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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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43 Own result · 15 Sources not found · 10 Own interpretation · 7 No basis given · 3 Own method · 1 Not checked yet
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“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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“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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“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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“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
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“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 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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“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 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 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 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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“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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“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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“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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“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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“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 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 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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“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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“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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“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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“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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“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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“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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“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 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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“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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“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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None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“Current work has narrowed the active substance down to glucagon (22), secretin (23-25), or pancreozymin (26).”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Discussion
What the sources say
- Not matchedcites [22]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [23]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [24]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [25]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [26]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not matched
In the paper
“the interpretation in- voked by Seltzer, Fajans, and Conn (3), that the occurrence of symptomatic postprandial hypogly- cemia in patients with mild diabetes mellitus might be due to delayed initial release of insulin followed by subsequent excessive hormonal secretion”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Introduction
What the sources say
- Not matchedcites Seltzer, Fajans, and Conn (3)
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
hedgedconditional- Asserted: fails — The authors may not put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The authors may not put it forward as true.
- Not matched
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“An acute rise or fall of blood glucose level directly induces an increase or decrease, respec- tively, of insulin release (1, 2, 8, 9).”
§ Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohy- drate Intolerance in Mild Diabetes Mellitus * > Methods
What the sources say
- Not matchedcites [1]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [2]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [8]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [9]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably 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
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably 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.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably 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.
boosted- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably 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
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably 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.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably 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
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably 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.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably 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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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.
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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
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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
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Cited by
Sorted by citations
Items 101–200 of 818
Fu, M., Shen, W., Gao, W., Namujia, L., Yang, X., Cao, J., & Sun, L. (2021) · Bioorganic Chemistry · doi:10.1016/j.bioorg.2021.105235 · Cited by 81
Insulin Sensitivity and β-Cell Function in Women With Polycystic Ovary Syndrome
Vrbíková, J., Bendlová, B., Hill, M., Vaňková, M., Vondra, K., & Stárka, L. (2002) · Diabetes Care · doi:10.2337/diacare.25.7.1217 · Cited by 81
Holdsworth, C. D., & Besser, G. M. (1968) · The Lancet · doi:10.1016/s0140-6736(68)90747-2 · Cited by 80
Treviño, S., Waalkes, M. P., Hernández, J. A. F., León‐Chávez, B. A., Aguilar‐Alonso, P., & Brambila, E. (2015) · Archives of Biochemistry and Biophysics · doi:10.1016/j.abb.2015.07.010 · Cited by 82
Hyperinsulinism and polycystic ovary syndrome (PCOS): role of insulin clearance
Amato, M. C., Vesco, R., Vigneri, E., Ciresi, A., & Giordano, C. S. D. S. (2015) · Journal of Endocrinological Investigation · doi:10.1007/s40618-015-0372-x · Cited by 84
“β-cell function was determined by fasting insulin, Insulinogenic Index (the ratio of the incremental insulin concentration to the incremental glucose concentration at the 30 min sample) [27] and the AUC2h Insulin during OGTT.”
MethodHashimoto, K., Ikewaki, K., Yagi, H., Nagasawa, H., Imamoto, S., Shibata, T., & Mochizuki, S. (2005) · Diabetes Care · doi:10.2337/diacare.28.5.1182 · Cited by 79
“Family history 35 (26) 23 (32) 7 (14) 5 (38) 0.”
BackgroundChu, P.-C., CONWAY, M. J., KROUSE, H. A., & Goodner, C. J. (1968) · Annals of Internal Medicine · doi:10.7326/0003-4819-68-4-757 · Cited by 79
β-Cell failure in type 2 diabetes
Leibowitz, G., Kaiser, N., & Cerasi, E. (2011) · Journal of Diabetes Investigation · doi:10.1111/j.2040-1124.2010.00094.x · Cited by 78
Characteristic features of insulin secretion in the streptozotocin-induced NIDDM rat model
Tsuji, K., Taminato, T., Usami, M., Ishida, H., Kitano, N., Fukumoto, H., Koh, G., Kurose, T., Yamada, Y., Yano, H., et al. (1988) · Metabolism · doi:10.1016/0026-0495(88)90064-9 · Cited by 76
McMonagle, J. R., & Felig, P. (1975) · Metabolism · doi:10.1016/0026-0495(75)90142-0 · Cited by 78
Mechanisms of insulin resistance in man
Rizza, R. A., Mandarino, L. J., & Gerich, J. E. (1981) · The American Journal of Medicine · doi:10.1016/0002-9343(81)90423-x · Cited by 79
Gastric inhibitory polypeptide (GIP) and insulin release after small-bowel resection in man
Lauritsen, K. B., Moody, A. J., Christensen, K. C., & Lindkár Jensen, S. (1980) · Scandinavian Journal of Gastroenterology · doi:10.3109/00365528009181538 · Cited by 77
Lee, W.-J., Chong, K., Chen, C.-Y., Chen, S. C., Lee, Y. C., Ser, K., & Chuang, L. (2011) · Obesity Surgery · doi:10.1007/s11695-011-0401-6 · Cited by 77
“Early insulin secreting response to specific glycemic response was measured by “ insulinogenic index” (Ii) [19].”
MethodMeier, J. J., Gallwitz, B., Askenas, M., Vollmer, K., Deacon, C. F., Holst, J. J., Schmidt, W. E., & Nauck, M. A. (2005) · Diabetologia · doi:10.1007/s00125-005-1863-7 · Cited by 77
“tion in response to oral glucose stimulation [22].”
BackgroundAcute and steady-state insulin responses to glucose in nonobese diabetic subjects
Lerner, R. L., & Porte, D. (1972) · Journal of Clinical Investigation · doi:10.1172/jci106963 · Cited by 76
Wagner, R. J., Jaghutriz, B. A., Gerst, F., Oquendo, M. B., Machann, J., Schick, F., Loeffler, M. W., Nadalin, S., Fend, F., Königsrainer, A., et al. (2020) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/clinem/dgaa435 · Cited by 76
“Insulin secretion was measured from stimulated insulin and C-peptide levels using the insulinogenic index (13) and area under the curve (AUC)-C-peptide0-30/AUC-glucose0-30.”
MethodMoreira‐Lucas, T., Duncan, A. M., RABASA-LHORET, R. P. R., Vieth, R., Gibbs, A. L., Badawi, A. F., & Wolever, T. M. S. (2016) · Diabetes Obesity and Metabolism · doi:10.1111/dom.12794 · Cited by 76
“The IGI was calculated by dividing the rise in insulin by the rise in glucose from 0 to 30 minutes (ΔI0 − 30/ΔG0 − 30).(19) ISSI-2 is defined as the ratio of the insulin AUC to the glucose AUC multiplied by the Matsuda index.”
MethodThe Effect of Rate and Dose of Glucose Infusion on the Acute Insulin Response in Man
CHEN, M., & Porte, D. (1976) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jcem-42-6-1168 · Cited by 75
The Role of Carbohydrates in Appetite, Hunger and Obesity
Geiselman, P. J., & Novin, D. (1982) · Appetite · doi:10.1016/s0195-6663(82)80017-2 · Cited by 77
Kacerovsky-Bielesz, G., Chmelik, M., Ling, C., Pokan, R., Szendroedi, J., Farukuoye, M., Kacerovsky, M., Schmid, A. I., Gruber, S., Wolzt, M., et al. (2009) · Diabetes · doi:10.2337/db08-1240 · Cited by 75
Diabetes in the Undernourished: Coincidence or Consequence?
Rao, R. H. (1988) · Endocrine Reviews · doi:10.1210/edrv-9-1-67 · Cited by 75
Insulin Secretion in Diabetes Mellitus
KIPNIS, D. M. (1968) · Annals of Internal Medicine · doi:10.7326/0003-4819-69-5-891 · Cited by 76
The significance and interpretation of mildly abnormal oral glucose tolerance
ALFORD, F. P., Martin, P. I. R., & Pearson, M. J. (1971) · Diabetologia · doi:10.1007/bf01212550 · Cited by 75
Kruszynska, Y. T., Harry, D. S., Bergman, R. N., & McIntyre, N. (1993) · Diabetologia · doi:10.1007/bf00400692 · Cited by 71
“glucose [ 34 , 35] as well as to oral glucose [34, 36, 37].”
BackgroundScott, R. C. (1975) · American Heart Journal · doi:10.1016/0002-8703(75)90314-2 · Cited by 71
BAIRD, J. D. (1973) · Proceedings of The Nutrition Society · doi:10.1079/pns19730040 · Cited by 71
Boden, G., Soeldner, J. S., Gleason, R. E., & Marble, A. (1968) · Journal of Clinical Investigation · doi:10.1172/jci105768 · Cited by 71
Miettinen, T. A., Taskinen, M., Pelkonen, R., & Nikkilä, E. A. (1969) · Acta Medica Scandinavica · doi:10.1111/j.0954-6820.1969.tb01473.x · Cited by 70
Nonsense mutation of glucokinase gene in late-onset non-insulin-dependent diabetes mellitus
Katagiri, H., Asano, T., Ishihara, H., Inukai, K., Anai, M., Yazaki, Y., Oka, Y., & Miyazaki, J. (1992) · The Lancet · doi:10.1016/0140-6736(92)92494-z · Cited by 68
Tse, T. F., Clutter, W. E., Shah, S. D., Miller, J. P., & Cryer, P. E. (1983) · Journal of Clinical Investigation · doi:10.1172/jci110966 · Cited by 68
Endogeneous Insulin and Growth Hormone Response in Children with Newly Diagnosed Diabetes Mellitus
DRASH, A. L., Field, J. B., Garces, L. Y., Kenny, F. M., Mintz, D. H., & Vazquez, A. M. (1968) · Pediatric Research · doi:10.1203/00006450-196803000-00004 · Cited by 68
Kinoshita, Y., Fujii, H., Takeshita, A., Taguchi, M., Miyakawa, M., Oyama, K., Yamada, S., & Takeuchi, Y. (2011) · European Journal of Endocrinology · doi:10.1530/eje-10-1096 · Cited by 68
Kim, J. D., Kang, S. J., Lee, M. K., Park, S. E., Rhee, E., Park, C., Oh, K. W., Park, S. W., & Lee, W. (2016) · Endocrinology and Metabolism · doi:10.3803/enm.2016.31.2.320 · Cited by 70
Insulin levels in thyrotoxicosis and primary myxoedema: Response to intravenous glucose and glucagon
Andreani, D., Menzinger, G., Fallucca, F., et al. (1970) · Diabetologia · doi:10.1007/bf00425884 · Cited by 66
INSULIN EXCESS AS THE INITIAL LESION IN DIABETES
Jackson, W. P. U., Mieghem, W. V., & Keller, P. (1972) · The Lancet · doi:10.1016/s0140-6736(72)91221-4 · Cited by 66
Chirakalwasan, N., Amnakkittikul, S., Wanitcharoenkul, E., Charoensri, S., Saetung, S., Chanprasertyothin, S., Chailurkit, L., Panburana, P., Bumrungphuet, S., Thakkinstian, A., et al. (2018) · Journal of Clinical Sleep Medicine · doi:10.5664/jcsm.6972 · Cited by 70
“…and insulin sensitivity as obtained from MTT. Homeostatic model assessment of insulin resistance (an index of fasting insulin resistance), 29 the insulinogenic index (an estimate of early insulin secretion), 30 and the Matsuda index (an index of whole body insulin sensitivity) 31 were calculated.”
Effects of Two-Week Sleep Extension on Glucose Metabolism in Chronically Sleep-Deprived Individuals
So-ngern, A., Chirakalwasan, N., Saetung, S., Chanprasertyothin, S., Thakkinstian, A., & Reutrakul, S. (2019) · Journal of Clinical Sleep Medicine · doi:10.5664/jcsm.7758 · Cited by 69
Effects of meal size and composition on incretin, α-cell, and β-cell responses
Rijkelijkhuizen, J. M., McQuarrie, K., Girman, C. J., Stein, P. P., Mari, A., Holst, J. J., Nijpels, G., & Dekker, J. M. (2009) · Metabolism · doi:10.1016/j.metabol.2009.07.039 · Cited by 67
Suzuki, H., Fukushima, M., Usami, M., Ikeda, M., Taniguchi, A., Nakai, Y., Matsuura, T., Kuroe, A., Yasuda, K., Kurose, T., et al. (2003) · Diabetes Care · doi:10.2337/diacare.26.4.1211 · Cited by 65
“As the index of insulin secretion, we used the insulinogenic index, the change in the ratio of insulin to glucose level during the first 30 min of OGTT (30-min insulin level fasting insulin)/(30-min PG FPG) (15,16).”
MethodRaverdy, V., Baud, G., Pigeyre, M., Verkindt, H., Torres, F., Preda, C., Thuillier, D., Gelé, P., Vantyghem, M., Caiazzo, R. J., et al. (2016) · Annals of Surgery · doi:10.1097/sla.0000000000001915 · Cited by 69
“HOMA2 B and HOMA2 S was calculated using the HOMA2 calculator version 2.2.3 to assess insulin resistance from the mean baseline levels of glucose and insulin a s described by Levy et al. 30 yBeta-cell mass was assessed by the fasting c-peptide to fasting glucose ratio as described by Meier et al.31 zPost prandial beta…”
MethodInfluentialAssociation of Insulin Gene VNTR Polymorphism with Polycystic Ovary Syndrome
Vaňková, M., Vrbíková, J., Hill, M., Cinek, O., & Bendlová, B. (2002) · Annals of the New York Academy of Sciences · doi:10.1111/j.1749-6632.2002.tb04317.x · Cited by 65
Insulin Resistance and Insulin Receptors in Hepatic Cirrhosis
Blei, A. T., Robbins, D. C., DROBNY, E. C., Baumann, G. P., & Rubenstein, A. H. (1982) · Gastroenterology · doi:10.1016/s0016-5085(82)80127-3 · Cited by 64
Biosynthetic human growth hormone in burned patients: a pilot study
BELCHER, H. J. C. R., Mercer, D., Judkins, K. C., Shalaby, S., Wise, S., Marks, V., & Tanner, N. S. B. (1989) · Burns · doi:10.1016/0305-4179(89)90138-1 · Cited by 65
Insulin Resistance and Human Disease: A Short History
Reaven, G. M. (1998) · Journal of Basic and Clinical Physiology and Pharmacology · doi:10.1515/jbcpp.1998.9.2-4.387 · Cited by 65
Normalization of plasma insulin profiles with intraperitoneal insulin infusion in diabetic man
Schade, D. S., Eaton, R. P., Friedman, N. M., et al. (1980) · Diabetologia · doi:10.1007/bf00258308 · Cited by 64
“for assessing insulin availability [11].”
MethodTHE BASAL PLASMA GLUCOSE: A SIMPLE RELEVANT INDEX OF MATURITY‐ONSET DIABETES
HOLMAN, R. R., & TURNER, R. C. (1981) · Clinical Endocrinology · doi:10.1111/j.1365-2265.1981.tb00196.x · Cited by 64
Hulman, A., Vistisen, D., Glümer, C., Bergman, M., Witte, D. R., & Færch, K. (2018) · Diabetologia · doi:10.1007/s00125-017-4468-z · Cited by 60
Dietary acid load, insulin sensitivity and risk of type 2 diabetes in community-dwelling older men
Xu, H., Jia, T., Huang, X., Risérus, U., Cederholm, T., Ärnlöv, J., Sjögren, P., Lindholm, B., & Carrero, J. J. (2014) · Diabetologia · doi:10.1007/s00125-014-3275-z · Cited by 63
“The Insulinogenic Index (IGI) for beta cell function was calculated using the following formula: IGI=(insulin30 min− insulin0 min)/ (glucose30 min−glucose0 min) [20].”
MethodComparison of Algorithms for the Closed-Loop Control of Blood Glucose Using the Artificial Beta Cell
Broekhuyse, H. M., Nelson, H. D., Zinman, B., & Albisser, A. M. (1981) · IEEE Transactions on Biomedical Engineering · doi:10.1109/tbme.1981.324661 · Cited by 61
The β Cell in Diabetes: Integrating Biomarkers With Functional Measures
Kahn, S. E., Chen, Y., Esser, N., Taylor, A. J., van Raalte, D. H., Zraika, S., & Verchere, C. B. (2021) · Endocrine Reviews · doi:10.1210/endrev/bnab021 · Cited by 75
“While in the beginning, oral glucose ingestion formed the basis of estimating insulin responses (473, 474), it was not long after that it was demonstrated that intravenous glucose elicited insulin responses that could also be used to address how the β cell was performing (477, 508).”
BackgroundMethodCarbohydrate metabolism in lichen planus
Lowe, N. J., Cudworth, A. G., CLOUGH, S. A., et al. (1976) · British Journal of Dermatology · doi:10.1111/j.1365-2133.1976.tb15530.x · Cited by 62
Glycemic control is impaired in the evening in prediabetes through multiple diurnal rhythms
Sonnier, T. J., Rood, J., Gimble, J. M., & Peterson, C. M. (2014) · Journal of Diabetes and its Complications · doi:10.1016/j.jdiacomp.2014.04.001 · Cited by 62
Cho, H., Kumar, S., Yang, D., Vaidyanathan, S. R., Woo, K., Garcia, I., Shue, H. J., Yoon, Y.-Z., Ferreri, K., & Choo, H. (2018) · ACS Sensors · doi:10.1021/acssensors.7b00864 · Cited by 63
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9Carbohydrate metabolism in trauma
Wilmore, D. W. (1976) · Clinics in Endocrinology and Metabolism · doi:10.1016/s0300-595x(76)80048-5 · Cited by 62
Glucose Intolerance in Hyperthyroidism: Role of Glucagon
Kabadi, U. M., & Eisenstein, A. B. (1980) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jcem-50-2-392 · Cited by 60
Newcomer, J. W., Ratner, R. E., Eriksson, J. W., Emsley, R. A., Meulien, D., Miller, F., Leonova-Edlund, J., Leong, R. W., & Brecher, M. (2009) · The Journal of Clinical Psychiatry · doi:10.4088/jcp.08m04132 · Cited by 62
Tharakan, G., Behary, P., Albrechtsen, N. J. W., Chahal, H., Kenkre, J. S., Miras, A. D., Ahmed, A. R., Holst, J. J., Bloom, S. R., & Tan, T. (2017) · European Journal of Endocrinology · doi:10.1530/eje-17-0446 · Cited by 65
“The insulinogenic index was calculated as the ratio of incremental insulin concentration to glucose concentration at 30 min (22).”
Emptying of the Gastric Substitute After Total Gastrectomy
Miholic, J., Meyer, H.-J., Kotzerke, J., et al. (1989) · Annals of Surgery · doi:10.1097/00000658-198908000-00005 · Cited by 61
The metabolism of circulating maltose in man
Young, S. J. M., & Weser, E. (1971) · Journal of Clinical Investigation · doi:10.1172/jci106592 · Cited by 60
Kosáka, K., Hagura, R., Kuzuya, T., & Kuzuya, N. (1974) · Diabetologia · doi:10.1007/bf01219540 · Cited by 60
“Diabetologia 10, 775--782 (1974) 9 by Springer-Verlag 1974”
Ma, R.-L., Deng, Y., Wang, Y.-F., Zhu, S.-Y., Ding, X.-S., & Sun, A.-J. (2021) · Chinese Medical Journal · doi:10.1097/cm9.0000000000001712 · Cited by 90
“Matsuda index = 10,000/square root of ([fasting glucose (mg/dL) fasting insulin (mIU/L)] [mean glucose mean insulin]).([18])”
BackgroundQian, J., Yeh, B., Rakshit, K., Colwell, C. S., & Matveyenko, A. V. (2015) · Endocrinology · doi:10.1210/en.2015-1516 · Cited by 61
Mari, A., Tura, A., Pacini, G., Kautzky‐Willer, A., & Ferrannini, E. (2008) · Diabetic Medicine · doi:10.1111/j.1464-5491.2008.02441.x · Cited by 59
Zhang, J., Xing, C., Cheng, X., & He, B. (2022) · Frontiers in Endocrinology · doi:10.3389/fendo.2022.1003238 · Cited by 60
“The AUCIns/ AUCGlu ratio is relevant to pancreatic beta-cell dysfunction and the incidence of diabetes (48).”
Backgroundβ-Cell preservation with thiazolidinediones
Campbell, I. W., & Mariz, S. (2006) · Diabetes Research and Clinical Practice · doi:10.1016/j.diabres.2006.08.015 · Cited by 57
Early insulin responses to glucose and to tolbutamide in maturity-onset diabetes
Varsano-Aharon, N., Echemendia, E., Yalow, R. S., & Berson, S. A. (1970) · Metabolism · doi:10.1016/0026-0495(70)90092-2 · Cited by 58
Li, J., Kaneko, T., Qin, L., Wang, J., Wang, Y., & Sato, A. (2003) · Metabolism · doi:10.1016/s0026-0495(03)00159-8 · Cited by 57
Chung, J. O., Cho, D. H., Chung, D. J., & Chung, M. Y. (2012) · The Korean Journal of Internal Medicine · doi:10.3904/kjim.2012.27.1.66 · Cited by 57
“The indices of insulin secretion and insulin resistance were calculated as follows [10-13]:”
MethodWhat is a Normal Glucose Value?
Piché, M., Arcand-Bossé, J.-F., Després, J., Përusse, L., Lemieux, S., & Weisnagel, S. J. (2004) · Diabetes Care · doi:10.2337/diacare.27.10.2470 · Cited by 57
Liu, P., Chang, Y., Jiang, Y., Chen, W. J., Chang, T., Kuo, S., Lee, K., Hsiao, P., Chiu, K. C., & Chuang, L. (2009) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2009-0609 · Cited by 57
“The insulinogenic index was calculated as [insulin at 30 min insulin at 0 min (pmol/liter)]/[glucose at 30 min glucose at 0 min (mmol/liter)] (17).”
MethodChouinard-Castonguay, S., Weisnagel, S. J., Tchernof, A., & Robitaille, J. (2013) · European Journal of Endocrinology · doi:10.1530/eje-12-0939 · Cited by 57
Han, S. J., Kim, H. J., Kim, D. J., Lee, K. W., & Cho, N. H. (2016) · Diabetes Research and Clinical Practice · doi:10.1016/j.diabres.2016.10.004 · Cited by 57
Cholinergic Modification of Glucose-Induced Biphasic Insulin Release in Vitro
Sharp, R. A., Culbert, S. J., Cook, J., Jennings, A. S., & Burr, I. M. (1974) · Journal of Clinical Investigation · doi:10.1172/jci107609 · Cited by 54
Matveyenko, A. V., Veldhuis, J. D., & Butler, P. C. (2008) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.90451.2008 · Cited by 54
Yen, S. S. C., TSAI, C. C., & Vela, P. (1971) · American Journal of Obstetrics and Gynecology · doi:10.1016/0002-9378(71)90490-x · Cited by 54
Sato, Y., Nishikawa, M., Shinkai, H., & Sukegawa, E. (1991) · Diabetes Research and Clinical Practice · doi:10.1016/0168-8227(91)90130-6 · Cited by 54
Cockburn, B. N., Bermano, G., Boodram, L.-L. G., Teelucksingh, S., Tsuchiya, T., Mahabir, D., Allan, A. B., Stein, R. W., Docherty, K., & Bell, G. I. (2004) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2003-031282 · Cited by 55
Cho, N. H., Oh, T. J., Kim, K. M., Choi, S. H., Lee, J. H., Park, K. S., Jang, H. C., Kim, J. Y., Lee, H. K., & Lim, S. K. (2015) · Scientific Reports · doi:10.1038/srep18565 · Cited by 53
Todd, J. F., Edwards, C. M. B., Ghatei, M. A., Mather, H. M., & Bloom, S. R. (1998) · Clinical Science · doi:10.1042/cs0950325 · Cited by 53
Mechanisms of starvation diabetes: a study with double tracer and indirect calorimetry
Féry, F., D’Attellis, N., & Balasse, E. O. (1990) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.1990.259.6.e770 · Cited by 54
Noori, M., Davoodi, A., Iraji, A., Dastyafteh, N., Khalili, M., Asadi, M., Mohammadi‐Khanaposhtani, M., Mojtabavi, S., Dianatpour, M., Faramarzi, M. A., et al. (2022) · Scientific Reports · doi:10.1038/s41598-022-18455-7 · Cited by 55
Is there a Delay in the Plasma Insulin Response of Patients with Chemical Diabetes Mellitus?
Reaven, G. M., Shen, S.-W., Silvers, A., & Farquhar, J. W. (1971) · Diabetes · doi:10.2337/diab.20.6.416 · Cited by 52
Stauffacher, W., Orci, L., Cameron, D. P., Burr, I. M., & Renold, A. E. (1971) · Elsevier eBooks · doi:10.1016/b978-0-12-571127-2.50026-2 · Cited by 52
Oh, T. J., Lim, S. K., Kim, K. M., Moon, J. H., Choi, S. H., Cho, Y. M., Park, K. S., Jang, H. C., & Cho, N. H. (2016) · Clinical Endocrinology · doi:10.1111/cen.13280 · Cited by 51
INSULIN RATHER THAN GLUCOSE HOM$OElig;OSTASIS IN THE PATHOPHYSIOLOGY OF DIABETES
TURNER, R. (1976) · The Lancet · doi:10.1016/s0140-6736(76)91739-6 · Cited by 51
Hofeldt, F. D. (1975) · Metabolism · doi:10.1016/0026-0495(75)90156-0 · Cited by 50
Itou, M., Kawaguchi, T., Taniguchi, E., et al. (2007) · Journal of Gastroenterology and Hepatology · doi:10.1111/j.1440-1746.2007.05183.x · Cited by 50
Diabetes mellitus and sexual ateliotic dwarfism: a comparative study
Merimée, T. J., Fineberg, S. E., McKusick, V. A., et al. (1970) · Journal of Clinical Investigation · doi:10.1172/jci106325 · Cited by 50
The mechanism of insulin secretion after oral glucose administration
Hommel, H., & Fischer, U. (1977) · Diabetologia · doi:10.1007/bf01219711 · Cited by 50
Cho, N. H., Kim, K. M., Choi, S. H., Park, K. S., Jang, H. C., Kim, S. S., Sattar, N. A., & Lim, S. K. (2015) · Diabetes Care · doi:10.2337/dc14-1931 · Cited by 49
“The insulinogenic index (IGI), which is an estimate of early insulin secretion, was calculated by dividing the increase in insulin during the first 60 min by the increase in glucose during the same period, as follows: 60–0 min insulin (in international units per milliliter)/60–0 min glucose (in millmoles per liter) (2…”
MethodOverproduction of insulin in the chromium-deficient rat
Striffler, J. S., Polansky, M. M., & Anderson, R. A. (1999) · Metabolism · doi:10.1016/s0026-0495(99)90207-x · Cited by 49
Meyre, D., Boutin, P., Tounian, A., Deweirder, M., Aout, M., Jouret, B., Heude, B., Weill, J., Tauber, M., Tounian, P., et al. (2005) · Journal of Clinical Endocrinology and Metabolism · doi:10.1210/jc.2004-1468 · Cited by 58
Godoy-Parejo, C., Deng, C., Liu, W., & Chen, G. (2019) · Stem Cells · doi:10.1002/stem.3026 · Cited by 48
Measurement of pulsatile insulin secretion in the rat: direct sampling from the hepatic portal vein
Matveyenko, A. V., Veldhuis, J. D., & Butler, P. C. (2008) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.90335.2008 · Cited by 47
“Since the latter constitutes the majority of insulin secretion, it is not surprising that insulin secretion is therefore deficient in type 2 diabetes mellitus (20, 29, 32) and is restored to normal if the insulin secretory burst mass is restored (11).”
BackgroundPatterns of insulin response to glucose in protein-calorie malnutrition
Becker, D. J., Pimstone, B. L., HANSEN, J. D. L., Machutchon, B., & Drysdale, A. (1972) · American Journal of Clinical Nutrition · doi:10.1093/ajcn/25.5.499 · Cited by 48
“too � This abnormal pattern has been described in a number of other disorders including maturity-onset diabetes ( 8-10 ), obesity (17, 18), acute starvation (19, 20), and liver disease (21, 22).”
BackgroundInfluentialEffects of Nonglucose Nutrients on Insulin Secretion and Action in People With Pre-Diabetes
Bock, G., Man, C. D., Campioni, M., Chittilapilly, E. G., Basu, R., TOFFOLO, G. M., Cobelli, C., & Rizza, R. A. (2007) · Diabetes · doi:10.2337/db06-1272 · Cited by 50
“It has been long known that even a minimal elevation in plasma glucose concentration is associated with a decreased -cell response to glucose (30,31).”
BackgroundHyperglycemia with Relative Hypoinsulinemia in Diphenylhydantoin Toxicity
Peters, B. H., & Samaan, N. A. (1969) · New England Journal of Medicine · doi:10.1056/nejm196907102810208 · Cited by 47
Martínez‐Sánchez, F. D., Vargas-Abonce, V. P., Guerrero-Castillo, A. P., Santos-Villavicencio, M. D. L., Eseiza-Acevedo, J., Meza-Arana, C. E., Gulías-Herrero, A., & Gómez-Sámano, M. Á. (2020) · Primary care diabetes · doi:10.1016/j.pcd.2020.10.006 · Cited by 48
Gumbiner, B., Cauter, E. V., Beltz, W. F., Ditzler, T. M., Griver, K., Polonsky, K. S., & Henry, R. R. (1996) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jcem.81.6.8964829 · Cited by 46
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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