Plasma Insulin Activity after Glucose: An Index of Insulogenic Reserve in Normal and Diabetic Man

Seltzer, Holbrooke S.; Smith, Walter L.

doi:10.2337/diab.8.6.417

Cited by 87 publications

(35 citation statements)

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“…In 9 of 13 dogs the pancreaticoduodenal vein insulin was greater after intraduodenal glucose than after intravenous glucose loading; the difference in the means of the peak levels was not statistically significant, thus confirming to a degree the findings of Grossman and Gold 4 and of Seltzer (23). However, in all but 3 of the 13 dogs the "insulinogenic index" (24), determined here by dividing the area of the insulin increment by the area of the increment of vena cava glucose during the first 20 min 5 after glucose administration, was greater in the intraduodenal experiment (Table VI). This was true in both "isometric" and "isoglycemic" experiments, but the difference between the groups was only slightly significant (P < 0.05).…”

Section: Resultsmentioning

confidence: 99%

Characterization of the responses of circulating glucagon-like immunoreactivity to intraduodenal and intravenous administration of glucose

Unger¹,

Ohneda²,

Valverde³

et al. 1968

J. Clin. Invest.

281

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A B S T R A C T The effects of ingested and infused glucose upon circulating glucagon-like immunoreactivity (GLI) were compared in 14 triply catheterized conscious dogs. Within 60 min after the intraduodenal administration of 2 g/kg of glucose, the mean level of glucagon-like immunoreactivity in the vena caval plasma more than doubled, whereas after intravenous infusion of the same dose over a 90 min period no change in the mean vena caval level was observed; during glucose infusion mean glucagon-like immunoreactivity in the pancreatic venous effluent declined, suggesting that hyperglycemia suppresses rather than stimulates pancreatic glucagon secretion.To determine if the rise in glucagon-like immunoreactivity that occurs during glucose absorption was of pancreatic origin, the effect of pancreatectomy performed 1 hr after the intraduodenal administration of glucose was determined. Although circulating insulin disappeared after resection of the pancreas, the level of glucagon-like immunoreactivity continued to rise, establishing its extrapancrentic origin. In other experiments, measurements j. 'cagon-like immunoreactivity in plasma obtained simultaneously from pancreatico-

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Section: Resultsmentioning

confidence: 99%

Characterization of the responses of circulating glucagon-like immunoreactivity to intraduodenal and intravenous administration of glucose

Unger¹,

Ohneda²,

Valverde³

et al. 1968

J. Clin. Invest.

281

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“…Figure 3 shows the patterns of "insulin: glucose ratios" obtained by dividing plasma insulin enhancement above fasting value by corresponding net increase of blood glucose. After both test loads, normal subjects showed a prompt, sustained rise in the insulin: glucose ratio compared to a much slower 8 Figure 4 illustrates how the index of insulinogenic reserve was used to semiquantitate insulin secretory capacity, both to compare the initial hormonal output with the cumulative and "total" responses in each clinical group and to enable comparison between groups. The index was calculated by dividing the area circumscribed by the insulin curve (i.e., increment above fasting level) by the corresponding area circumscribed by the glucose curve.…”

Section: Resultsmentioning

confidence: 99%

“…Interpretations derived from our findings (see Discussion) depend upon the validity of the following causal relationships between blood glucose concentration and insulin secretion: 1) An acute rise or fall of blood glucose level directly induces an increase or decrease, respectively, of insulin release (1,2,8,9). 2) 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.2 3) Differences between the insulin secretory responsiveness of normal versus diabetic beta cells can be semiquantitated by expressing the magnitude of insulin output per unit of glycemic stimulus, with the resulting ratio representing an empirical "index of insulinogenic reserve" (see Results and Figure 4).…”

Section: Methodsmentioning

confidence: 99%

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

Seltzer¹,

Allen²,

Herron³

et al. 1967

J. Clin. Invest.

774

387

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Summary. 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 * Submitted for publication September 13, 1965; ac- were matched, the apparent hyperinsulinemia associated with obesity was again reduced to insignificance. At the same time, a tendency toward perpetuation of higher insulin levels in overweight normal subjects and mild diabetics, in response to both glucose loads, suggested that obesity per se does induce a state of peripheral insulin resistance.The data indicate that normal beta cells respond instantly to a glycemic stimulus, whereas diabetic islets react sluggishly, and that proportionally greater insulinogenesis accounts for faster disposal of postprandial hyperglycemia in nondiabetics than in diabetics, in both nonobese and obese individuals. By tracing a rational sequence of events within the beta cell-fro...

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“…Very recently Seltzer and Smith (41), employing the rat diaphragm assay of Vallance-Owen and Hurlock (33), have reported insulin concentrations one hour after glucose, in tolbutamide-sensitive adult diabetics, almost in the normal range, but significantly lower values were observed in juvenile diabetics and adult tolbutamide-insensitive diabetics. To resolve the present finding of a higher than normal integrated insulin output in diabetics during the glucose tolerance test with sustained hyperglycemia in these patients, it must be concluded that the tissues of the maturity-onset diabetic do not respond to his insulin as well as the tissues of the nondiabetic subject respond to his insulin.…”

Section: Discussionmentioning

confidence: 99%

Immunoassay of Endogenous Plasma Insulin in Man

Yalow¹,

Berson²

1960

J. Clin. Invest.

2,738

509

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Plasma Insulin Activity after Glucose: An Index of Insulogenic Reserve in Normal and Diabetic Man

Cited by 87 publications

References 0 publications

Characterization of the responses of circulating glucagon-like immunoreactivity to intraduodenal and intravenous administration of glucose

Characterization of the responses of circulating glucagon-like immunoreactivity to intraduodenal and intravenous administration of glucose

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

Immunoassay of Endogenous Plasma Insulin in Man

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