Plasma Concentrations of Insulin, Glucose, Free Fatty Acids and Ketone Bodies in the Foetal and Newborn Sheep and the Response to a Glucose Load Before and After Birth
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The relationship between in vivo insulin-stimulated glucose utilization (euglycemic clamp technique) and various estimates of the plasma insulin response to oral glucose was defined in 62 subjects with normal glucose tolerance. Both the incremental insulin increase above fasting (r = 0.61) and the total integrated insulin response (r = 0.65) were highly correlated (P less than 0.001) with in vivo insulin action, and the relationship between total insulin response and insulin action remained significant (r = 0.61, P less than 0.001) when corrected for variations in total glucose response, age, and obesity. In a subset of these subjects (N = 27) we were also able to assess state of habitual physical activity by estimating maximal oxygen consumption during bicycle ergometry. A significant correlation also existed between insulin action and response in these subjects (r = 0.67, P less than 0.001), which remained significant (r = 0.65) when differences in total glucose response, obesity, age, and maximal oxygen consumption were taken into account. These data demonstrate that there is a significant correlation between insulin response and insulin action in normal individuals that can account for approximately one-third of the total variance in insulin action seen in subjects with normal glucose tolerance. Thus, determination of plasma insulin levels after an oral glucose challenge can only provide a qualitative estimate of insulin-stimulated glucose utilization.
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BTS 67 582 (1,1-dimethyl-2(2-morpholinophenyl)guanidine fumarate) is being developed as a short-acting anti-diabetic insulin secretagogue. The effect of BTS 67 582 on the phasic pattern of insulin release was assessed in anaesthetized normal rats by measuring arterial plasma insulin concentrations while arterial glucose concentrations were fixed at 6, 8.5 and 12.5 mM. Intravenous BTS 67 582 (10 mg kg(-1)) induced an immediate but transient increase in insulin concentrations which declined by 10 min (first phase). This was followed by a smaller but sustained increase in insulin concentrations (second phase). The increment from basal to peak insulin release (0-2 min) was independent of glucose, but the first phase was maintained for longer and the second phase was greater at the highest concentration of glucose (12.5 mM). BTS 67 582 also extended the first-phase insulin response to a standard intravenous glucose challenge and enhanced the rate of glucose disappearance by approximately 12%. Thus BTS 67 582 causes biphasic stimulation of insulin release and augments the insulin-releasing effect of glucose.
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Evidence that Glucose Load Is an Important Determinant of Plasma Insulin Response in Normal Subjects
Two consecutive oral glucose tolerance tests were performed on twelve healthy, malemedical students, in which each subject received 20 and 40 gm. of glucose per square meter body surface area. The tests were conducted one week apart, and the sequence in which the two glucose loads was given was randomized. The larger glucose load elicited anincrease in both plasma glucose and immunoreactive insulin response. However, the increase in the plasma insulin response was much greater than the increase in plasma glucoseresponse. Thus, the insulinogenic index, denned as the plasma insulin level divided bythe plasma glucose level, significantly increased as the glucose load increased. These results indicate that glucose load is an important determinant of plasma insulin response, and that in any individual the plasma insulin response is not a simple linear function of coexisting plasma glucose concentration.
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This study aimed at determining the release and action of insulin in liver cirrhosis. Eight non-diabetic patients with alcoholic liver cirrhosis and eight age-, sex-, and weight-matched controls were investigated. The clearance and hypoglycemic action of insulin were determined after a brief intravenous infusion of insulin (10 mU/kg). Glucose tolerance and insulin response were determined after rapid intravenous infusion of 25 g glucose. In the cirrhotic patients the decrease in glucose tolerance was associated with a) an unchanged insulin clearance, b) a decreased hypoglycemic action of insulin, and c) a marked impairment in the early insulin response and a slight, but not significant, increase in the late insulin response. In the cirrhotic group glucose tolerance varied with the early (and late) insulin response and with the hypoglycemic action of insulin. It is concluded that both insulin action and the early insulin response are impaired in alcoholic liver cirrhosis and that deterioration of the early insulin release plays an important role for deterioration of glucose tolerance.
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Oral glucose tolerance and the plasma immunoreactive insulin response to oral glucose were measured in 42 elderly hypertensive patients. Twenty-four of these patients showed abnormal glucose tolerance curves an 18 had normal curves. Patients with abnormal glucose tolerance showed significantly lower plasms immunoreactive insulin concentrations at 30 min and 60 min after the glucose load compared with patients with normal glucose tolerance. The patients in the two groups did not appear to differ in any other clinical or biochemical characteristics.
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We examined the hindlimb lymph insulin profile during simulated intravenous glucose tolerance tests (IVGTTs) in anesthetized dogs to test the following hypotheses: 1) the biphasic insulin response to intravenous glucose can be seen as a priming bolus and a secondary infusion that effect a rapid stepwise increase in the interstitial insulin concentration and 2) the activation of glucose utilization (rate of glucose uptake [Rd]) during an IVGTT is more similar to the dynamics of the interstitial insulin profile than that of the arterial plasma. Three insulin profiles were infused: a normal biphasic pattern, a second phase infusion only, and a biphasic pattern with a fourfold greater first phase and a normal second phase. During the normal biphasic infusion, lymph insulin quickly reached and maintained a steady-state concentration (10 min, 26.42 +/- 0.86 microU/ml). With second phase only, it took lymph insulin 35 min to reach a steady state of lower concentration (13.13 +/- 0.46 microU/ml) than the normal. And with a fourfold greater first phase, lymph insulin plateaued quickly (16 min, 140.87 +/- 1.68 microU/ml), but for a shorter duration than the normal. For each profile, the time course of activation of Rd did not follow the time course of insulin in the plasma, but was more similar to that of insulin in the interstitial fluid. These results show that the biphasic response allows interstitial insulin to rapidly reach and maintain a steady state beneficial to activation and maintenance of glucose utilization.
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ABSTRACT Plasma glucose and insulin responses to orally administered glucose were determined in rats of varying ages and weights. The results indicated that glucose tolerance tends to deteriorate as rats grow from 1 month to 9 months of age. This change in glucose tolerance was associated with an increase in the response of plasma insulin to glucose, consistent with the hypothesis that the decline in glucose tolerance is due to a loss of normal insulin sensitivity. The changes in glucose and insulin responses could not be explained entirely on the basis of the associated weight gain. They seemed to be at least partially secondary to either age or an age‐related factor other than obesity.
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Feed-back inhibition of insulin secretion in subjects with high and low insulin response to glucose.
The plasma insulin response to two successive stimulations by glucose was measured in 12 healthy subjects, 5 of whom demonstrated subnormal insulin responses to glucose infusion (low insulin responders). 15 g of glucose were injected rapidly i.v. at 0 and 20 min, and blood glucose and plasma insulin levels determined at intervals of 2-10 min. In both groups, the peak elevation of plasma insulin, and the peak insulinogenic index, were significantly inhibited at the second stimulation. The degree of inhibition was smaller in subjects with low insulin response. The integrated insulin response and the integrated insulinogenic index during the 20 min following glucose administration were also significantly inhibited at the second glucose challenge in subjects with low insulin responders. The degree of inhibition of the second insulin response (20-40 min) shows significant correlation with the insulinogenic index of the first response (0-20 min) in the total material. It is suggested that this inhibition of insulin release on repeating the stimulus, (a) may offer an explanation sustained stimulation by glucose; (b) is probably generated by the phenomenon of insulin secretion, and (c) might thus represent a negative feed-back loop in insulin secretion. (d) Decreased insulin secretion in low responders is not due to the presence of increased inhibition.
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Insulin oscillation
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