Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohydrate intolerance in Mild Diabetes Mellitus*

May combine two claims.

Mildly diabetic patients exhibited delayed hyperinsulinemia in concert with prolonged hyperglycemia during oral glucose tolerance tests.

“since the latter exhibited delayed hyperinsulinemia in concert with prolonged hyperglycemia.”

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Whether blood glucose descended from an acutely imposed hyperglycemic apex or first rose and then fell postprandially, the insulin secretory response was always much greater in normal subjects than in mild diabetics, and was even lower in moderate diabetics.

“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.”

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Both the speed of insulin release and the quantity of insulin secreted per unit of glycemic stimulus are much greater in normal subjects than in the mildest diabetic patients, in both nonobese and obese individuals.

“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.”

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Although obese nondiabetics and mild diabetics tended to produce higher plasma insulin concentrations after both glucose loads, they otherwise exhibited the same patterns of insulinogenic response as their nonobese counterparts.

“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.”

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During the oral glucose tolerance test in nonobese individuals, the insulinogenic index for the first 30 minutes was 3.07 ± 0.34 in normal controls and 1.14 ± 0.21 in mild diabetics, and respective indexes for the entire test were 4.93 ± 0.54 and 2.43 ± 0.39.

“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).”

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When individual secretory response was expressed per unit of glycemic stimulus, the much greater absolute hyperinsulinemia of obesity lost statistical meaning because glucose tolerance of overweight subjects was sufficiently higher than in nonobese controls.

“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.”

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Normal subjects responded immediately and maximally to the massive glycemic stimulus, in contrast to progressively blunted secretory responses in the diabetic groups.

“Normal subjects responded immediately and max- imally to the massive glycemic stimulus, in con- trast to progressively blunted secretory responses in the diabetic groups.”

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For the initial 30 minutes after oral glucose, the mean insulin:glucose ratio for control subjects was 3.37 ± 0.32, and the corresponding value for mild diabetics was 1.28 ± 0.14 (p < 0.001).

“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).”

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Mean insulinogenic indexes for obese subjects were not statistically greater than those for nonobese controls, since corresponding glucose tolerance curves were also higher.

“Since corresponding glucose tolerance curves were also higher, the mean insulinogenic indexes for obese subjects were not statistically greater.”

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In moderate diabetics, mean fasting glucose of 126 ± 8 mg per 100 ml rose to 342 ± 17 mg per 100 ml in 5 minutes with no increase above the fasting plasma insulin level of 24 ± 5 μU per ml.

“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”

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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.

“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.”

May combine two claims. The quote only partly states this claim.

In mild diabetics, the 5-minute blood glucose level of 294 ± 17 mg per 100 ml elicited only a modest rise of plasma insulin from a fasting value of 12 ± 2 to 45 ± 9 μU per ml (p < 0.001 compared to the 5-minute value in normal subjects), and plasma insulin plateaued at a maximum of 47 ± 8 μU per ml as circulating glucose slowly receded to the normal fasting range by 120 minutes.

“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.”

Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

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 glucose load greatly exceeded 160 mg per 100 ml and 120 mg per 100 ml, respectively.

“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.”

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During the first 10 minutes after intravenous glucose, the mean insulin:glucose ratio for normal subjects was 0.56 ± 0.03, and the corresponding ratio in mild diabetics was 0.22 ± 0.06 (p < 0.001).

“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).”

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Thereafter, in normal subjects, blood glucose dropped rapidly to a normal fasting level by 60 minutes, accompanied by a similar swift decline in circulating insulin concentration.

“Thereafter, blood glucose dropped rapidly to a normal fasting level by 60 minutes, accompanied by a similar swift decline in circulating insulin concentration.”

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For the intravenous test, the total insulinogenic index was 0.66 ± 0.07 (100%) for normal subjects, 0.31 ± 0.06 (47%) for mild diabetics, and 0.12 ± 0.04 (18%) for moderate diabetics.

“For the intravenous test, the”

May combine two claims. The quote only partly states this claim.

In mild diabetics during the oral glucose test, fasting blood glucose of 80 ± 3 mg per 100 ml rose to 201 ± 11 mg per 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.

“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.”

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Corresponding over-all insulinogenic indexes after oral glucose were 4.93 ± 0.54 (100%), 2.43 ± 0.39 (49%), and 0.47 ± 0.13 (10%).

“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).”

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The relatively greater normal secretory response declared itself shortly after administration of glucose by either route and was maintained throughout both tests.

“This relatively greater normal secretory response de- clared itself shortly after the administration of glucose by either route, and was maintained throughout both tests.”

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Despite higher absolute hormonal output after oral glucose in mild diabetics, the insulinogenic index revealed that insulin release in normal subjects was proportionally more than twice as great.

“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.”

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In moderate diabetics during the oral glucose test, 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 to 103 ± 29 μU per ml at 120 minutes.

“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.”

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The present findings did show much greater insulin release after oral glucose loads in all three clinical groups, and regardless of body weight.

“Nevertheless, the present findings did show much greater insulin release after oral glucose loads in all three clinical groups, and regardless of body weight.”

Classified as probably not a substantial claim.

Each patient was given intravenous and oral glucose in random order and at intervals of a few days.

“each patient was given intravenous and oral glucose, in random order and at intervals of a few days.”

Probably not a substantial claim: may not pass S3 (load-bearing).

Current work has narrowed the active substance down to glucagon, secretin, or pancreozymin.

“Current work has narrowed the active substance down to glucagon (22), secretin (23-25), or pancreozymin (26).”

• cites [22]Not matched

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• cites [23]Not matched

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• cites [24]Not matched

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• cites [25]Not matched

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• cites [26]Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

Probably not a substantial claim: may not pass S1 (asserted).

Symptomatic postprandial hypoglycemia in patients with mild diabetes mellitus might be due to delayed initial release of insulin followed by subsequent excessive hormonal secretion.

“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”

• cites Seltzer, Fajans, and Conn (3)Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

May combine two claims.

An acute rise or fall of blood glucose level directly induces an increase or decrease, respectively, of insulin release.

“An acute rise or fall of blood glucose level directly induces an increase or decrease, respec- tively, of insulin release (1, 2, 8, 9).”

• cites [1]Not matched

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• cites [2]Not matched

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• cites [8]Not matched

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• cites [9]Not matched

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Probably not a substantial claim: may not pass S3 (load-bearing).

In a carefully controlled study of comparably mild diabetics, Perley and Kipnis concluded that the diabetic state is associated with reduced insulin secretory capacity, regardless of body weight.

“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.”

• cites [16]Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

Probably not a substantial claim: may not pass S3 (load-bearing).

The finding that plasma insulin became significantly higher in obese mild diabetics at 20 minutes after intravenous glucose suggested an anti-insulin effect of obesity.

“which finding again sug- gested an anti-insulin effect of obesity.”

Probably not a substantial claim: may not pass S3 (load-bearing).

The general phenomenon of greater hormonal response to glucose loads in overweight normal subjects suggests that the obese state somehow engenders peripheral insulin resistance.

“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).”

• cites [14]Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

• cites [15]Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

Probably not a substantial claim: may not pass S3 (load-bearing).

Glucose-induced insulinogenesis does not alter pancreatic venous blood flow.

“previous work (2) having established that glucose-induced insulinogenesis does not alter pancreatic venous blood flow.”

• cites [2]Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

Probably not a substantial claim: may not pass S3 (load-bearing).

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.

“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.”

Classified as probably not a substantial claim. May combine two claims.

Yalow and Berson found subnormal plasma insulin concentrations at 30 minutes during glucose tolerance testing of mild diabetics but supernormal levels at 2 hours.

“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.”

• cites Yalow and Berson (4)Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

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 radioimmunoassay technique.

“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.”

Classified as probably not a substantial claim.

During continuous changes in circulating glucose concentrations after carbohydrate loads, the rate of insulin secretion is directly, but not necessarily linearly, proportional to the simultaneous blood glucose level.

“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.”

• cites Metz (1)Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

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In its initial stage, diabetes mellitus remains fundamentally a disease of deficient insulin secretion, but one of rate rather than magnitude.

“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.”

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The blunted capability of mildly diabetic islets to release insulin after the same intravenous bolus of glucose implied an obtunded islet response to oral glucose as well, which relative lack of early insulin activity on hepatic and posthepatic tissues could reasonably account for the delay in metabolizing ingested glucose.

“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.”

May combine two claims.

Normal immediate hormonal release after sudden intense hyperglycemia suggested that a similarly fast response, but smaller and peripherally undetectable, was also activated by postprandially rising blood sugar, and this brisk insulinogenesis should promote avid hepatic and peripheral glucose uptake, which in turn would clear absorptive hyperglycemia with dispatch.

“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.”

• cites [27]Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.