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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
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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).
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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
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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
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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
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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.
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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
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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
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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
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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
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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
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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
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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
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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
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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
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“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
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“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
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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
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“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
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“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
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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
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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
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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
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“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
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“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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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]
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- Not matchedcites [26]
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- 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)
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- Not matched
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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
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Cited by
Sorted by citations
Items 401–500 of 818
Preexercise Carbohydrate Ingestion and Transient Hypoglycemia: Fasting versus Feeding
KONDO, S., Tanisawa, K., Suzuki, K., Terada, S., & Higuchi, M. (2018) · Medicine & Science in Sports & Exercise · doi:10.1249/mss.0000000000001773 · Cited by 17
Human Physiology of Genetic Defects Causing Beta-cell Dysfunction
Kettunen, J. L. T., & Tuomilehto, J. (2020) · Journal of Molecular Biology · doi:10.1016/j.jmb.2019.12.038 · Cited by 18
“Dinsulin Dglucose 1⁄4 insulinðat 30 Þ insulinðat fastingÞ glucoseðat 300 Þ glucoseðat fastingÞ [30], 30-min values occasionally substituted by 60-min values) and corrected insulin response (CIR30 or CIR120, insulin1⁄2mU=mL ðresponse; usually at 30=1200Þ 100 glucose1⁄2mg=dl ðresponse; usually at 300=1200Þ 70 1⁄4 insuli…”
Aynsley-Green, A., & Alberti, K. G. M. M. (1973) · Diabetologia · doi:10.1007/bf01225998 · Cited by 17
Postoperative Glucose Metabolism in Diabetic and Nondiabetic Patients
Lindseth, R. E. (1972) · Archives of Surgery · doi:10.1001/archsurg.1972.04180110064016 · Cited by 17
Lee, H.-O., Yim, J., Kim, Y.-S., & Choue, R. (2014) · Nutrition Research and Practice · doi:10.4162/nrp.2014.8.4.469 · Cited by 16
“After calorie restriction, weight, body fat percentage, hip circumference, BP, TC, HDL-C, LDL-C, plasma glucose at fasting, insulin at fasting and 120 min, AUCglu and the insulin area under the curve all decreased significantly (all P 0.05), while insulin sensitivity (HOMA-IR, QUICKI and Matsuda index) measured by OGT…”
BackgroundInfluentialKobayashi, Y., Kawaguchi, Y., Mizuta, T., Kuwashiro, T., Oeda, S., Oza, N., Takahashi, K., Iwane, S., Eguchi, Y., Anzai, K., et al. (2010) · Journal of Gastroenterology · doi:10.1007/s00535-010-0338-x · Cited by 16
“The insulinogenic index (II) [ 24 ], a marker of earlyphase insulin secretion, was calculated as (SI30 - FSI)/ (PG30 - FPG).”
MethodComplement C3 Is the Strongest Predictor of Whole-Body Insulin Sensitivity in Psoriatic Arthritis
Ursini, F., D’Angelo, S., Russo, E., Nicolosi, K., Gallucci, A., Chiaravalloti, A., Bruno, C., Naty, S., Sarro, G. D., Olivieri, I., et al. (2016) · PLoS ONE · doi:10.1371/journal.pone.0163464 · Cited by 16
Huard, B., Bridgewater, A., & Angelova, M. N. (2017) · Journal of Theoretical Biology · doi:10.1016/j.jtbi.2017.01.039 · Cited by 17
“In T2DM, it is well known that this initial release is reduced [32] (for a more in-depth look at the dynamics of insulin secretion, see [31]).”
BackgroundMurata, M., Adachi, H., Oshima, S., & Kurabayashi, M. (2017) · Diabetes Research and Clinical Practice · doi:10.1016/j.diabres.2017.07.007 · Cited by 17
“5 h] − fasting plasma glucose [mg/dL]) [24].”
Fat feeding potentiates the diabetogenic effect of dexamethasone in Wistar rats
Sivabalan, S., Renuka, S., & Menon, V. P. (2008) · International Archives of Medicine · doi:10.1186/1755-7682-1-7 · Cited by 17
Li, M., Qureshi, A. R., Ellis, E. C. S., & Axelsson, J. (2013) · Nephrology Dialysis Transplantation · doi:10.1093/ndt/gft337 · Cited by 17
“The homoeostasis model assessment of insulin resistance (HOMA-IR) and early phase insulin secretion (insulinogenic index) were calculated as described [10].”
MethodGodoy‐Matos, A. F., Valério, C. M., Moreira, R. O., Momesso, D., & Bittencourt, L. K. (2018) · Diabetology & Metabolic Syndrome · doi:10.1186/s13098-018-0375-9 · Cited by 17
Temple, K. A., Tjaden, A. H., Atkinson, K. M., Barengolts, E., Hannon, T. S., Mather, K. J., Utzschneider, K. M., Edelstein, S. L., Ehrmann, D. A., Mokhlesi, B., et al. (2019) · Diabetes Care · doi:10.2337/dc19-0538 · Cited by 16
“The C-peptide index (CPI) (DC-peptide0–30/Dglucose0–30) and insulinogenic index (IGI) (Dinsulin0–30/ Dglucose0–30) were calculated using the 0- and 30-min samples from the OGTT (21,22).”
MethodKakutani‐Hatayama, M., Kadoya, M., Morimoto, A., Miyoshi, A., Kosaka‐Hamamoto, K., Kusunoki, Y., Shoji, T., & Koyama, H. (2020) · Metabolism Open · doi:10.1016/j.metop.2020.100033 · Cited by 16
“The following indices were calculated in this study: Insulinogenic index 1⁄4 (IRI30 pmol/L-IRI0 pmol/L)/(Glu30 mmol/L e Glu0 mmol/ L) [30], corrected insulin response (CIR) 1⁄4 [(100 IRI30 pmol/L)/ (Glu30 mmol/L) (Glu30 mmol/L - 3.”
Yoshimura, K., Hirano, S., Takata, H., Funakoshi, S., Ohmi, S., Amano, E., Nishi, Y., Inoue, M., Fukuda, Y., Hayashi, H., et al. (2017) · Journal of Diabetes Investigation · doi:10.1111/jdi.12622 · Cited by 16
Rehfeld, J. F., Juhl, E., & Hilden, M. (1973) · PubMed · Cited by 16
Nordlander, S., Östman, J., Cerasi, E., Luft, R., & Ekelund, L. (1973) · Acta Medica Scandinavica · doi:10.1111/j.0954-6820.1973.tb10532.x · Cited by 16
The significance of an increased RQ after sucrose ingestion during prolonged aerobic exercise
Benad�, A. J. S., JANSEN, C. R., Rogers, G. G., Wyndham, C. H., & Strydom, N. B. (1973) · Pflügers Archiv - European Journal of Physiology · doi:10.1007/bf00591368 · Cited by 16
“This implies tha t the effect of the increased concentration of insulin in the blood reported after sucrose ingestion [4,10,11,13] was to enhance the uptake of glucose mainly derived from the ingested sucrose.”
BackgroundDynamics of Insulin Secretion in Early Diabetes in Humans
Yalow, R. S., & Berson, S. A. (1970) · Elsevier eBooks · doi:10.1016/b978-0-12-027361-4.50017-x · Cited by 16
Effect of Age on Intravenous Glucose Tolerance and Insulin Secretion*
Feldman, J. M., & Plonk, J. W. (1976) · Journal of the American Geriatrics Society · doi:10.1111/j.1532-5415.1976.tb03245.x · Cited by 16
“For each IVGTT, the cumulative insulin output per unit of secretory stimulus (“the insulinogenic index” or AI/AG) was calculated from 0 to 60 minutes (9).”
MethodNormalization effect of preceding protein meals on "diabetic" oral glucose tolerance in Eskimos.
Schæfer, O., Crockford, P. M., & Romanowski, B. (1972) · PubMed Central · Cited by 16
Hormonal and metabolic disturbances during acute and subacute myocardial infarction in man
Boden, G. (1971) · Diabetologia · doi:10.1007/bf01219479 · Cited by 15
Ohkura, T., Inoue, K., Fujioka, Y., Nakanishi, R., Shiochi, H., Sumi, K., Yamamoto, N., Matsuzawa, K., Izawa, S., Ohkura, H., et al. (2013) · BMC Research Notes · doi:10.1186/1756-0500-6-453 · Cited by 14
“Insulinogenic Index = [(insulin at 30 min) - (insulin at 0 min)]/[(glucose at 30 min) - (glucose at 0 min)] [13].”
O'Connor, S. E., Julien, P., Weisnagel, S. J., Gagnon, C., & Rudkowska, I. (2019) · Current Developments in Nutrition · doi:10.1093/cdn/nzz083 · Cited by 20
“Insulin sensitivity from the OGTT was assessed using the Matsuda index: 10,000/ {[fasting glucose (mmol/L) × fasting insulin (pmol/L)] × [mean glucose OGTT (mmol/L) × mean insulin OGTT (pmol/L)]} (4).”
BackgroundMethodInfluentialInsulin secretory capacity and insulin sensitivity in impaired fasting glucose in Japanese
Mitsui, R., Fukushima, M., Taniguchi, A., Nakai, Y., Aoyama, S., Takahashi, Y., Tsuji, H., Yabe, D., Yasuda, K., Kurose, T., et al. (2012) · Journal of Diabetes Investigation · doi:10.1111/j.2040-1124.2012.00201.x · Cited by 15
Two Japanese infants with congenital generalized lipodystrophy due to BSCL2 mutations
Nishiyama, A., Yagi, M., Awano, H., Okizuka, Y., Maeda, T., Yoshida, S., Takeshima, Y., & Matsuo, M. (2009) · Pediatrics International · doi:10.1111/j.1442-200x.2009.02863.x · Cited by 15
Elder, D. A., Woo, J. G., & D’Alessio, D. A. (2009) · Pediatric Diabetes · doi:10.1111/j.1399-5448.2009.00601.x · Cited by 14
“This differs with the classic descriptions of β-cell function in adults with type 2 diabetes in whom the insulin response to oral glucose is lower (13–15) and in whom firstphase insulin secretion in response to glucose is nearly absent (15, 16).”
BackgroundBan, Y., Koba, S., Tsunoda, F., Yokota, Y., Ezumi, H., Kondo, T., Suzuki, H., & Katagiri, T. (2006) · Circulation Journal · doi:10.1253/circj.70.393 · Cited by 15
Heterogeneity of insulin secretion in type II diabetes
Fajans, S. S. (1986) · Diabetes/Metabolism Reviews · doi:10.1002/dmr.5610020308 · Cited by 15
Interrelationships of insulin, glucose, lipid and anthropometric data in a natural population
Gibson, T. C., Horton, E., & Whorton, E. B. (1975) · American Journal of Clinical Nutrition · doi:10.1093/ajcn/28.12.1387 · Cited by 15
Sugiyama, K., Yonemura, Y., & Okamoto, H. (1991) · International Journal of Pancreatology · doi:10.1007/bf02930227 · Cited by 15
“Total insulin, insulinogenic index, and total insulinogenic index were calculated according to Seltzer et al. ( 9 ,10).”
MethodCarbohydrate tolerance in the very aged
Smith, M. J., & Hall, M. R. P. (1973) · Diabetologia · doi:10.1007/bf01239433 · Cited by 15
Rosselin, G., Claude, J., Eschwège, É., Patois, E., Warnet, J., & Richard, J. L. (1971) · Diabetologia · doi:10.1007/bf02346252 · Cited by 15
Baronio, F., Mazzanti, L., Girtler, Y., Tamburrino, F., Fazzi, A., Lupi, F., Longhi, S., & Radetti, G. (2016) · Hormone Research in Paediatrics · doi:10.1159/000448841 · Cited by 14
Swauger, S. E., Hornung, L. N., Elder, D. A., Balamurugan, A. N., Vitale, D. S., Lin, T. K., Nathan, J. D., & Abu‐El‐Haija, M. A. (2022) · Diabetes Care · doi:10.2337/dc21-1222 · Cited by 14
Poomthavorn, P., Nantarakchaikul, P., Mahachoklertwattana, P., Chailurkit, L., & Khlairit, P. (2013) · Clinical Endocrinology · doi:10.1111/cen.12337 · Cited by 14
Insulin secretion and carbohydrate metabolism in experimental protein malnutrition
Khardori, R. K., Bajaj, J. S., Deo, M. G., et al. (1980) · Journal of Endocrinological Investigation · doi:10.1007/bf03348275 · Cited by 14
Radetti, G., Grugni, G., Lupi, F., Marazzi, N., Longhi, S., Fanolla, A., & Sartório, A. (2017) · Journal of Endocrinological Investigation · doi:10.1007/s40618-017-0705-z · Cited by 15
Hansson, S., Zhou, A., Vachet, P., Eriksson, J. W., Pereira, M. J., Skrtic, S., Wallin, H. J., Ericsson‐Dahlstrand, A., Karlsson, D., Ahnmark, A., et al. (2018) · PLoS ONE · doi:10.1371/journal.pone.0196601 · Cited by 14
Factors responsible for elevation of 1-h postchallenge plasma glucose levels in Japanese men
Harada, N., Fukushima, M., Toyoda, K., Mitsui, R., Izuka, T., Taniguchi, A., Nakai, Y., Yamada, Y., Seino, Y., & Inagaki, N. (2008) · Diabetes Research and Clinical Practice · doi:10.1016/j.diabres.2008.04.011 · Cited by 15
“were evaluated by insulinogenic index [23] and ISI composite [24,25].”
BackgroundMethodOhmi, S., Ono, M., Takata, H., Hirano, S., Funakoshi, S., Nishi, Y., Yoshimura, K., Amano, E., Terada, Y., Saibara, T., et al. (2017) · Diabetology & Metabolic Syndrome · doi:10.1186/s13098-017-0264-7 · Cited by 15
“As insulin secretion indices, insulinogenic index (IGI) and HOMA-β were calculated using the following formula [10, 11]: IGI: [I30 − I0 (pmol/L)]/ [G30 − G0 (mmol/L)]; HOMA-β: I0 (μU/mL) × 20/[G0 (mmol/L) − 3.”
Glucoregulatory disorders in school refusal students
Iwatani, N., Miike, T., Kai, Y., Kodama, M., Mabe, H., Tomoda, A., Fukuda, K., & Jodoi, T. (1997) · Clinical Endocrinology · doi:10.1046/j.1365-2265.1997.2191095.x · Cited by 14
Burr, I. M., TAFT, H. P., Stauffacher, W., & Renold, A. E. (1971) · Annals of the New York Academy of Sciences · doi:10.1111/j.1749-6632.1971.tb45253.x · Cited by 14
Insulin Secretion in Diabetes Mellitus
Cerasi, E. (1988) · Springer eBooks · doi:10.1007/978-3-642-72691-0_11 · Cited by 14
Tripolt, N. J., Hofer, S. J., Pferschy, P. N., Aziz, F., Durand, S., Aprahamian, F., Nirmalathasan, N., Waltenstorfer, M., Eisenberg, T., Obermayer, A. M., et al. (2023) · Nutrients · doi:10.3390/nu15030511 · Cited by 16
“and the ratio of the incremental insulin (Ins30) to glucose response (Glc30) over the first 30 min during the OGTT ∆Ins30/∆Glc30 [17].”
BackgroundInfluentialSato, H., Ishikawa, A., Yoshioka, H., et al. (2024) · Scientific Reports · doi:10.1038/s41598-024-76256-6 · Cited by 13
Sanctis, V. D., Soliman, A. T., Tzoulis, P., Daar, S., Karimi, M., Yassin, M. A., Pozzobon, G. C., & KATTAMIS, C. A. (2022) · Acta bio-medica dell'Ateneo parmense/Acta biomedica · doi:10.23750/abm.v92i6.12366 · Cited by 18
Garvey, W. T., Cohen, R. M., Butera, N. M., Kazemi, E. J., Younes, N., Rosin, S. P., Suratt, C. E., Ahmann, A., Hollander, P. A., Krakoff, J. A., et al. (2024) · Diabetes Care · doi:10.2337/dc23-1782 · Cited by 14
Colombo, C., Alicandro, G., Gambazza, S., et al. (2018) · Pediatric Pulmonology · doi:10.1002/ppul.24212 · Cited by 13
“tion at 30min minus fasting insulin to the difference in glucose at the same time points.(23) The insulinogenic index was also computed by using C-peptide concentrations.”
MethodLee, J.-E., Oh, T. J., Moon, J. H., Park, K. S., Jang, H. C., & Choi, S. H. (2019) · Frontiers in Endocrinology · doi:10.3389/fendo.2019.00043 · Cited by 14
Estimation of β-cell function from the data of the oral glucose tolerance test
Sakaue, S., 石丸伸司, Ikeda, D., Ohtsuka, Y., Honda, T., Suzuki, J.-I., Kawakami, Y., Ishii, J., & Nishimura, M. (2007) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00341.2006 · Cited by 13
“As a surrogate of AIR, the insulinogenic index [IGI, the increment of serum insulin level divided by the increment of plasma glucose (PG) level for the first 30 min of the oral glucose tolerance test (OGTT)] (19) has been also used, because the IGI is correlated with AIR (10, 17).”
MethodThe response to intravenous glucose of patients on maintenance hemodialysis: Effects of dialysis
Ferrannini, E., PILO, A., & Tuoni, M. (1979) · Metabolism · doi:10.1016/0026-0495(79)90077-5 · Cited by 13
Normal glucose, insulin, and growth hormone responses to oral glucose in Huntington's disease
Davidson, M. B., Green, S. A., & Menkes, J. H. (1974) · Journal of Laboratory and Clinical Medicine · doi:10.5555/uri:pii:0022214374901784 · Cited by 13
Neuropeptides in the Control of the Islets of Langerhans
Wood, S. M., Polak, J. M., & Bloom, S. R. (1983) · Advances in metabolic disorders · doi:10.1016/b978-0-12-027310-2.50021-9 · Cited by 13
Kin, S., STEPHANIAN, E., Gores, P. F., et al. (1992) · Journal of Surgical Research · doi:10.1016/0022-4804(92)90132-j · Cited by 13
Hormonal and metabolic disturbances during acute and subacute myocardial infarction in man
Boden, G. (1971) · Diabetologia · doi:10.1007/bf01211875 · Cited by 13
F�rster, H., Haslbeck, M., Geser, C. A., & Mehnert, H. (1970) · Diabetologia · doi:10.1007/bf01211888 · Cited by 13
Stinson, S. E., Alzola, I. F. D. R., Hovendal, E. D. B., Lund, M. A. V., Fonvig, C. E., Holm, L. A., Jonsson, A. E., Frithioff‐Bøjsøe, C., Christiansen, M., Pedersen, O. B., et al. (2023) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/clinem/dgad728 · Cited by 12
“The insulinogenic index (IGI) was calculated as (insulin 30 – insulin 0 )/(glucose 30 – glucose 0 ) (29), which has been shown to correlate with acute insulin response (30).”
MethodWagner, R. J., Hieronimus, A., Lamprinou, A., Heni, M., Hatziagelaki, E. E., Ullrich, S., Stefan, N., Staiger, H., Häring, H., & Fritsche, A. (2014) · Molecular Metabolism · doi:10.1016/j.molmet.2014.07.001 · Cited by 12
“in 1967 [13], and has been since then validated several times as a reliable measure of insulin secretion utilizing insulin and glucose measurements during the first 30 min of an OGTT [14,15].”
β cell function and insulin resistance in lean cases with polycystic ovary syndrome
Pande, A. K., Guleria, A., Singh, S. D., Shukla, M. K., & Dabadghao, P. (2017) · Gynecological Endocrinology · doi:10.1080/09513590.2017.1342165 · Cited by 12
“The homeostasis model assessment Insulin resistance index (HOMA-IR), QUICKI Matsuda index, [8] homeostasis model assessment b cell function (HOMA-B) [9], Disposition index [10], area under the curve during OGTT for glucose (AUCglu) and insulin (AUCins), [11] and free androgen index (FAI) were calculated as before [12]…”
MethodSanctis, V. D., Soliman, A. T., Tzoulis, P., Daar, S., Maio, S. D., Fiscina, B., & KATTAMIS, C. A. (2021) · Mediterranean Journal of Hematology and Infectious Diseases · doi:10.4084/mjhid.2021.051 · Cited by 15
“Calculations of variables: a) Insulin secretion index: For the evaluation of acutephase serum insulin response, during OGTT, the insulinogenic index (IGI) was calculated as the incremental change in insulin concentration during the first 30 min of the OGTT divided by the incremental change in glucose during the same p…”
MethodEarly impaired β-cell function in chinese women with polycystic ovary syndrome.
Tao, T., Li, S., Zhao, A., Mao, X., & Liu, W. (2012) · Europe PMC (PubMed Central) · Cited by 12
Impairment of Glucose Tolerance in Normal Adults Following a Lowered Carbohydrate Intake.
Wang, P.-Y., Kaneko, T., Wang, Y., et al. (1999) · The Tohoku Journal of Experimental Medicine · doi:10.1620/tjem.189.59 · Cited by 12
The heritability of beta cell function parameters in a mixed meal test design
Simonis-Bik, A. M. C., Boomsma, D. I., Dekker, J. M., Diamant, M., de Geus, E. J. C., Hart, L. M. ‘., Heine, R. J., Kramer, M. H. H., Maassen, J. A., Mari, A., et al. (2011) · Diabetologia · doi:10.1007/s00125-011-2060-5 · Cited by 12
“The insulinogenic index is a classically calculated estimate of early insulin response in OGTT, described as early as 1967 [22].”
BackgroundHou, X., Chen, P., Hu, G., Wei, L., Jiao, L., Wang, H., Liang, Y., Bao, Y., & Jia, W. (2018) · Obesity · doi:10.1002/oby.22183 · Cited by 14
“Assessment of beta-cell function based on OGTT test Early-phase insulin secretion was evaluated using the insulinogenic index (14), the ratio of incremental insulin to incremental glucose responses during the first 30 minutes of the OGTT (Ins30 2 Ins0 / Gluc30 2 Gluc0).”
MethodEarly-phase insulin secretion is disturbed in obese subjects with glucose intolerance
Mizuno, A., Arai, H., Fukaya, M., Sato, M., Yamanaka-Okumura, H., Takeda, E., & Doi, T. (2007) · Metabolism · doi:10.1016/j.metabol.2007.01.017 · Cited by 12
“Several studies have reported that incretin action is usually disturbed in patients with type 2 DM [19,20].”
BackgroundMori, Y., KITAHARA, Y., Miura, K., Mine, T., & Tajima, N. (2004) · Diabetes Obesity and Metabolism · doi:10.1111/j.1462-8902.2004.00367.x · Cited by 12
Olefsky, J. M., Batchelder, T., Farquhar, J. W., & Reaven, G. M. (1973) · Metabolism · doi:10.1016/0026-0495(73)90273-4 · Cited by 11
The initial distribution volume of glucose and cardiac output after haemorrhage in dogs
Shimodate, Y., Ishihara, H., & Matsuki, A. (1994) · Canadian Journal of Anesthesia/Journal canadien d anesthésie · doi:10.1007/bf03009842 · Cited by 12
Hales, C. N. (1967) · The Lancet · doi:10.1016/s0140-6736(67)92008-9 · Cited by 12
Metabolic basis of human atherosclerosis
Kuo, P. T. (1969) · Metabolism · doi:10.1016/0026-0495(69)90075-4 · Cited by 12
Zöllner, N., & Heuckenkamp, P. U. (1970) · Research in Experimental Medicine · doi:10.1007/bf02044685 · Cited by 12
Zhu, Y., Lin, S., Zhang, Y., Yu, J., Fu, J., Li, Y., Shan, C., Cai, J., Liu, W. X., & Tao, T. (2024) · Scientific Reports · doi:10.1038/s41598-024-77645-7 · Cited by 13
“…determined using the following formula: HOMA-IR = insulin (mIU/L) × glucose (mmol/L) / 22.5 23 ; Insulinogenic Index = (Ins30– Ins0) / (Glu30–Glu0) 24 ; Deposition Index (DI) = Insulinogenic index / HOMA-IR 25 ; Matsuda Index (MI) = 10 000/square root of (fasting glucose × fasting insulin) ×…”
InfluentialTang, L., Tong, Y., Cao, H., Xie, S., Yang, Q., Zhang, F., Zhu, Q., Huang, L., Lu, Q., Yang, Y., et al. (2014) · Gene · doi:10.1016/j.gene.2014.06.028 · Cited by 11
Niakaris, K., Magkos, F., Geladas, N. D., & Sidossis, L. S. (2005) · Journal of Sports Sciences · doi:10.1080/02640410400023241 · Cited by 11
“Finally, the product of the areas under the glucose and insulin response curves (AUCG 6 AUCI), proposed by Levine and Haft (1970), as well as the ratio of insulin to glucose in the fasting state (I0/G0), referred to as the insulinogenic index by Seltzer et al. (1967), were also calculated.”
MethodBone Healing of Tooth Extraction Socket in Type 2 Diabetes
Sakai, D., Okazaki, J., & Komasa, Y. (2008) · Journal of oral tissue engineering · doi:10.11223/jarde.5.134 · Cited by 11
Benadé, A. J. S., Wyndham, C. H., JANSEN, C. R., Rogers, G. G., & Bruin, E. J. P. D. (1973) · Pflügers Archiv - European Journal of Physiology · doi:10.1007/bf00591369 · Cited by 11
Bagdade, J. D., Bierman, E. L., & Porte, D. (1971) · Metabolism · doi:10.1016/0026-0495(71)90022-9 · Cited by 11
On the pathogenesis of maturity-onset diabetes mellitus
Luft, R., & Efendić, S. (1978) · Acta Diabetologica · doi:10.1007/bf02581002 · Cited by 11
Johansen, K. (1973) · Acta Medica Scandinavica · doi:10.1111/j.0954-6820.1973.tb19424.x · Cited by 11
Insulin Sensitivity of Forearm Tissues in Prediabetic Man
Pozefsky, T., Santis, M. R., Soeldner, J. S., & Tancredi, R. G. (1973) · Journal of Clinical Investigation · doi:10.1172/jci107338 · Cited by 11
INSULIN RESERVE IN ELDERLY SUBJECTS
Joffe, B. I., Vinik, A. I., & Jackson, W. P. U. (1969) · The Lancet · doi:10.1016/s0140-6736(69)92226-0 · Cited by 11
STUDIES IN SUBJECTS WITH POSITIVE POSTPRANDIAL CLINISTIXr TEST
Lundquist, I., Nordén, Å., & Scherstén, B. (1970) · Acta Medica Scandinavica · doi:10.1111/j.0954-6820.1970.tb02927.x · Cited by 11
Significance of the Duodenum for Carbohydrate Metabolism in Patients After Total Gastrectomy
Bittner, R., & Beger, H. G. (1979) · Springer eBooks · doi:10.1007/978-3-642-67368-9_35 · Cited by 11
Rundle, M., Fiamoncini, J., Thomas, E. L., Wopereis, S., Afman, L. A., Brennan, L., Drevon, C. A., Gundersen, T. E., Daniel, H., Perez, I. G., et al. (2023) · American Journal of Clinical Nutrition · doi:10.1016/j.ajcnut.2023.07.002 · Cited by 11
“Insulin sensitivity indices such as HOMA-IR and HOMA for β -cell function (HOMA-β ), and Matsuda index (MI) were calculated [14 – 18].”
MethodUchida, J., Iwai, T., Kuwabara, N., Machida, Y., Iguchi, T., Naganuma, T., Kumada, N., Kawashima, H., & Nakatani, T. (2011) · Transplant Immunology · doi:10.1016/j.trim.2011.02.001 · Cited by 10
Wang, Y., Zhou, W., Wu, C., Zhang, Y., Lin, T.-C., Sun, Y. W., Liu, W. X., & Tao, T. (2018) · Reproductive Biology and Endocrinology · doi:10.1186/s12958-018-0331-4 · Cited by 10
“10,000/square root of [(fasting glucose x fasting insulin) x (mean glucose x mean insulin during OGTT)] [31].”
BackgroundPrior, S. L., Churm, R., Min, T., Dunseath, G. J., Barry, J. D., & Stephens, J. W. (2020) · Obesity Surgery · doi:10.1007/s11695-020-04457-9 · Cited by 10
Ma, N., Xu, N., Yin, D., Liu, W. W., Wu, M., & Cheng, X. (2020) · Medicine · doi:10.1097/md.0000000000020737 · Cited by 10
“The quantitative insulin check index (QUICKI) was calculated as an index of insulin sensitivity using the formula([13]) QUICKI=1 / [log10 fasting glucose (mg/dL)+ log10 fasting insulin (mIU/L)].”
MethodBrooks‐Worrell, B., Tjaden, A. H., Edelstein, S. L., PALOMINO, B. M., Utzschneider, K. M., Arslanian, S. A., Mather, K. J., Buchanan, T. A., Nadeau, K. J., Atkinson, K. M., et al. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.640251 · Cited by 11
Yoon, J. W., Jung, H. S., Jang, J. Y., Kim, M. J., Kim, J. H., Ohn, J. H., Kim, J. H., Lee, H. M., Kim, H., Lee, K. B., et al. (2014) · Cell Transplantation · doi:10.3727/096368914x682440 · Cited by 10
“As for the non-OAD group, preoperative OGTT 2-h glucose was lower than that of the OAD group (p 0.05).”
MethodInfluentialBistrian, B. R. (2011) · Critical Care Medicine · doi:10.1097/ccm.0b013e31820eb763 · Cited by 10
“However, could there be additional factors that differentiate parenteral from enteral feeding that would make hypoglycemia and blood glucose variability more likely with enteral feeding and perhaps serve in part to explain the very positive outcome in Van den Berghe’s surgical study that was not reproducible in subseq…”
BackgroundVigneault, J., Lemieux, S., Garneau, V., Weisnagel, S. J., Tchernof, A., & Robitaille, J. (2014) · Obesity · doi:10.1002/oby.20940 · Cited by 10
“Both obesity and GDM have been positively associated with maternal and neonatal outcomes, metabolic deteriorations, and important T2D risk factors (9,11-13).”
BackgroundMethodOhkura, T., Fujioka, Y., Sumi, K., Nakanishi, R., Shiochi, H., Yamamoto, N., Matsuzawa, K., Izawa, S., Ohkura, H., Kato, M., et al. (2014) · Diabetes Therapy · doi:10.1007/s13300-014-0071-1 · Cited by 10
“The insulinogenic index was calculated as previously described [23]: Insulinogenic index 1⁄4 insulin 1⁄2 f pmol=L ð Þ at 30 min insulin pmol= ð 1⁄2 LÞ at 0 min g= glucose 1⁄2 f mmol=L ð Þ at 30 min glucose mmol=L ð Þ at 0 min 1⁄2 g.”
Murai, N., Saito, N., Kodama, E., Iida, T., Mikura, K., Imai, H., Kaji, M., Hashizume, M., Kigawa, Y., Koizumi, G., et al. (2020) · Journal of the Endocrine Society · doi:10.1210/jendso/bvaa066 · Cited by 10
“7 doi: 10.1210/jendso/bvaa066 | Journal of the Endocrine Society | 1–12 Received 31 March 2020 Accepted 29 May 2020 First Published Online 5 June 2020 Corrected and Typeset 25 June 2020 Abbreviations: β, insulin secretion; BMI, body mass index; bpm, beats per minute; DBP, diastolic blood pressure; DM, diabetes mellitu…”
BackgroundMethodInfluentialKo, G. T.-C., Tong, P. C.-Y., So, W., et al. (2007) · Chinese Medical Journal · doi:10.1097/00029330-200712020-00015 · Cited by 10
Cigarette smoking as a dieting strategy in a university population
Klesges, R. C., & Klesges, L. M. (1988) · International Journal of Eating Disorders · doi:10.1002/1098-108x(198805)7:3 · Cited by 184
Biochemical Precursors of Atherosclerosis
Ostrander, L. D. (1974) · Archives of Internal Medicine · doi:10.1001/archinte.1974.00320200034003 · Cited by 10
Oral Hypoglycemic Agents and the Mechanism of Diabetes Mellitus
Davidoff, F. F. (1968) · New England Journal of Medicine · doi:10.1056/nejm196801182780306 · Cited by 10
Glucose Intolerance in Nonischemic Cardiac Disease
Ettinger, P. O., Oldewurtel, H. A., Dzindzio, B. S., Sethi, V., & Regan, T. J. (1971) · Circulation · doi:10.1161/01.cir.43.6.809 · Cited by 10
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
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