EFFECT OF TWO SULPHONYLUREAS ON THE DOSE KINETICS OF GLUCOSE – INDUCED INSULIN RELEASE IN NORMAL AND DIABETIC SUBJECTS

1979 ◽  
Vol 91 (2) ◽  
pp. 282-293 ◽  
Author(s):  
Erol Cerasi ◽  
Suad Efendic ◽  
Christina Thornqvist ◽  
Rolf Luft
Keyword(s):  
Glucose Tolerance ◽  
Insulin Release ◽  
Dose Response ◽  
Insulin Dose ◽  
Insulin Response ◽  
Normal Glucose Tolerance ◽  
Response Curves ◽  
Normal Glucose ◽  
Slow Rise ◽  
The Right

The effect of two second generation sulphonylureas, gliquidone and glibenclamide, on insulin secretion has been studied in the basal state and in combination with glucose infusions in normal controls, patients with mild maturity-onset diabetes, and subjects with normal glucose tolerance but low insulin response. When injected intravenously, gliquidone caused rapid elevation of plasma insulin, peaking at 5 min in all groups, while glibenclamide induced a slow rise in insulin. Insulin response was somewhat smaller than normal in diabetics and low insulin responders. In all groups, 25 μg/kg glibenclamide and 200 μg/kg gliquidone were equipotent in generating an insulin response at the basal state. Equipotent amounts of sulphonylureas were combined with glucose infusions at three different dose levels. The glucose-insulin dose relationships, established by giving glucose alone, demonstrated curves that were flatter, and shifted to the right of the control in diabetics and low insulin responders, the changes being more marked in the former group. Addition of sulphonylurea induced a left shift in the dose-response relationships in controls and low insulin responders; under these conditions the effect of glibenclamide was more pronounced than that of gliquidone. The doseresponse relation for glucose-induced insulin release was completely normalized in low responders when sulphonylureas were added. In the group of mild diabetics, insulin response to glucose was enhanced by sulphonylureas only to a modest extent, the dose-response curves remaining grossly abnormal. It is concluded that, under acute experiments, sulphonylureas correct the deficient insulin response only in subjects with minimal abnormalities of the glucose tolerance; their effect in diabetics, even very mild ones, is marginal.

POTENTIATION OF INSULIN RELEASE BY GLUCOSE IN MAN

1975 ◽  
Vol 79 (3) ◽  
pp. 511-534 ◽  
Author(s):  
Erol Cerasi
Keyword(s):  
Blood Glucose ◽  
Insulin Release ◽  
Dose Response ◽  
Pancreatic Beta Cell ◽  
Insulin Response ◽  
Initial Response ◽  
Normal Glucose Tolerance ◽  
Glucose Infusion ◽  
Clear Cut ◽  
The Right

ABSTRACT Glucose-induced potentiation of glucose-induced insulin release was quantitatively evaluated in 14 non-obese subjects with normal glucose tolerance but decreased insulin response, and in six non-obese patients with mild, adult-onset diabetes, by measuring the insulin responses to two consecutive glucose infusion tests, administered with 40 or 70 min interval. Enhancement of the second insulin response occurred in both groups. In low insulin responders, the dose-response relationship between blood glucose and plasma insulin was flatter and shifted to the right when compared to the control. Pretreatment with glucose increased strikingly the slope of this relationship, the responses now being within the normal range. The enhancement induced by glucose seems to be of multiplicative type. In mildly diabetic subjects, insulin response to glucose infusion was low and sluggish, only a minor initial response being observed. Pretreatment with glucose modified the profile of the insulin response, a clear-cut initial response of greater magnitude being obtained at least in some of the patients. The sensitivity of the islet to the potentiating action of glucose was higher in low insulin responders than in controls, the minimal glucose concentration needed to induce potentiation of the forthcoming response being much lower. The dose-response curve for the relationship between the blood glucose level of the preinfusion period and the percentual enhancement of the insulin response obtained at the second stimulation was, in low insulin responders, higher than and shifted to the left of the curve of the control subjects. In the group of diabetics, sensitivity for potentiation by glucose seemed not different from the controls. These studies indicate that the ability of glucose to initiate insulin release and its ability to generate time-bound potentiation in the islet correspond to two distinct functions. In the early stages of the diabetic syndrome, only the recognition of glucose as the initiator of an insulinogenic signal is impaired. The pancreatic beta-cell in these subjects seems to recognize normally glucose as the promotor of the potentiation.

Effects of exercise and lack of exercise on glucose tolerance and insulin sensitivity

1983 ◽  
Vol 55 (2) ◽  
pp. 512-517 ◽  
Author(s):  
G. W. Heath ◽  
J. R. Gavin ◽  
J. M. Hinderliter ◽  
J. M. Hagberg ◽  
S. A. Bloomfield ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Insulin Response ◽  
Insulin Binding ◽  
Normal Glucose Tolerance ◽  
Residual Effects ◽  
Oral Glucose ◽  
Glucose Load ◽  
Plasma Insulin Concentration ◽  
Normal Glucose ◽  
Blood Glucose Concentrations

Physically trained individuals have a markedly blunted insulin response to a glucose load and yet have normal glucose tolerance. This phenomenon has generally been ascribed to long-term adaptations to training which correlate with maximal oxygen uptake (VO2max) and reduced adiposity. Our study was undertaken to test the hypothesis that residual effects of the last bouts of exercise play an important role in this phenomenon. Eight well-trained subjects stopped training for 10 days. There were no significant changes in VO2max (58.6 +/- 2.2 vs. 57.6 +/- 2.1 ml/kg), estimated percent body fat (12.5 +/- 0.7 vs. 12.5 +/- 0.8%), or body weight. The maximum rise in plasma insulin concentration in response to a 100-g oral glucose load was 100% higher after 10 days without exercise than when the subjects were exercising regularly. Despite the increased insulin levels, blood glucose concentrations were higher after 10 days without exercise. Insulin binding to monocytes also decreased with physical inactivity. One bout of exercise after 11 days without exercise returned insulin binding and the insulin and glucose responses to an oral 100-g glucose load almost to the initial “trained” value. These results support our hypothesis.

Clinical, endocrine and metabolic effects of acarbose, an α-glucosidase inhibitor, in PCOS patients with increased insulin response and normal glucose tolerance

2001 ◽  
Vol 16 (10) ◽  
pp. 2066-2072 ◽  
Author(s):  
Lilliana Ciotta ◽  
Aldo E. Calogero ◽  
Marco Farina ◽  
Vincenzo De Leo ◽  
Antonio La Marca ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Insulin Response ◽  
Normal Glucose Tolerance ◽  
Metabolic Effects ◽  
Glucosidase Inhibitor ◽  
Normal Glucose

Hyperuricemia is associated with the increase of insulin release in non-obese subjects with normal glucose tolerance

2016 ◽  
Vol 42 (1) ◽  
pp. 1-5 ◽  
Author(s):  
Luis E. Simental-Mendía ◽  
Esteban Simental-Mendía ◽  
Martha Rodríguez-Morán ◽  
Fernando Guerrero-Romero
Keyword(s):  
Glucose Tolerance ◽  
Insulin Release ◽  
Normal Glucose Tolerance ◽  
Normal Glucose ◽  
Obese Subjects

scholarly journals Regional Variations of Insulin Secretion and Insulin Sensitivity in Japanese Participants With Normal Glucose Tolerance

2021 ◽  
Vol 8 ◽  
Author(s):  
Kiriko Watanabe ◽  
Moritake Higa ◽  
Yoshimasa Hasegawa ◽  
Akihiro Kudo ◽  
Richard C. Allsopp ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Regional Differences ◽  
Insulin Response ◽  
Normal Glucose Tolerance ◽  
Sensitivity Index ◽  
Insulinogenic Index ◽  
Genetic Traits ◽  
Normal Glucose

Purpose: Regional differences in dietary patterns in Asian countries might affect the balance of insulin response and sensitivity. However, this notion is yet to be validated. To clarify the regional differences in the insulin response and sensitivity and their relationship to nutrients, we compared the insulin secretory response during an oral glucose tolerance test in Japanese participants.Methods: This observational retrospective cohort study analyzed the data from participants with normal glucose tolerance (NGT) from four distinct areas of Japan with regard to the food environment: Fukushima, Nagano, Tokushima, and Okinawa based on data available in the Japanese National Health Insurance database.Results: Although the glucose levels were comparable among the four regions, the insulin responses were significantly different among the regions. This difference was observed even within the same BMI category. The plot between the insulin sensitivity index (Matsuda index) and insulinAUC/glucoseAUC or the insulinogenic index showed hyperbolic relationships with variations in regions. The indices of insulin secretion correlated positively with fat intake and negatively with the intake of fish, carbohydrate calories, and dietary fiber.Conclusions: We found that significant regional differences in insulin response and insulin sensitivity in Japanese participants and that nutritional factors may be linked to these differences independently of body size/adiposity. Insulin response and insulin sensitivity can vary among adult individuals, even within the same race and the same country, and are likely affected by environmental/lifestyle factors as well as genetic traits.

PLASMA CORTICOSTEROID, PLASMA INSULIN AND BLOOD SUGAR OF NORMAL FASTING AND DIABETIC SUBJECTS WITH OR WITHOUT HYPERCORTICISM

1968 ◽  
Vol 58 (4) ◽  
pp. 643-654 ◽  
Author(s):  
Vivian Harding Asfeldt ◽  
Kai R. Jørgensen
Keyword(s):  
Glucose Tolerance ◽  
Blood Sugar ◽  
Plasma Insulin ◽  
Insulin Response ◽  
Tolerance Test ◽  
Normal Glucose Tolerance ◽  
Oral Glucose ◽  
Acth Stimulation ◽  
Normal Glucose ◽  
Plasma Insulin Response

ABSTRACT Transient, maximum stimulation with β1–24 corticotrophin has been carried out in nine normal fasting subjects, in two fasting diabetics without hypercorticism and in three fasting diabetics with hypercorticism. Fluorimetric determinations of corticosteroids and determinations of immunological detectable insulin in plasma and blood sugar were made during stimulation. No significant variation in the blood sugar or the plasma insulin during transient, maximum ACTH stimulation was found either in normal fasting subjects or in fasting diabetics with or without hypercorticism. Moreover, in two diabetics with hypercorticism the plasma insulin response was measured during an oral glucose tolerance test. After treatment for approximately seven months with glucocorticosteroids, a reduced glucose tolerance and an increased plasma insulin response were found in one of these two patients. Four and a half months after the termination of steroid treatment, normal glucose tolerance and normal insulin responses were observed. In one patient, after several years of hypercorticism, a reduced glucose tolerance and a markedly reduced plasma insulin response were found.

DIMINISHED SENSITIVITY OF THE INSULIN RESPONSE TO GLUCOSE FOLLOWING GROWTH HORMONE INFUSION IN MAN

1976 ◽  
Vol 81 (4) ◽  
pp. 735-742 ◽  
Author(s):  
Ulf Adamson ◽  
Erol Cerasi
Keyword(s):  
Growth Hormone ◽  
Blood Glucose ◽  
Insulin Release ◽  
Dose Response ◽  
Plasma Insulin ◽  
Insulin Dose ◽  
Insulin Response ◽  
Insulinogenic Index ◽  
K Value ◽  
Insulin Response To Glucose

ABSTRACT The acute effect of growth hormone (GH) administration on the dose-kinetics of glucose-stimulated insulin release was investigated in eight healthy, non-obese male subjects. The glucose-insulin dose-response relationship in these subjects was established by performing glucose infusions at three different dose levels. In a second series of experiments, the glucose infusions were preceded by a 30 min infusion of GH (40 μg/kg body weight), terminated 60 min before administration of glucose. GH induced small but significant reductions in the basal levels of blood glucose and plasma insulin. The glucose tolerance (k-value) was diminished after GH at all glucose doses. Both the initial late phases of insulin response to glucose were impaired following GH treatment. This effect was most pronounced when the intermediary glucose dose (eliciting a blood glucose level around 300 mg/100 ml) was used. Thus, the insulinogenic index (whole period of stimulation) was reduced by GH to 88.9 ± 7.6, 60.4 ± 7.1 and 74.3 ± 11.0% of the respective controls when the smallest, the intermediate, and the largest glucose loads, respectively, were given. The blood glucose-plasma insulin dose-response curves were shifted to the right of the control ones when glucose infusion was preceded by GH. These findings suggest that GH diminishes the sensitivity of the islet for the insulin releasing action of glucose. Some possible mechanisms by which GH may modify insulin release are discussed.

Fat metabolism in human obesity

1994 ◽  
Vol 266 (4) ◽  
pp. E600-E605 ◽  
Author(s):  
P. J. Campbell ◽  
M. G. Carlson ◽  
N. Nurjhan
Keyword(s):  
Insulin Resistance ◽  
Fat Mass ◽  
Dose Response ◽  
Insulin Dose ◽  
Fat Free Mass ◽  
Maximal Response ◽  
Response Curves ◽  
Ffa Metabolism ◽  
Obese Subjects ◽  
The Right

Excessive fat turnover and oxidation might cause the insulin resistance of carbohydrate metabolism in obese humans. We studied the response of free fatty acid (FFA) metabolism in lean and obese volunteers to sequential insulin infusions of 4, 8, 25, and 400 mU.m-2.min-1. The insulin dose-response curves for suppression of FFA concentration, FFA turnover ([1-14C]palmitate), and lipolysis ([2H5]glycerol) were shifted to the right in the obese subjects (insulin concentrations that produced a half-maximal response, lean vs. obese: 103 +/- 21 vs. 273 +/- 41, 96 +/- 11 vs. 264 +/- 44, and 101 +/- 23 vs. 266 +/- 44 pM, all P < 0.05), consistent with insulin resistance of FFA metabolism in obesity. After the overnight fast, FFA turnover per fat mass was decreased in obese subjects (37 +/- 4 vs. 20 +/- 3 mumol.kg fat mass-1.min-1, P < 0.01) as the result of suppression of lipolysis by the hyperinsulinemia of obesity and an increased fractional reesterification of FFA before leaving the adipocyte (primary FFA reesterification; 0.14 +/- 0.03 vs. 0.35 +/- 0.06, P < 0.05). Nevertheless, FFA turnover per fat-free mass (FFM) was also greater in the obese volunteers (8.5 +/- 0.7 vs. 11.0 +/- 1.0 mumol.kg FFM-1.min-1, P < 0.05) but only as the result of increased reesterification of intravascular FFA (secondary reesterification; 1.8 +/- 0.5 vs. 4.8 +/- 1.1 mumol.kg FFM-1.min-1, P < 0.01), since FFA oxidation was the same in the two groups throughout the insulin dose-response curve.(ABSTRACT TRUNCATED AT 250 WORDS)

Diminished Serum Insulin Response to Glucose in Genetic Prediabetic Males with Normal Glucose Tolerance

Diabetes ◽  
1968 ◽  
Vol 17 (1) ◽  
pp. 17-26 ◽  
Author(s):  
J. S. Soeldner ◽  
R. E. Gleason ◽  
R. F. Williams ◽  
M. J. Garcia ◽  
D. M. Beardwood ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Serum Insulin ◽  
Insulin Response ◽  
Normal Glucose Tolerance ◽  
Normal Glucose ◽  
Insulin Response To Glucose
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