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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
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Cited by
Sorted by citations
Glucose clamp technique: a method for quantifying insulin secretion and resistance.
DeFronzo, R. A., Tobin, J. D., & Andres, R. (1979) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.1979.237.3.e214 · Cited by 7,425
“In order to relate the response of the beta-cell (as assessed by changes in plasma insulin concentration) to the everchanging stimulus of the plasma glucose concentration, the use of an “insulinogenic index” has been proposed and widely used (11, 15).”
BackgroundMethodReduced incretin effect in Type 2 (non-insulin dependent) diabetes
Nauck, M., Stöckmann, F., Ebert, R., & Creutzfeldt, W. (1986) · Diabetologia · doi:10.1007/bf02427280 · Cited by 1,307
Diabetogenic action of streptozotocin: relationship of dose to metabolic response
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“(11) in nonobese diabetics, using his "insulinogenic index," while Colwell and Lein have observed qualitatively and quantitatively almost identical alterations in prediabetic patients (25).”
MethodResultPlasma Insulin Responses to Oral and Intravenous Glucose: Studies in Normal and Diabetic Subjects*
Perley, M. J., & Kipnis, D. M. (1967) · Journal of Clinical Investigation · doi:10.1172/jci105685 · Cited by 917
“(24) and Cerasi and Luft (25) that insulin secretion is impaired in diabetes mellitus.”
BackgroundVelazquez, E. M., Mendoza, S., Hamer, T., Sosa, F., & Glueck, C. J. (1994) · Metabolism · doi:10.1016/0026-0495(94)90209-7 · Cited by 865
Ducimetière, P., Eschwège, É., Papoz, L., Richard, J. L., Claude, J., & Rosselin, G. (1980) · Diabetologia · doi:10.1007/bf00275270 · Cited by 746
“The insulin/glucose ratio has been proposed [26, 27] as a”
BackgroundDose-response characteristics for effects of insulin on production and utilization of glucose in man
Rizza, R. A., Mandarino, L. J., & Gerich, J. E. (1981) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.1981.240.6.e630 · Cited by 705
Bagdade, J. D., Bierman, E. L., & Porte, D. (1967) · Journal of Clinical Investigation · doi:10.1172/jci105646 · Cited by 672
“Discussion The elevation of basal (fasting) insulin levels found in obese subjects is in accord with other recent observations (9-13).”
ResultPhillips, D. I. W., Clark, P. M., Hales, C. N., & Osmond, C. (1994) · Diabetic Medicine · doi:10.1111/j.1464-5491.1994.tb00273.x · Cited by 631
Brunzell, J. D., Robertson, R. P., Lerner, R. L., Hazzard, W. R., Ensinck, J. W., Bierman, E. L., & Porte, D. (1976) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jcem-42-2-222 · Cited by 511
Chen, C., Cohrs, C. M., Stertmann, J., Bozsak, R., & Speier, S. (2017) · Molecular Metabolism · doi:10.1016/j.molmet.2017.06.019 · Cited by 506
Validation of the insulin sensitivity index (ISI0,120): comparison with other measures
Gutt, M., Davis, C. L., Spitzer, S. B., Llabre, M. M., Kumar, M., Czarnecki, E. M., Schneiderman, N., Skyler, J. S., & Marks, J. B. (2000) · Diabetes Research and Clinical Practice · doi:10.1016/s0168-8227(99)00116-3 · Cited by 470
“The ‘insulinogenic index’ refers to the ratio of fasting insulin to fasting glucose [9,10].”
BackgroundShen, S.-W., Reaven, G. M., & Farquhar, J. W. (1970) · Journal of Clinical Investigation · doi:10.1172/jci106433 · Cited by 494
Turner, R. C., Holman, R. R., Matthews, D., Hockaday, T. D. R., & Peto, J. (1979) · Metabolism · doi:10.1016/0026-0495(79)90146-x · Cited by 388
Strawbridge, R. J., Dupuis, J., Prokopenko, I., Barker, A., Ahlqvist, E., Rybin, D., Petrie, J. R., Travers, M. E., Bouatia-Naji, N., Dimas, A. S., et al. (2011) · Diabetes · doi:10.2337/db11-0415 · Cited by 356
“The insulinogenic index (27), which measures dynamic insulin secretion during the first 30 min after an oral glucose load and was available in 14,956 subjects, showed nominal associations for four loci.”
Færch, K., Torekov, S. S., Vistisen, D., Johansen, N. B., Witte, D. R., Jonsson, A., Pedersen, O., Hansen, T., Lauritzen, T., Sandbæk, A., et al. (2015) · Diabetes · doi:10.2337/db14-1751 · Cited by 321
“These findings are in agreement with the glucoregulatory effects of GLP-1 (33,34) and with studies showing that infusion of the GLP-1 receptor antagonist exendin-(9-39) reduced first-phase insulin release and decreased insulin action in healthy individuals and in patients with type 2 diabetes (35,36).”
BackgroundMethodResultInfluentialMeyre, D., Bouatia‐Naji, N., Tounian, A., Samson, C., Lecœur, C., Vatin, V., Ghoussaini, M., Wachter, C., Herçberg, S., Charpentier, G., et al. (2005) · Nature Genetics · doi:10.1038/ng1604 · Cited by 316
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“Second, impairment of 'early-phase' insulin response to glucose is characteristic of diabetic metabolism [14, 16].”
BackgroundMethodInsulin secretion capacity in the development from normal glucose tolerance to type 2 diabetes
Fukushima, M., Suzuki, H., & Seino, Y. (2004) · Diabetes Research and Clinical Practice · doi:10.1016/j.diabres.2003.11.024 · Cited by 313
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MethodFehse, F., Trautmann, M., Holst, J. J., Halseth, A. E., Nanayakkara, N., Nielsen, L. L., Fineman, M. S., Kim, D. D., & Nauck, M. A. (2005) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2005-1093 · Cited by 297
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BackgroundElkind-Hirsch, K., Marrioneaux, O., Bhushan, M., Vernor, D., & Bhushan, R. (2008) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2008-0115 · Cited by 276
“I/Glu30–0) and corrected I response at Glu peak (CIRgp), indexes of -cell activity, were computed from Glu-I values obtained during the OGTT ( 26 , 27).”
MethodAltered Myocardial Function and Metabolism in Chronic Diabetes Mellitus without Ischemia in Dogs
Regan, T. J., Ettinger, P. O., Khan, M. I., Jesrani, M. U., Lyons, M. M., Oldewurtel, H. A., & Weber, M. A. (1974) · Circulation Research · doi:10.1161/01.res.35.2.222 · Cited by 276
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“Insulin secretion was also expressed in terms of the insulinogenic index (II): 0–30 min insulin increment (μU/ ml)/0–30 min PG increment (mg/dl) [23].”
BackgroundZhang, L., Chen, C., Zhou, N., Fu, Y., & Cheng, X. (2017) · Clinica Chimica Acta · doi:10.1016/j.cca.2017.10.034 · Cited by 182
Gut hormones and diabetes mellitus
Creutzfeldt, W., & Nauck, M. (1992) · Diabetes/Metabolism Reviews · doi:10.1002/dmr.5610080206 · Cited by 176
Scott, R. A., Fall, T., Pasko, D., Barker, A., Sharp, S. J., Arriola, L., Balkau, B., Barricarte, A., Barroso, I., Boeing, H., et al. (2014) · Diabetes · doi:10.2337/db14-0319 · Cited by 173
“We investigated the association of these risk scores with euglycemichyperinsulinemic clamp (22) and oral glucose tolerance test (OGTT)-based measures of insulin sensitivity and secretion (23,24).”
BackgroundLee, W., Ser, K., Chong, K., Lee, Y.-C., Chen, S., Tsou, J.-J., Chen, J., & Chen, C. (2009) · Surgery · doi:10.1016/j.surg.2009.10.059 · Cited by 174
First-phase insulin secretion: does it exist in real life? Considerations on shape and function
Caumo, A., & Luzi, L. (2004) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00139.2003 · Cited by 181
“Another evidence that the insulin responses to intravenous and oral glucose are closely related comes from the observation that, in patients with IGT or in the early stages of type 2 diabetes, the first-phase insulin response to an IVGTT or a hyperglycemic clamp is almost invariably impaired, and this defect is mirror…”
BackgroundAcute and 2-week exposure to prednisolone impair different aspects of β-cell function in healthy men
van Raalte, D. H., Nofrate, V., Bunck, M. C., van Iersel, T., Elassaiss Schaap, J., Nässander, U. K., Heine, R. J., Mari, A., Dokter, W. H. A., & Diamant, M. (2010) · European Journal of Endocrinology · doi:10.1530/eje-09-1034 · Cited by 170
Thyroid Hormones, Gonadal and Adrenocortical Steroids and the Function of the Islets of Langerhans
Lenzen, S., & Bailey, C. J. (1984) · Endocrine Reviews · doi:10.1210/edrv-5-3-411 · Cited by 168
Functional Assessment of Pancreatic β-Cell Area in Humans
Meier, J. J., Menge, B. A., Breuer, T. G. K., Müller, C., Tannapfel, A., Uhl, W. H., Schmidt, W. E., & Schrader, H. (2009) · Diabetes · doi:10.2337/db08-1611 · Cited by 164
Ellingsen, C., Dassau, E., Zisser, H., Grosman, B., Percival, M. W., Jovanovic, L. G., & Doyle, F. J. (2009) · Journal of Diabetes Science and Technology · doi:10.1177/193229680900300319 · Cited by 153
“if G(k) Gss(k) > 0 IG(k) = {G(k) Gss(k)} ‧ CF else IG(k) = 0, (6)”
BackgroundEffects of Bariatric Surgery on Glucose Homeostasis and Type 2 Diabetes
Bradley, D. P., Magkos, F., & Klein, S. (2012) · Gastroenterology · doi:10.1053/j.gastro.2012.07.114 · Cited by 154
Færch, K., Vaag, A. A., Holst, J. J., Glümer, C., Pedersen, O. B., & Borch‐Johnsen, K. (2008) · Diabetologia · doi:10.1007/s00125-008-0951-x · Cited by 144
“An estimate of firstphase insulin secretion was also calculated from the OGTT using the insulinogenic index (ΔI30/ΔG30) [21].”
MethodHormonal Responses and Their Effect on Metabolism
Wilmore, D. W. (1976) · Surgical Clinics of North America · doi:10.1016/s0039-6109(16)41029-7 · Cited by 142
Matveyenko, A. V., & Butler, P. C. (2006) · Diabetes · doi:10.2337/db05-1672 · Cited by 144
“Glucose-induced insulin secretion is defective in individuals at risk of developing type 2 diabetes (8,9), a defect that becomes more pronounced in those who develop type 2 diabetes (7,10,11).”
BackgroundMetabolic Effects of Chronic Cannabis Smoking
Muniyappa, R., Sable, S., Ouwerkerk, R., Mari, A., Gharib, A. M., Walter, M. F., Courville, A. B., Hall, G., Chen, K. Y., Volkow, N. D., et al. (2013) · Diabetes Care · doi:10.2337/dc12-2303 · Cited by 140
“In addition, insulinogenic index (IGI) was derived from plasma insulin and glucose concentrations during an OGTT as previously described (24).”
MethodWhy Syndrome X? From Harold Himsworth to the Insulin Resistance Syndrome
Reaven, G. M. (2005) · Cell Metabolism · doi:10.1016/j.cmet.2004.12.001 · Cited by 143
Qian, J., Block, G. D., Colwell, C. S., & Matveyenko, A. V. (2013) · Diabetes · doi:10.2337/db12-1543 · Cited by 141
“Type 2 diabetes mellitus (T2DM) is characterized by islet failure due to loss of b-cell function and mass (1,2).”
Saito, K., Yaginuma, N., & Takahashi, T. (1979) · Tohoku journal of experimental medicine · doi:10.1620/tjem.129.273 · Cited by 156
To The Pathogenesis of Diabetes Mellitus
van BEEK, C. (1954) · Gastroenterology · doi:10.1016/s0016-5085(54)80036-9 · Cited by 134
Loss of beta cell function as fasting glucose increases in the non-diabetic range
Godsland, I. F., Jeffs, J. A. R., & Johnston, D. G. (2004) · Diabetologia · doi:10.1007/s00125-004-1454-z · Cited by 131
“The key role of loss of first-phase insulin secretion in deteriorating glucose homeostasis has long been recognised [36, 37, 38] and the increased late-phase insulin secretion necessary to correct the initial deficit provided the original explanation for the hyperinsulinaemia seen in impaired glucose homeostasis.”
BackgroundRuth, M. R., Port, A. M., Shah, M., Bourland, A. C., Istfan, N. W., Nelson, K. P., Gokce, N., & Apovian, C. M. (2013) · Metabolism · doi:10.1016/j.metabol.2013.07.006 · Cited by 137
“The area under the curve for glucose and insulin were calculated according to Seltzer’s methods as published elsewhere [18,19].”
MethodHaganes, K. L., Silva, C. P., Eyjólfsdóttir, S. K., Steen, S., Grindberg, M., Lydersen, S., Hawley, J. A., & Moholdt, T. T. (2022) · Cell Metabolism · doi:10.1016/j.cmet.2022.09.003 · Cited by 136
Experimental reduction of B‐cell mass: Implications for the pathogenesis of diabetes
Weir, G. C., Leahy, J. L., & Bonner‐Weir, S. (1986) · Diabetes/Metabolism Reviews · doi:10.1002/dmr.5610020108 · Cited by 127
Vardi, P., Crisa, L., Jackson, R. A., Dumont Herskowitz, R., Wolfsdorf, J. I., Einhorn, D., Linarelli, L., Dolinar, R., Wentworth, S., Brink, S. J., et al. (1991) · Diabetologia · doi:10.1007/bf00500379 · Cited by 122
“It is also important to note that loss of 1st phase insulin secretion is not an abnormality specific to Type i diabetes but occurs with Type 2 diabetes [13] and following partial pancreatectomy [14].”
BackgroundD’Alessio, D. A., Vogel, R., Prigeon, R. L., Laschansky, E. C., Koerker, D. J., Eng, J., & Ensinck, J. W. (1996) · Journal of Clinical Investigation · doi:10.1172/jci118380 · Cited by 119
“To determine the overall effect of GLP-1 on glucose disposition after a meal we studied a group of healthy, conscious baboons before and after intragastric glucose administration during infusions of saline, and two treatments to eliminate the action of GLP-1: ( a ) exendin-[9-39] (Ex-9), a peptide receptor antagonist…”
BackgroundMethodInfluentialRadiosurgery of acoustic neurinomas
Flíckinger, J. C., Lunsford, L. D., Coffey, R. J., Linskey, M. E., Bissonette, D. J., Maitz, A. H., & Kondziolka, D. S. (1991) · Cancer · doi:10.1002/1097-0142(19910115)67:2 · Cited by 149
Self-citationGrowth Hormone Stimulates Protein Synthesis during Hypocaloric Parenteral Nutrition
Manson, J., Smith, R. J., & Wilmore, D. W. (1988) · Annals of Surgery · doi:10.1097/00000658-198808000-00002 · Cited by 121
Glucose Intolerance and Insulin Resistance in Patients With Liver Disease
Collins, J. R. (1969) · Archives of Internal Medicine · doi:10.1001/archinte.1969.00300180014003 · Cited by 125
Wollheim, C. B., Kikuchi, M., Renold, A. E., & Sharp, G. W. G. (1978) · Journal of Clinical Investigation · doi:10.1172/jci109146 · Cited by 119
IMPROVEMENT IN INSULIN SECRETION IN DIABETES AFTER DIAZOXIDE
Greenwood, R. H., Mahler, R., & Hales, C. N. (1976) · The Lancet · doi:10.1016/s0140-6736(76)91473-2 · Cited by 118
Tzagournis, M., Chiles, R. P., Ryan, J. M., et al. (1968) · Circulation · doi:10.1161/01.cir.38.6.1156 · Cited by 117
Ehrmann, D. A., Temple, K. A., Rue, A., Barengolts, E., Mokhlesi, B., Cauter, E. V., Sam, S., Miller, M. A., Kahn, S. E., Atkinson, K. M., et al. (2018) · Diabetes Care · doi:10.2337/dc18-0243 · Cited by 121
“TheC-peptide index (CPI;ΔC30/ΔG30) and insulinogenic index (IGI; ΔI30/ΔG30) were calculated using the 0- and 30-min samples (12,13).”
MethodLevine, R., & Haft, D. E. (1970) · New England Journal of Medicine · doi:10.1056/nejm197007232830405 · Cited by 114
Cario, H., Holl, R. W., Debatin, K., & KOHNE, E. (2003) · European Journal of Pediatrics · doi:10.1007/s00431-002-1121-7 · Cited by 113
“In contrast, several previous studies reported a normal or even reduced insulin response to oral glucose [6, 15, 26 ].”
BackgroundResultCerasi, E., Efendić, S., & Luft, R. (1973) · The Lancet · doi:10.1016/s0140-6736(73)90599-0 · Cited by 113
Galvin, P., Ward, G. M., Walters, J. M., Pestell, R. G., Koschmann, M., Vaag, A. A., Martin, I. K., Best, J. D., & ALFORD, F. P. (1992) · Diabetic Medicine · doi:10.1111/j.1464-5491.1992.tb01732.x · Cited by 111
Quddusi, S., Vahl, T. P., Hanson, K., Prigeon, R. L., & D’Alessio, D. A. (2003) · Diabetes Care · doi:10.2337/diacare.26.3.791 · Cited by 111
“finding in type 2 diabetes (29,30), and is a”
BackgroundKjems, L., Kirby, B. M., Welsh, E. M., Veldhuis, J. D., Straume, M., McIntyre, S. S., Yang, D., Lefèbvre, P., & Butler, P. C. (2001) · Diabetes · doi:10.2337/diabetes.50.9.2001 · Cited by 108
Targeting β-Cell Mass in Type 2 Diabetes: Promise and Limitations of New Drugs Based on Incretins
Salehi, M., Aulinger, B. A., & D’Alessio, D. A. (2008) · Endocrine Reviews · doi:10.1210/er.2007-0031 · Cited by 107
Plasma Insulin and Glucose Profiles in Normal, Obese, and Diabetic Persons
GENUTH, S. M. (1973) · Annals of Internal Medicine · doi:10.7326/0003-4819-79-6-812 · Cited by 109
Bottin, J. H., Swann, J. R., Cropp, E., Chambers, E. S., Ford, H. E., Ghatei, M. A., & Frost, G. S. (2016) · British Journal Of Nutrition · doi:10.1017/s0007114516001872 · Cited by 106
“Postprandial insulin sensitivity was estimated using the Matsuda Index((26)), β-cell output was estimated using the insulinogenic index((27)) and β-cell function in the context of insulin resistance was estimated using the disposition index((28)).”
MethodRuchat, S.-M., Elks, C. E., Loos, R. J. F., Vohl, M., Weisnagel, S. J., Rankinen, T., Bouchard, C., & Përusse, L. (2008) · Acta Diabetologica · doi:10.1007/s00592-008-0080-5 · Cited by 107
“The C-peptide/glucose ratio (P30/G30: C-peptide 30 min - C-peptide 0 min/glucose 30 min - glucose 0 min) [40] quantifies the pancreatic C-peptide response to glucose during the first 30 minutes of the OGTT, and the insulogenic index (I30/G30: insulin 30 min - insulin 0 min/glucose 30 min - glucose 0 min) [41] the panc…”
MethodNon-insulin-dependent diabetes mellitus: Interplay between B-cell inadequacy and insulin resistance
Weir, G. C. (1982) · The American Journal of Medicine · doi:10.1016/0002-9343(82)90321-7 · Cited by 104
Senft, G., Schultz, G., Munske, K., & Hoffmann, M. (1968) · Diabetologia · doi:10.1007/bf01211766 · Cited by 104
Insulin resistance and insulin secretion in chronic hepatitis C virus infection
Narita, R., Abe, S., Kihara, Y., Akiyama, T., Tabaru, A., & Otsuki, M. (2004) · Journal of Hepatology · doi:10.1016/j.jhep.2004.03.020 · Cited by 102
“To estimate b-cell function and insulin resistance, various indices derived either from the fasting plasma glucose, insulin and C-peptide or from OGTT were calculated as shown in Table 1 [18,20–23].”
BackgroundMethodInsulin-independent diabetes mellitus: Metabolic characteristics
Reaven, G. M. (1980) · Metabolism · doi:10.1016/0026-0495(80)90170-5 · Cited by 99
Morimoto, A., Tatsumi, Y., Deura, K., Mizuno, S., Ohno, Y., Miyamatsu, N., & Watanabe, S. (2013) · Diabetologia · doi:10.1007/s00125-013-2932-y · Cited by 100
“Insulinogenic index (Insulin30 − Insulin0)/(Glucose30 − Glucose0) [17] 0.”
MethodImpaired β-cell function and insulin sensitivity in Japanese subjects with normal glucose tolerance
Kuroe, A., Fukushima, M., Usami, M., Ikeda, M., Nakai, Y., Taniguchi, A., Matsuura, T., Suzuki, H., Kurose, T., Yasuda, K., et al. (2002) · Diabetes Research and Clinical Practice · doi:10.1016/s0168-8227(02)00177-8 · Cited by 100
Fritsche, A., Wagner, R. J., Heni, M., Kantartzis, K., Machann, J., Schick, F., Lehmann, R., Peter, A., Dannecker, C., Fritsche, L., et al. (2021) · Diabetes · doi:10.2337/db21-0526 · Cited by 104
“Insulin secretion was calculated with the insulinogenic index (IGI) (22).”
MethodCretti, A., Lehtovirta, M., Bonora, E., Brunato, B., Zenti, M., Tosi, F., Caputo, M., Caruso, B., Groop, L., Muggeo, M., et al. (2001) · European Journal of Clinical Investigation · doi:10.1046/j.1365-2362.2001.00827.x · Cited by 99
Functional Role of miR-155 in the Pathogenesis of Diabetes Mellitus and Its Complications
Jankauskas, S. S., Gambardella, J., Sardu, C., Lombardi, A., & Santulli, G. (2021) · Non-Coding RNA · doi:10.3390/ncrna7030039 · Cited by 104
Successful Versus Failed Adaptation to High-Fat Diet–Induced Insulin Resistance
Matveyenko, A. V., Gurlo, T., Daval, M., Butler, A. E., & Butler, P. C. (2009) · Diabetes · doi:10.2337/db08-1464 · Cited by 98
Impaired Carbohydrate Metabolism during a Mild Viral Illness
Rayfield, E. J., Curnow, R. T., George, D. T., & Beisel, W. R. (1973) · New England Journal of Medicine · doi:10.1056/nejm197309202891207 · Cited by 98
Chromium improves insulin response to glucose in rats
Striffler, J. S., Law, J. S., Polansky, M. M., Bhathena, S. J., & Anderson, R. A. (1995) · Metabolism · doi:10.1016/0026-0495(95)90036-5 · Cited by 93
Epstein, F. H. (1967) · Circulation · doi:10.1161/01.cir.36.4.609 · Cited by 92
Insulin Response to Glucose in Hypermetabolic Burn Patients
Wilmore, D. W., Mason, A. D., & Pruitt, B. A. (1976) · Annals of Surgery · doi:10.1097/00000658-197603000-00018 · Cited by 86
Impaired insulin secretion in the spontaneous diabetes rats.
Kimura, K., Toyota, T., KAKIZAKI, M., KUDO, M., Takebe, K., & Gotō, Y. (1982) · The Tohoku Journal of Experimental Medicine · doi:10.1620/tjem.137.453 · Cited by 87
Suzuki, H., Fukushima, M., Okamoto, S., Takahashi, O., Shimbo, T., Kurose, T., Yamada, Y., Inagaki, N., Seino, Y., & Fukui, T. (2005) · Metabolism · doi:10.1016/j.metabol.2005.06.006 · Cited by 84
“The insulinogenic index (II) [14], the ratio of the incremental serum insulin to plasma glucose concentration during the first 30 minutes after glucose ingestion calculated by OGTT (IIOGTT), has been commonly used as a measure of early-phase insulin secretion [15-18] since it was proposed by Seltzer et al [19] in 1967.”
MethodRijkelijkhuizen, J. M., Girman, C. J., Mari, A., Alssema, M., Rhodes, T., Nijpels, G., Kostense, P. J., Stein, P. P., Eekhoff, E. M. W., Heine, R. J., et al. (2008) · Diabetes Research and Clinical Practice · doi:10.1016/j.diabres.2008.11.017 · Cited by 86
Boquist, L., Hellman, B., Lernmark, Å., & Täljedal, I. ‐. (1974) · The Journal of Cell Biology · doi:10.1083/jcb.62.1.77 · Cited by 83
Reaven, G. M., & Olefsky, J. M. (1977) · Diabetologia · doi:10.1007/bf01219700 · Cited by 83
Intravenous Glucose Tolerance Test in Depression
Mueller, P. S. (1969) · Archives of General Psychiatry · doi:10.1001/archpsyc.1969.01740220086010 · Cited by 81
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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