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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
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 801–818 of 818
Ryang, S., Kim, J., Kim, M., Im, M., Kim, D., Kim, J. M., Yi, W., Jang, M. H., Kim, Y. J., Kang, H., et al. (2024) · SSRN Electronic Journal · doi:10.2139/ssrn.5070283
Yamashita, A., Kaku, M., Ideguchi, T., Nishida, S., Kinoshita, H., & Nishikawa, T. (2025) · Endocrine Journal · doi:10.1507/endocrj.ej24-0486 · Cited by 1
Au/Go Based Partially Uncladded SMF for Detection of Glucose Concentration
Fauzi, N. S., Mukhtar, W. M., Halim, R. M., et al. (2025) · Applied Mechanics and Materials · doi:10.4028/p-4lw10j
“To maintain blood sugar concentration following ingesting carbohydrate, the body requires insulin, produced and released from the B-(or b) cells of the pancreas, to transport glucose into cells for subsequent metabolism [2].”
InfluentialYamashita, A., Kaku, M., Matsunaga, M., Inoue, S., Arizono, K., Ideguchi, T., Watanabe, T., Nishida, S., & Nishikawa, T. (2025) · Diabetes Research and Clinical Practice · doi:10.1016/j.diabres.2025.112930
Li, J. H., Szczerbiński, Ł., Tripputi, M., Liu, H., Nam, S., Mújica, E., Emmanouilidou, A., Wangden, T. Y., Citko, A., Konopka, P., et al. (2025) · medRxiv · doi:10.1101/2025.10.07.25336827
Steger, F. L., Donnelly, J. E., Montgomery, R. N., Clark, L., Martin, C. K., Miles, J. M., Grdinovac, K., Henderson, A. E., & Thyfault, J. P. (2025) · Contemporary Clinical Trials · doi:10.1016/j.cct.2025.108118
“We will calculate the insulinogenic index to assess early-phase insulin secretion [44], and the Matsuda Index to estimate whole body insulin sensitivity [45].”
Protective Role of Serum β-Hydroxybutyrate in Early Diabetic Kidney Disease: A Longitudinal Study
Kim, S. R., Lee, M. Y., Lee, Y., Kang, E. S., Soo, B., & Lee, B. (2025) · Diabetes Therapy · doi:10.1007/s13300-025-01819-3
Das Wachstumshormon und die Entwicklung der diabetischen Gefäßkrankheit
Cerasi, E., & Luft, R. (1975) · Springer eBooks · doi:10.1007/978-3-642-66033-7_17
腹部中〓穴 (CV12) への鍼通電刺激が経静脈糖負荷試験および Hyperinsulinemic Euglycemic Clamp 時の糖消費に及ぼす効果
石崎直人, 矢野, 忠., & 山村, 義. (2006) · Medical Entomology and Zoology · doi:10.11390/onki1962.69.109
Clinical investigation on abnormal glucose tolerance in liver cirrhosis
Kato, K., Kikuchi, S., & Ito, M. (1976) · Gastroenterologia Japonica · doi:10.1007/bf02775448
Kim, D., Kim, J., Im, M., Ryang, S., Kim, M., Kim, Y. J., Kim, I. J., Kim, Y. K., Kang, H., Chung, S. T., et al. (2026) · Frontiers in Endocrinology · doi:10.3389/fendo.2025.1726006
Blood glucose homeostasis in patients with mild to moderate Spinocerebellar Ataxia type 2Preprint
Aguilera‐Rodríguez, R., Almaguer‐Gotay, D., Sosa, A. Á., Anidos-Machado, M., Silva-Ricardo, Y., Cuello‐Almarales, D., Estupiñán‐Rodríguez, A., & Almaguer‐Mederos, L. E. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.01.25.701567
“Additionally, the insulinogenic index (IGI) (78), Stumvoll phase 1 (PH1) and 2 (PH2) (77), and the ratio of the area under the curve for insulin from 0 to 120 minutes to the area under the curve for glucose from 0 to 120 minutes (AUC-i/g) (76), were used as surrogate markers of insulin secretion.”
Ryang, S., Kim, J., Kim, M., Im, M., Kim, D., Kim, Y. J., Kang, H., Kim, Y. J., Kim, I. J., Chung, S. T., et al. (2026) · Diabetes Research and Clinical Practice · doi:10.1016/j.diabres.2026.113131
Yang, M. A., Pu, F., Guo, Y., Yang, Y., Tang, R., Luo, Y., Li, Q., & Fan, Y. (2026) · Diabetes Research and Clinical Practice · doi:10.1016/j.diabres.2026.113221 · Cited by 2
Ludwig, M. S., Heck, T. G., Minguetti‐Câmara, V. C., Schroeder, H. T., Muller, C. H. D. L., Bittencourt, A., Scomazzon, S. P., Bruxel, M. A., Porto, R. R., Bandeira, B. B., et al. (2026) · Cell Stress and Chaperones · doi:10.1016/j.cstres.2026.100180
“123,124 For the conversion of insulin to SI units, we assumed 5807.57 g/mol, 125 so that 1 μU = 5.975 fmol e 1 μU/mL = 5.975 pmol/L ( ≈ 6 pM).”
InfluentialAguilera‐Rodríguez, R., Almaguer‐Gotay, D., Sosa, A. Á., Anidos-Machado, M., Silva-Ricardo, Y., Cuello‐Almarales, D., Estupiñán‐Rodríguez, A., & Almaguer‐Mederos, L. E. (2026) · The Cerebellum · doi:10.1007/s12311-026-02076-1
“Additionally, the insulinogenic index (IGI) [79], Stumvoll phase 1 (PH1) and 2 (PH2) [78], and the ratio of the area under the curve for insulin from 0 to 120 min to the area under the curve for glucose from 0 to 120 min (AUC-i/g) [ 77], were used as surrogate markers of insulin secretion.”
Andersson-Hall, U. K., Kristiansson, E., Åberg, S., Törnqvist, M., Wallenius, K., Sengpiel, V., & Holmäng, A. B. (2026) · Journal of Diabetes Research · doi:10.1155/jdr/7103883
Dosaggio radioimmunologico dell’insulina (IRI): Metodo di calcolo con elaboratore elettronico
Ghidini, O., Bistaffa, R., Marabini, A., et al. (1972) · La Ricerca in Clinica e in Laboratorio · doi:10.1007/bf03054783
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.
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