral glucose as well-which relative lack of early in- sulin activity on hepatic and posthepatic tissues could reasonably account for the delay in metabo- lizing ingested glucose.”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Discussion
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Normal immediate hormonal release after sudden intense hyperglycemia suggested that a similarly fast response, but smaller and peripherally unde- tectable, was also activated by postprandially rising blood sugar, and this brisk insulinogenesis should promote avid hepatic and peripheral glucose up- take (27), which in turn would clear absorptive hyperglycemia with dispatch.”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Discussion
What the sources say
- Not matchedcites [27]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Not matched
The authors state this as an assumption.
The concentration of glucose in antecubital venous blood is directly proportional to the concomitant glucose level in pancreatic arterial blood.
“the concentration of glucose in antecubital venous blood is directly proportional to the concomitant glucose level in pancreatic arterial blood”
The authors state this as an assumption.
The insulin content of antecubital venous plasma directly reflects the simultaneous concentration in pancreatic venous plasma.
“the insulin content of antecubital venous plasma directly reflects the simul- taneous concentration in pancreatic venous plasma.”
The authors state this as an assumption.
Events in the peripheral circulation of man reflect those occurring in the pancreas.
“Assuming that events in the peripheral circulation of man reflect those occurring in the pancreas”
The paper relies on this without support.
Frequently monitored peripheral plasma insulin concentrations reflect actual insulin secretion.
“to the extent that frequently monitored peripheral plasma insulin concentra- tions reflected actual insulin secretion”
Citations
Cites
A PHOTOMETRIC ADAPTATION OF THE SOMOGYI METHOD FOR THE DETERMINATION OF GLUCOSE
Nelson, N. (1944) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(18)71980-7 · Cited by 10,376
Immunoassay of endogenous plasma insulin in man
Yalow, R. S., & Berson, S. A. (1960) · Journal of Clinical Investigation · doi:10.1172/jci104130 · Cited by 3,041
Plasma Insulin Response to Oral and Intravenous Glucose Administration1
ELRICK, H., STIMMLER, L., HLAD, C. J., & ARAI, Y. (1964) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jcem-24-10-1076 · Cited by 857
Promotion of Insulin Secretion by Glucagon
Samols, E., Marri, G., & Marks, V. (1965) · The Lancet · doi:10.1016/s0140-6736(65)90761-0 · Cited by 521
Rabinowitz, D. L., & Zierler, K. L. (1962) · Journal of Clinical Investigation · doi:10.1172/jci104676 · Cited by 505
IMMUNOASSAY OF ENDOGENOUS PLASMA INSULIN IN MAN
Yalow, R. S., & Berson, S. A. (1996) · Obesity Research · doi:10.1002/j.1550-8528.1996.tb00274.x · Cited by 459
Effects of carbohydrates on secretion of insulin from isolated rat pancreas
Grodsky, G. M., Batts, A. A., Bennett, L. L., Vcella, C., McWilliams, N. B., & Smith, D. F. (1963) · American Journal of Physiology-Legacy Content · doi:10.1152/ajplegacy.1963.205.4.638 · Cited by 430
Intestinal Factors in the Control of Insulin Secretion
McIntyre, N., Holdsworth, C. D., & Turner, D. S. (1965) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jcem-25-10-1317 · Cited by 382
Perley, M., & Kipnis, D. M. (1966) · Diabetes · doi:10.2337/diab.15.12.867 · Cited by 330
Hypertension, the Potassium Ion and Impaired Carbohydrate Tolerance
Conn, J. W. (1965) · New England Journal of Medicine · doi:10.1056/nejm196511182732106 · Cited by 329
Flagged first, then by citations
3 of the 30 references couldn’t be matched to a known paper.
Research works printed but not linked: 4
- Elrick, H., L. Stimmler, C. J. Hlad, Jr., and Y. Arai. Plasma insulin response to oral and intra- venous glucose administration. J. clin. Endocr. 1964, 24, 1076.
- Dupre, J. Effect of route of administration on dis- posal of glucose loads. J. Physiol. (Lond.) 1964, 175, 58.
- Ketterer, H., A. Ohneda, J. Dupre, A. Eisentraut, and R. H. Unger. Effects of enteric hormones on insulin and glucagon secretion. J. Lab. clin. Med. 1966, 68, 888.
- Schonfeld, G., and D. M. Kipnis. Studies of extra- cellular and tissue fatty acid pools and glucose metabolism in striated muscle. J. clin. Invest. 1966, 45, 1071.
Cited by
Sorted by citations
Items 201–300 of 818
Cederholm, J., & Wibell, L. B. (1985) · Scandinavian Journal of Clinical and Laboratory Investigation · doi:10.3109/00365518509155289 · Cited by 46
Dynamics of Insulin Release from the Foetal and Neonatal Rat Pancreas
Asplund, K. (1973) · European Journal of Clinical Investigation · doi:10.1111/j.1365-2362.1973.tb00360.x · Cited by 45
Gertler, M. M., Leetma, H. E., Saluste, E., et al. (1972) · Circulation · doi:10.1161/01.cir.46.1.103 · Cited by 46
First-phase insulin secretion: can its evaluation direct therapeutic approaches?
Di Giuseppe, G., Ciccarelli, G., Soldovieri, L., Capece, U., Cefalo, C. M. A., Moffa, S., Nista, E. C., Brunetti, M., Cinti, F., Gasbarrini, A., et al. (2023) · Trends in Endocrinology & Metabolism · doi:10.1016/j.tem.2023.02.001 · Cited by 46
Lim, S. K., An, J. H., Shin, H., Khang, A. R., Lee, Y., Ahn, H. Y., Yoon, J. W., Kang, S. M., Choi, S. H., Cho, Y. M., et al. (2011) · Clinical Endocrinology · doi:10.1111/j.1365-2265.2011.04240.x · Cited by 46
Impact of Glucose Tolerance Status, Sex, and Body Size on Glucose Absorption Patterns During OGTTs
Færch, K., Pacini, G., Nolan, J. J., Hansen, T. F., Tura, A., & Vistisen, D. (2013) · Diabetes Care · doi:10.2337/dc13-0592 · Cited by 49
“Surrogate markers of first-phase insulin secretion (b-cell function) were estimated from the OGTT by various methods: 1) the insulinogenic index (27), modeling the change in serum insulin divided by the change in plasma glucose from 0 to 30 min; 2) the Stumvoll first-phase insulin secretion index (28), which includes…”
MethodWon, J. C., Park, C., Park, H.-S., Kim, J. H., Choi, E. S., Rhee, E., Lee, W., Oh, K. W., Kim, S. W., & Park, S. W. (2009) · Diabetes Research and Clinical Practice · doi:10.1016/j.diabres.2009.01.002 · Cited by 45
“In addition, even in the prediabetic range of glycemia, subjects with low serum 1,5-AG levels had a decreased insulinogenic index (DI30–0/ DG30–0) indicating a reduced capacity for early phase insulin secretion [16].”
BackgroundThe Role of Insulin Resistance in the Pathogenesis of Diabetes Mellitus
Reaven, G. M., & Olefsky, J. M. (1978) · Advances in metabolic disorders · doi:10.1016/b978-0-12-027309-6.50021-5 · Cited by 44
WACHMAN, A., Hattner, R. S., George, B., & Bernstein, D. S. (1970) · Metabolism · doi:10.1016/0026-0495(70)90009-0 · Cited by 44
Oral Glucose Tolerance and Hormonal Response in Heroin-dependent Males
Reed, J. L., & Ghodse, A. H. (1973) · BMJ · doi:10.1136/bmj.2.5866.582 · Cited by 44
Diabetes mellitus in childhood: A review
DRASH, A. L. (1971) · The Journal of Pediatrics · doi:10.1016/s0022-3476(71)80421-3 · Cited by 44
Endocrine Cephalic Phase Responses to Food Cues: A Systematic Review
Lasschuijt, M. P., Mars, M., de Graaf, C., & Smeets, P. A. M. (2020) · Advances in Nutrition · doi:10.1093/advances/nmaa059 · Cited by 43
Kawaguchi, Y., Mizuta, T., Oza, N., et al. (2009) · Liver International · doi:10.1111/j.1478-3231.2009.01993.x · Cited by 43
“Changes in fasting plasma glucose and serum insulin levels In sustained responders, the FPG levels increased significantly from 85.9 1.5 mg/dl before therapy to 90.6 1.5 mg/dl (P = 0.0006) after therapy, whereas FSI levels did not change (Fig.”
MethodInfluentialInsulin resistance and excess risk of diabetes in Mexican-Americans: the San Antonio Heart Study.
Lorenzo, C., Hazuda, H., & Haffner, S. (2012) · Journal of Clinical Endocrinology and Metabolism · doi:10.1210/jc.2011-2272 · Cited by 44
“We selected the following indices of insulin resistance and insulin secretion to assess to which extent these indices accounted for the difference in diabetes incidence between Mexican-Americans and non-Hispanic whites: 1) homeostasis model assessment of insulin resistance and -cell function using published formulas (…”
MethodSAKAMOTO, N., Nishiike, T., Iguchi, H., & SAKAMOTO, K. (2000) · Clinical Nutrition · doi:10.1054/clnu.2000.0102 · Cited by 43
Long-term changes in the diabetic state induced by different doses of streptozotocin in rats.
Tancrède, G., Rousseau-Migneron, S., & Nadeau, A. (1983) · PubMed · Cited by 43
Does Disruption of Circadian Rhythms Contribute to Beta-Cell Failure in Type 2 Diabetes?
Rakshit, K., Thomas, A. P., & Matveyenko, A. V. (2014) · Current Diabetes Reports · doi:10.1007/s11892-014-0474-4 · Cited by 42
Ohkura, T., Fujioka, Y., Nakanishi, R., et al. (2014) · Diabetology & Metabolic Syndrome · doi:10.1186/1758-5996-6-106 · Cited by 42
“Insulinogenic index was measured by [insulin (pmol/L) at 30 min – insulin (pmol/L) at 0 min]/[glucose (mmol/L) at 30 min – glucose (mmol/L) at 0 min] [22].”
MethodMcCulloch, D. K., Kahn, S. E., Schwartz, M. W., Koerker, D. J., & Palmer, J. P. (1991) · Journal of Clinical Investigation · doi:10.1172/jci115145 · Cited by 41
Zern, R. T., Bird, J. L., & Feldman, J. M. (1980) · Diabetologia · doi:10.1007/bf00251017 · Cited by 42
Effect of Exercise on Glucose and Insulin Response to Glucose Infusion
Pruett, E. D. R., & OSEID, S. (1970) · Scandinavian Journal of Clinical and Laboratory Investigation · doi:10.3109/00365517009046234 · Cited by 41
Crockford, P. M., & Salmon, P. A. (1970) · PubMed Central · Cited by 41
Ørskov, H., & Christensen, N. J. (1971) · Scandinavian Journal of Clinical and Laboratory Investigation · doi:10.3109/00365517109080189 · Cited by 41
Kusaka, I., Nagasaka, S., Horie, H., & Ishibashi, S. (2008) · Diabetes, Obesity and Metabolism · doi:10.1111/j.1463-1326.2008.00857.x · Cited by 40
The incretin effect in K orean subjects with normal glucose tolerance or type 2 diabetes
Oh, T. J., Kim, M. Y., Shin, J. Y., Lee, J. C., Kim, S., Park, K. S., & Cho, Y. M. (2013) · Clinical Endocrinology · doi:10.1111/cen.12167 · Cited by 41
Mitsui, R., Fukushima, M., Nishi, Y., Ueda, N., Suzuki, H., Taniguchi, A., Nakai, Y., Kawakita, T., Kurose, T., Yamada, Y., et al. (2005) · Metabolism · doi:10.1016/j.metabol.2005.07.006 · Cited by 40
Inhibition of Insulin Secretion by Catecholamines in Pheochromocytoma
Colwell, J. A. (1969) · Annals of Internal Medicine · doi:10.7326/0003-4819-71-2-251 · Cited by 40
Myocardial metabolism in open-heart surgery
Moffitt, E. A., Rosevear, J. W., Molnar, G. D., & McGoon, D. C. (1970) · Journal of Thoracic and Cardiovascular Surgery · doi:10.1016/s0022-5223(19)42430-6 · Cited by 40
Morimoto, A., Tatsumi, Y., Soyano, F., Miyamatsu, N., Sonoda, N., Godai, K., Ohno, Y., Noda, M., & Deura, K. (2014) · PLoS ONE · doi:10.1371/journal.pone.0105827 · Cited by 39
“The insulinogenic index was calculated using the formula: insulinogenic index = (Insulin30 [pmol/l]2Insulin0 [pmol/l])/(Glucose30 [mmol/l]2Glucose0 [mmol/l]) [8].”
Rigas, A. N., Bittles, A. H., Hadden, D. R., et al. (1968) · BMJ · doi:10.1136/bmj.4.5622.25 · Cited by 39
Tao, T., Wu, P., Wang, Y., & Liu, W. (2018) · BMC Endocrine Disorders · doi:10.1186/s12902-018-0243-5 · Cited by 38
“2) Whole-body insulin sensitivity was calculated by the Matsuda index [11] as follows:”
MethodHirsch, F. F., Pareja, J. C., Geloneze, S. R., Chaim, É. A., Cazzo, E., & Geloneze, B. (2012) · Obesity Surgery · doi:10.1007/s11695-012-0589-0 · Cited by 38
“The AUCs for the variables studied during the MTT were calculated using the trapezoidal rule.”
MethodInfluentialOlsson, A. H., Rönn, T., Ladenvall, C., Parikh, H. M., Isomaa, B., Groop, L., & Ling, C. (2011) · European Journal of Endocrinology · doi:10.1530/eje-10-0995 · Cited by 39
The progression from obesity to type 2 diabetes in Alström syndrome
Bettini, V., Maffei, P., Pagano, C., Romano, S., Milan, G., Favaretto, F., Marshall, J. D., Paisey, R., Scolari, F., Greggio, N. A., et al. (2011) · Pediatric Diabetes · doi:10.1111/j.1399-5448.2011.00789.x · Cited by 38
“The last index, the insulinogenic index (9), estimates the early phase insulin secretion and was calculated as the ratio of the increment of serum insulin 30 min after an oral glucose load to blood glucose concentration 30 min after the glucose load:”
MethodIslet Morphometry in the Diabetic Pancreas of Man
Saito, K., TAKAHASHI, T., Yaginuma, N., & Iwama, N. (1978) · The Tohoku Journal of Experimental Medicine · doi:10.1620/tjem.125.185 · Cited by 38
Mechanism of glucose intolerance during fasting: Differences between lean and obese subjects
Göschke, H. (1977) · Metabolism · doi:10.1016/0026-0495(77)90042-7 · Cited by 38
Insulin release, insulin sensitivity, and glucose intolerance.
Efendić, S., Wajngot, A., Cerasi, E., & Luft, R. (1980) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.77.12.7425 · Cited by 38
Hales, C. N., Greenwood, F. C., Mitchell, F. L., & Strauss, W. T. (1968) · Diabetologia · doi:10.1007/bf01212536 · Cited by 38
So, W., Tong, P. C. Y., Ko, G. T. C., Ronald, C. W., Ozaki, R., Kong, A. P. S., Yang, X., Ho, C. S., Lam, C. C. F., & Chan, J. C. N. (2009) · Diabetes Research and Clinical Practice · doi:10.1016/j.diabres.2009.08.010 · Cited by 37
Immunoreactive insulin and growth hormone responses in patients with Prader-Willi syndrome
Parra, A., Cervantes, C., & Schultz, R. B. (1973) · The Journal of Pediatrics · doi:10.1016/s0022-3476(73)80219-7 · Cited by 37
Insulin secretion by the transplanted neonatal pancreas during food intake in fasted and fed rats
Strubbe, J. H., & van Wachem, P. B. (1981) · Diabetologia · doi:10.1007/bf00252633 · Cited by 37
“The delayed insulin response in the transplanted rats resembles the insulin response of human prediabetics, in whom a lower first phase response with a delayed and sometimes higher second phase insulin response is seen [24, 33-35].”
BackgroundInsulin Responses of Children with Chemical Diabetes Mellitus
Rosenbloom, A. L. (1970) · New England Journal of Medicine · doi:10.1056/nejm197005282822203 · Cited by 37
Adrenergic Modification of Glucose‐Induced Biphasic Insulin Release from Perifused Rat Pancreas
Burr, I. M., Balant, L., Stauffacher, W., & Renold, A. E. (1971) · European Journal of Clinical Investigation · doi:10.1111/eci.1971.1.4.216 · Cited by 37
Nishikawa, T., Ono, K., Hashimoto, S., Kinoshita, H., Watanabe, T., Araki, H., Otsu, K., Sakamoto, W., Harada, M., Toyonaga, T., et al. (2018) · Journal of Diabetes Investigation · doi:10.1111/jdi.12848 · Cited by 33
Inoue, H., Tamaki, Y., Kashihara, Y., Muraki, S., Kakara, M., Hirota, T., & Ieiri, I. (2018) · British Journal of Clinical Pharmacology · doi:10.1111/bcp.13807 · Cited by 41
Kraft, G., Vrba, A., Scott, M. F., Allen, E. J., Edgerton, D. S., Williams, P. E., Vafai, S. B., Azamian, B. R., & Cherrington, A. D. (2019) · Diabetes · doi:10.2337/db18-1209 · Cited by 38
“The ratio of the incremental insulin concentration to the incremental glucose concentration at the 30-min time point has been termed the insulinogenic index, a parameter that assesses b-cell function from OGTT data (35,36).”
Self-citationHarada, N., Hamasaki, A., Yamane, S., Muraoka, A., Joo, E., Fujita, K., & Inagaki, N. (2010) · Journal of Diabetes Investigation · doi:10.1111/j.2040-1124.2010.00078.x · Cited by 36
Kurauti, M. A., Dias, R. D. F., Ferreira, S. M., Vettorazzi, J. F., Nardelli, T. R., Araújo, H. N., dos Santos, G. J., Carneiro, E. M., Boschero, A. C., de Rezende, L. F., et al. (2016) · PLoS ONE · doi:10.1371/journal.pone.0160239 · Cited by 36
Goodner, C. J., Conway, M. J., & Werrbach, J. H. (1969) · Journal of Clinical Investigation · doi:10.1172/jci106154 · Cited by 36
“Since the ability to secrete insulin in response to various stimuli is impaired in diabetics (2-6, 8), the relatively lower basal levels with respect to glucose concentration might simply reflect impaired beta cell function or reduced beta cell mass.”
BackgroundCoates, P. A., Ismail, I. S., Luzio, S. D., Griffiths, I., Ollerton, R. L., Vølund, A., & Owens, D. R. (1995) · Diabetic Medicine · doi:10.1111/j.1464-5491.1995.tb00464.x · Cited by 36
Leahy, J. L., & Weir, G. C. (1991) · Diabetologia · doi:10.1007/bf00400993 · Cited by 36
Obesity, hyperinsulinism, and diabetes mellitus in childhood
Martin, M. M., & Martin, A. L. A. (1973) · The Journal of Pediatrics · doi:10.1016/s0022-3476(73)80154-4 · Cited by 36
GLUCOSE TOLERANCE, PLASMA LIPIDS AND SERUM INSULIN IN PATIENTS WITH ISCHAEMIC HEART DISEASES
Christiansen, I. S., Deckert, T., Kjerulf, K., Midtgaard, K., & WORNING, H. (1968) · Acta Medica Scandinavica · doi:10.1111/j.0954-6820.1968.tb02458.x · Cited by 36
Effect of Body Mass Index on Insulin Secretion or Sensitivity and Diabetes
Tatsumi, Y., Morimoto, A., Miyamatsu, N., Noda, M., Ohno, Y., & Deura, K. (2014) · American Journal of Preventive Medicine · doi:10.1016/j.amepre.2014.09.009 · Cited by 38
“IIS was defined using the insulinogenic index, calculated as follows: (serum insulin 30 minutes after OGTT [pmol/L] fasting serum insulin [pmol/ L]) / (plasma glucose 30 minutes after OGTT [mmol/L] fasting glucose [mmol/L]).(12) IIS was defined as an insulinogenic index r51.”
MethodDeakin, S., Leviev, I., Nicaud, V., Brulhart‐Meynet, M., Tiret, L., & James, R. W. (2002) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.87.3.1268 · Cited by 35
Insulin secretion: mechanism of the stimulation by glucose
Cerasi, E. (1975) · Quarterly Reviews of Biophysics · doi:10.1017/s0033583500001281 · Cited by 35
Steady State Plasma Insulin Response to Continuous Glucose Infusion in Normal and Diabetic Subjects
Reaven, G. M., Farquhar, J. W., & Nakanishi, R. H. (1969) · Diabetes · doi:10.2337/diab.18.5.273 · Cited by 34
Oral Glucose Tolerance Curve and Hypoglycemias in the Fed State
Freinkel, N., & Metzger, B. E. (1969) · New England Journal of Medicine · doi:10.1056/nejm196904102801508 · Cited by 35
Gastric Operations and Glucose Homeostasis
Breuer, R. I., Moses, H., Hagen, T. C., & Zuckerman, L. (1972) · Gastroenterology · doi:10.1016/s0016-5085(72)80078-7 · Cited by 35
Reproducibility and discrimination of different indices of insulin sensitivity and insulin secretion
Hudak, S., Huber, P., Lamprinou, A., Fritsche, L., Stefan, N., Peter, A., Birkenfeld, A. L., Fritsche, A., Heni, M., & Wagner, R. J. (2021) · PLoS ONE · doi:10.1371/journal.pone.0258476 · Cited by 34
“php OGTT OGIS 0, 90, 120 Glucose, Insulin, height, body weight, glucose dose [g] f ðG0;G90;G120; I0; I90;D0Þ whereby f is a complex function which can be programmed on a spreadsheet[30] Belfiore 0(, 60), 120 Glucose, Insulin 2 ðAUCInsulin�AUCGlucoseÞþ1”
Michishita, R., Shono, N., Kasahara, T., & Tsuruta, T. (2008) · Diabetes Research and Clinical Practice · doi:10.1016/j.diabres.2008.08.013 · Cited by 34
Okura, T., Ueta, E., Nakamura, R., Fujioka, Y., Sumi, K., Matsumoto, K., Shoji, K., Matsuzawa, K., Izawa, S., Nomi, Y., et al. (2017) · Journal of Diabetes Research · doi:10.1155/2017/5139750 · Cited by 34
“As IGI and ISI were developed from OGTTs, we propose that differences between consuming a test meal and a pure glucose load may also affect glucose and insulin levels.”
InfluentialHumphrey, C. S., Dykes, J. R. W., & Johnston, D. (1975) · BMJ · doi:10.1136/bmj.2.5963.112 · Cited by 34
Iselius, L., Lindsten, J., Morton, N. E., Efendiź, S., Cerasi, E., Haegermark, A., & Luft, R. (1982) · Clinical Genetics · doi:10.1111/j.1399-0004.1982.tb01432.x · Cited by 34
Hormonal genesis of glucose intolerance following hypoglycemia
Mintz, D. H., Finster, J. L., Taylor, A. L., & Fefer, A. (1968) · The American Journal of Medicine · doi:10.1016/0002-9343(68)90037-5 · Cited by 34
Diabetes Remission After LRYGBP With and Without Fundus Resection: a Randomized Clinical Trial
Kehagias, D., Lampropoulos, C., Georgopoulos, N. A., Habeos, I. G., Kalavrizioti, D., Vamvakas, S. M., Davoulou, P., & Kehagias, I. (2023) · Obesity Surgery · doi:10.1007/s11695-023-06857-z · Cited by 35
“Both phases were improved postoperatively in the two groups, leading to recovered b-cell function and significant increase of insuli-nogenic index ( p 0.05) [29].”
BackgroundInfluentialThe enteral insulin-stimulation after pancreas transplantation in the pig
Jensen, S. L., Nielsen, O. V., & K�hl, C. (1976) · Diabetologia · doi:10.1007/bf01220640 · Cited by 33
Kuo, P. T., & Feng, L. Y. (1970) · Metabolism · doi:10.1016/0026-0495(70)90134-4 · Cited by 33
Brodovicz, K. G., Girman, C. J., Simonis-Bik, A. M. C., Rijkelijkhuizen, J. M., Zelis, M., Bunck, M. C. M., Mari, A., Nijpels, G., Eekhoff, E. M. W., & Dekker, J. M. (2011) · Diabetes Research and Clinical Practice · doi:10.1016/j.diabres.2011.09.002 · Cited by 32
Bradley, S. J., Kingwell, B. A., Canny, B. J., & McConell, G. K. (2007) · Metabolism · doi:10.1016/j.metabol.2007.06.003 · Cited by 32
Davis, S. N., Piatti, P., Monti, L., Brown, M. D., Branch, W. J., Hales, C. N., & Alberti, K. G. M. M. (1993) · Metabolism · doi:10.1016/0026-0495(93)90168-n · Cited by 32
Hecht, A., Gershberg, H., & Hulse, M. (1973) · Metabolism · doi:10.1016/0026-0495(73)90244-8 · Cited by 32
Devices for the control of diabetes mellitus
Albisser, A. M. (1979) · Proceedings of the IEEE · doi:10.1109/proc.1979.11448 · Cited by 33
Mo, Y., Ma, X., Li, H., Ran, X., Yang, W., Li, Q., Peng, Y., Li, Y., Gao, X., Luan, X., et al. (2016) · Diabetes Research and Clinical Practice · doi:10.1016/j.diabres.2016.03.003 · Cited by 31
Wang, Y., Wang, P., Qin, L., Ganmaa, D., Kaneko, T., Xu, J., Murata, S., Katoh, R., & Sato, A. (2003) · Endocrine · doi:10.1385/endo:22:2:85 · Cited by 31
Burned Adults Develop Profound Glucose Intolerance
Rehou, S., Mason, S. A., Burnett, M., & Jeschke, M. G. (2016) · Critical Care Medicine · doi:10.1097/ccm.0000000000001605 · Cited by 31
“The insulinogenic index (IGI): (δ insulin [0–30 min] [μU/mL]/δ glucose [0–30 min] [mg/dL]) (14).”
Albisser, A. M., & LEIBEL, B. S. (1977) · Clinics in Endocrinology and Metabolism · doi:10.1016/s0300-595x(77)80047-9 · Cited by 31
Insulin secretion and body composition in obesity
El-Khodary, A. Z., Ball, M. F., Oweiss, I. M., & Canary, J. J. (1972) · Metabolism · doi:10.1016/0026-0495(72)90088-1 · Cited by 31
CAN DIET BE RESPONSIBLE FOR THE INITIAL LESION IN DIABETES ?
Wapnick, S., Kanengoni, E., Wicks, A. C. B., & Jones, J. J. (1972) · The Lancet · doi:10.1016/s0140-6736(72)92906-6 · Cited by 31
Sulfonylurea Signal Transduction
BOYD, A. E., Aguilar‐Bryan, L., Bryan, J., Kunze, D. L., Moss, L. G., Nelson, D. A., Rajan, A. S., Raef, H., XIANG, H., & Yaney, G. C. (1991) · Elsevier eBooks · doi:10.1016/b978-0-12-571147-0.50013-5 · Cited by 30
Jung, K. Y., Kim, K. M., Ku, E. J., Kim, Y. J., Lee, D.-H., Choi, S. H., Jang, H. C., Shin, C. S., Park, K. S., & Lim, S. K. (2015) · Osteoporosis International · doi:10.1007/s00198-015-3315-7 · Cited by 30
“The insulinogenic index (IGI), as an indicator of early-phase insulin release, was calculated according to the following formula: (30-min insulin− fasting insulin)/(30-min glucose−fasting glucose) [21].”
MethodChen, C.-Y., Rasmussen, H., Kamil, A., Du, P., & Blumberg, J. B. (2017) · Nutrients · doi:10.3390/nu9020130 · Cited by 30
“The insulinogenic index (IGI) was also calculated using the formula (insulint=30 − insulint=0)/(glucoset=30 − glucoset=0) [20], but the values were not different between the three study beverages.”
MethodHofeldt, F. D., Dippe, S. E., & Forsham, P. H. (1972) · American Journal of Clinical Nutrition · doi:10.1093/ajcn/25.11.1193 · Cited by 30
Islet Changes in Human Diabetes
Gepts, W. (1981) · Elsevier eBooks · doi:10.1016/b978-0-12-187820-7.50019-x · Cited by 30
Glipizide versus tolbutamide, an open trial
Fineberg, S. E., & Schneider, S. H. (1980) · Diabetologia · doi:10.1007/bf01228302 · Cited by 30
Glucose and Insulin Secretory Response Patterns Following Diet and Tolazamide Therapy in Diabetes
Turtle, J. R. (1970) · BMJ · doi:10.1136/bmj.3.5723.606 · Cited by 30
Pontiroli, A. E., Pizzocri, P., Caumo, A., Perseghin, G., & Luzi, L. (2004) · Acta Diabetologica · doi:10.1007/s00592-004-0147-x · Cited by 29
“By introducing ∆G as part of the ∆I/∆G at 60 min, we emphasise the response of insulin as a function of current glucose levels [18].”
MethodLim, S. K., Han, K. A., Yu, J., Chamnan, P., Kim, E. S., Yoon, K., Kwon, S. H., Moon, M. K., Lee, K. W., Kim, D., et al. (2016) · Diabetes Obesity and Metabolism · doi:10.1111/dom.12787 · Cited by 29
“The insulinogenic index was calculated at 30 minutes (IGI30) and 60 minutes (IGI60) using the following equation: [30 or 60minutes insulin − fasting insulin]/[30 or 60-minutes glucose − fasting glucose].(14) The disposition index, which reflects β-cell function adjusted for insulin sensitivity, was calculated as IGI ×…”
MethodKim, G., Oh, S. W., Jin, S., Hur, K. Y., Kim, J. H., & Lee, M. (2017) · Expert Opinion on Pharmacotherapy · doi:10.1080/14656566.2017.1353080 · Cited by 30
“5], and [post-load 60 min insulin − fasting insulin (μIU/mL)] /[post-load 60 min glucose – fasting glucose (mmol/L)], respectively [25,26].”
BackgroundENHANCEMENT OF GLUCOSE-STIMULATED INSULIN RELEASE BY AN INTESTINAL POLYPEPTIDE IN RATS
Turner, D. S., & Marks, V. (1972) · The Lancet · doi:10.1016/s0140-6736(72)91431-6 · Cited by 29
Glucose disappearance rate in rhesus monkeys: Some technical considerations
Jen, K.-L. C., & HANSEN, B. C. (1988) · American Journal of Primatology · doi:10.1002/ajp.1350140206 · Cited by 29
GORDON, E. S. (1970) · Advances in metabolic disorders · doi:10.1016/b978-0-12-027304-1.50012-0 · Cited by 29
Osanai, H., Kanayama, H., Miyazaki, Y., Fukushima, A., Shinoda, M., & Ito, T. (1998) · The American Journal of Cardiology · doi:10.1016/s0002-9149(97)01021-7 · Cited by 29
The mechanism of insulin secretion after oral glucose administration
Fischer, U., Hommel, H., ZIEGLER, M., & Jutzi, E. (1972) · Diabetologia · doi:10.1007/bf01212164 · Cited by 29
Drenick, E. J., Brickman, A. S., & Gold, E. M. (1972) · American Journal of Clinical Nutrition · doi:10.1093/ajcn/25.8.746 · Cited by 29
Nowak, C., Salihović, S., Ganna, A., Brandmaier, S., Tukiainen, T., Broeckling, C. D., Magnusson, P. K. E., Prenni, J. E., Wang‐Sattler, R., Peters, A., et al. (2016) · PLoS Genetics · doi:10.1371/journal.pgen.1006379 · Cited by 29
“At the 5% false discovery rate (FDR), 47, 15, and zero metabolites were associated with clamp M/I, log-DI and log-IGI30, respectively (Fig 2, S1 Table).”
BackgroundMethodInfluentialSuzuki, K., Nakagawa, O., & Aizawa, Y. (2008) · Clinical and Experimental Hypertension · doi:10.1080/10641960802269927 · Cited by 28
Stéphan, F., Reville, P., Thierry, R., & Schlienger, J.-L. (1972) · Diabetologia · doi:10.1007/bf01212261 · Cited by 28
The Influence of Rare Genetic Variation in SLC30A8 on Diabetes Incidence and β-Cell Function
Billings, L. K., Jablonski, K. A., Ackerman, R. J., Taylor, A., Fanelli, R. R., McAteer, J. B., Guiducci, C., Delahanty, L. M., Dabelea, D., Kahn, S. E., et al. (2014) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2013-2378 · Cited by 27
Harder, M. N., Appel, E. V. R., Grarup, N., Gjesing, A. P., Ahluwalia, T. S., Jørgensen, T., Christensen, C., Brandslund, I., Linneberg, A. R., Sørensen, T. I. A., et al. (2015) · PLoS ONE · doi:10.1371/journal.pone.0120890 · Cited by 27
Metadata
- Authors
- Seltzer, H. S., Allen, E. W., Herron, A. L., & Brennan, M. T.
- Affiliations
- United States Department of Veterans Affairs (US)
- Venue
- Journal of Clinical Investigation
- Published
- 1967-03-01
- Volume
- 46
- Issue
- 3
- Pages
- 323-335
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC297053
- OpenAlex
- W2110124224
- Semantic Scholar
- 886c6609c46718fd9d260ed280e4e8b81313135e
- Cited by
- 819
- References
- 30
- Citations by year
- 2026: 12 · 2025: 12 · 2024: 26 · 2023: 15 · 2022: 16 · 2021: 18 · 2020: 18 · 2019: 13 · 2018: 26 · 2017: 25 · 2016: 24 · 2015: 18 · 2014: 25 · 2013: 24 · 2012: 10
- FWCI
- 90.80
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (submittedVersion)
- Funders
- National Institutes of Health
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
- Keywords
- insulin secretion, carbohydrate intolerance, oral glucose tolerance, intravenous glucose tolerance, hyperinsulinemia, hyperglycemia, obesity, insulinogenic index
- MeSH terms
- Adult, Aged, Blood Glucose, Body Weight, Diabetes Mellitus, Female, Glucose, Glucose Tolerance Test, Humans, Insulin, Male, Middle Aged, Obesity, Carbohydrate Metabolism
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-10-14, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-14 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
