Insulin response to intravenous glucose in patients with anorexia nervosa showing low insulin response to oral glucose

1994 ◽  
Vol 79 (1) ◽  
pp. 217-222 ◽  
Author(s):  
T. Nozaki
Keyword(s):  
Anorexia Nervosa ◽  
Insulin Response ◽  
Oral Glucose ◽  
Intravenous Glucose ◽  
Low Insulin Response

FURTHER STUDIES ON HEALTHY SUBJECTS WITH LOW AND HIGH INSULIN RESPONSE TO GLUCOSE INFUSION

1967 ◽  
Vol 55 (2) ◽  
pp. 305-329 ◽  
Author(s):  
Erol Cerasi ◽  
Rolf Luft
Keyword(s):  
Healthy Subjects ◽  
Insulin Response ◽  
Glucose Infusion ◽  
Oral Glucose ◽  
Intravenous Glucose ◽  
The Family ◽  
High Insulin ◽  
History Of ◽  
Insulin Response To Glucose ◽  
Plasma Insulin Response

ABSTRACT In a previous paper it was shown that 15 out of 85 healthy subjects with a normal intravenous glucose tolerance demonstrated a low plasma insulin response to glucose infusion which was similar to that obtained in diabetic subjects. In the present paper it has been shown that the type of insulin response to glucose infusion was the same when the test was repeated. Low insulin responders to glucose infusion, as a group, also showed low insulin response to intravenous tolbutamide and oral glucose. This indicates that the type of insulin response is characteristic for a given subject irrespective of the stimulation used. There seemed to be no difference in the occurrence of diabetes in the family history of the groups of low and high insulin responders.

scholarly journals The Incretin Effect in Female Mice With Double Deletion of GLP-1 and GIP Receptors

2019 ◽  
Vol 4 (2) ◽  
Author(s):  
Bo Ahrén ◽  
Yuichiro Yamada ◽  
Yutaka Seino
Keyword(s):  
Insulin Secretion ◽  
Beta Cell ◽  
Beta Cell Function ◽  
Cell Function ◽  
Insulin Response ◽  
Oral Glucose ◽  
Incretin Effect ◽  
Intravenous Glucose ◽  
C Peptide ◽  
Female Mice

Abstract To establish the contribution of glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) for the incretin effect after oral glucose, studies were undertaken in female mice with genetic deletion of receptors for GIP and GLP-1 (double incretin receptor knockout [DIRKO] mice) and their wild-type (WT) counterparts. Insulin secretion was explored after oral glucose (doses ranging from 0 to 100 mg), after intravenous glucose (doses ranging from 0 to 0.75 g/kg), and after oral and intravenous glucose at matching circulating glucose. DIRKO mice had glucose intolerance after oral glucose challenges in association with impaired beta-cell function. Suprabasal area under the curve for C-peptide (AUCC-peptide) correlated linearly with suprabasal AUCglucose both in WT (r = 0.942, P = .017) and DIRKO mice (r = 0.972, P = .006). The slope of this regression was lower in DIRKO than in WT mice (0.012 ± 0.006 vs 0.031 ± 0.006 nmol C-peptide/mmol glucose, P = .042). In contrast, there was no difference in the insulin response to intravenous glucose between WT and DIRKO mice. Furthermore, oral and intravenous glucose administration at matching glucose levels showed that the augmentation of insulin secretion after oral glucose (the incretin effect) in WT mice (11.8 ± 2.3 nmol/L min) was entirely absent in DIRKO mice (3.3 ± 1.2 nmol/L min). We conclude that GIP and GLP-1 are required for normal glucose tolerance and beta-cell function after oral glucose in mice, that they are the sole incretin hormones after oral glucose at higher dose levels, and that they contribute by 65% to insulin secretion after oral glucose.

scholarly journals The effect of 8 days of strict bed rest on the incretin effect in healthy volunteers

2016 ◽  
Vol 120 (6) ◽  
pp. 608-614 ◽  
Author(s):  
Signe Tellerup Nielsen ◽  
Nina Majlund Harder-Lauridsen ◽  
Fabiana Braga Benatti ◽  
Anne-Sophie Wedell-Neergaard ◽  
Mark Preben Lyngbæk ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Blood Glucose ◽  
Physical Inactivity ◽  
Insulin Response ◽  
Bed Rest ◽  
Fat Free Mass ◽  
Oral Glucose ◽  
Incretin Effect ◽  
Intravenous Glucose ◽  
C Peptide

Bed rest and physical inactivity are the consequences of hospital admission for many patients. Physical inactivity induces changes in glucose metabolism, but its effect on the incretin effect, which is reduced in, e.g., Type 2 diabetes, is unknown. To investigate how 8 days of strict bed rest affects the incretin effect, 10 healthy nonobese male volunteers underwent 8 days of strict bed rest. Before and after the intervention, all volunteers underwent an oral glucose tolerance test (OGTT) followed by an intravenous glucose infusion (IVGI) on the following day to mimic the blood glucose profile from the OGTT. Blood glucose, serum insulin, serum C-peptide, plasma incretin hormones [glucagon-like peptide (GLP-1) and glucose-dependent insulinotropic peptide (GIP)], and serum glucagon were measured serially during both the OGTT and the IVGI. The incretin effect is calculated as the relative difference between the area under the curve for the insulin response during the OGTT and that of the corresponding IVGI, respectively. Concentrations of glucose, insulin, C-peptide, and GIP measured during the OGTT were higher after the bed rest intervention (all P < 0.05), whereas there was no difference in the levels of GLP-1 and Glucagon. Bed rest led to a mean loss of 2.4 kg of fat-free mass, and induced insulin resistance evaluated by the Matsuda index, but did not affect the incretin effect ( P = 0.6). In conclusion, 8 days of bed rest induces insulin resistance, but we did not see evidence of an associated change in the incretin effect.

Oral glucose tolerance test and insulin sensitivity in low insulin responders

1983 ◽  
Vol 104 (1) ◽  
pp. 77-84 ◽  
Author(s):  
A. Wajngot ◽  
R. Luft ◽  
S. Efendić
Keyword(s):  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Glucose Tolerance Test ◽  
Fasting Blood Glucose ◽  
Insulin Response ◽  
Tolerance Test ◽  
Oral Glucose ◽  
Infusion Test ◽  
Glucose Infusion Test ◽  
Low Insulin Response

Abstract. Oral and iv glucose tolerance, insulin response to iv and oral glucose load as well as insulin sensitivity were evaluated in 58 'low insulin responders'. They were selected from a group of 226 healthy subjects with normal fasting blood glucose and normal iv glucose tolerance test on the basis of a low insulin response during a standardized glucose infusion test (GIT). The insulin response to GIT was analysed by parameter identification in a mathematical model (parameter KI). Insulin sensitivity was also measured by computer analysis of GIT (parameter KG) and, in a limited group of subjects, by a somatostatin infusion test. Thirty-three low insulin responders had normal OGTT, whereas 5 demonstrated borderline-1, 16 borderline-2, and 4 decreased OGTT. The first group of subjects demonstrated normal or enhanced insulin sensitivity. Borderline and decreased OGTT, in most instances, was accompanied by decreased insulin sensitivity, implying that a subgroup of low insulin responders exhibited signs of both impaired insulin response to glucose and insulin resistance. Since these defects characterize manifest type-2 diabetes, these subjects possibly may run a high risk to develop this type of diabetes. On the other hand, low insulin response in combination with increased insulin sensitivity may reflect adaptation of the secretory capacity of B-cells to the need of insulin.

Importance of cholinergic innervation of the pancreas for glucose tolerance in the rat

1981 ◽  
Vol 241 (5) ◽  
pp. E337-E341
Author(s):  
E. R. Trimble ◽  
H. R. Berthoud ◽  
E. G. Siegel ◽  
B. Jeanrenaud ◽  
A. E. Renold
Keyword(s):  
Glucose Tolerance ◽  
Vagus Nerve ◽  
Insulin Release ◽  
Insulin Response ◽  
Pancreatic Tissue ◽  
Cholinergic Innervation ◽  
Oral Glucose ◽  
Oral Glucose Tolerance ◽  
Experimental Conditions ◽  
Intravenous Glucose

Because cholinergic innervation of the pancreas is of importance in control of oral glucose tolerance, it seems important to determine whether transplanted pancreatic tissue becomes reinnervated with cholinergic fibers. Oral and intravenous glucose tolerance tests (ivGTT) were performed with and without atropine treatment on streptozotocin-diabetic rats treated by intraportal transplantation of isogenic islets 13-15 wk previously and on sham-operated nondiabetic controls. Atropine had no effect on the ivGTT of transplanted rats or controls. In controls atropine caused a deterioration of the oral glucose tolerance, abolished the preabsorptive insulin release, and also diminished the early part of the glucose-induced insulin release in these animals. In the absence of atropine, transplanted rats had pathological oral glucose tolerance, preabsorptive insulin release was absent, and glucose-induced insulin release was diminished compared to controls. Atropine had little effect on the oral GTT of transplanted rats. The present results underline the importance of the vagus nerve in the control of oral glucose tolerance and show that the vagus nerve in rats, at least under these experimental conditions, does not modulate the insulin response to intravenous glucose. The results suggest that intraportally transplanted islets remain functionally vagotomized.

scholarly journals OR23-06 Is the Improved Glucose Homeostasis in Patients with Acromegaly Treated with Pegvisomant Caused by Improved Glucagon Secretion?

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Nanna Thurmann Jørgensen, miss ◽  
Trine Møller Erichsen ◽  
Marianne C Klose ◽  
Morten Buus Jørgensen ◽  
Thomas Idorn ◽  
...  
Keyword(s):  
Glucose Homeostasis ◽  
Insulin Response ◽  
Glucagon Secretion ◽  
Somatostatin Analogues ◽  
Favorable Effect ◽  
Oral Glucose ◽  
Diabetic Patients ◽  
Healthy Controls ◽  
Incretin Effect ◽  
Intravenous Glucose

Abstract Context: Active acromegaly is associated with impaired glucose metabolism, which improves upon treatment. Treatment with first generation somatostatin analogues (SSA) has a detrimental effect on insulin secretion, but the effect on glucose homeostasis is neutralized by the reduction in growth hormone (GH) and Insulin-like growth factor-1 (IGF-1). Treatment with GH receptor antagonists has a more favorable effect on glucose homeostasis. Objective: To describe the secretion of glucose, insulin, glucagon, glucagon-like peptide-1 (GLP1), and glucose-dependent insulinotropic polypeptide (GIP) in surgically treated patients with acromegaly treated or not with somatostatin analogues, either as monotherapy (SSA) or in co-treatment with pegvisomant (SSA+PEG), respectively, compared to healthy controls. Methods: Descriptive study of data from 23 surgically treated, non-diabetic patients with acromegaly and 6 healthy controls. After an overnight fast, all participants underwent a three-hour 75 g oral glucose tolerance test (OGTT) and subsequently a three-hour isoglycaemic intravenous glucose infusion on a separate day. Analysis: Baseline hormone concentrations, time to peak and area under the curve (AUC) on the OGTT-day, and the incretin effect in the patient groups and controls were compared using analysis of variance with post-hoc analysis. Results: The total group of patients treated with somatostatin analogues (N=15) had numerically impaired glucose, insulin, GLP1 and glucagon responses (AUC, P&gt;0.05 respectively), and an impaired GIP-response (AUC, P=0.007) during OGTT as compared to patients not treated with somatostatin analogues and healthy controls. Similarly, the incretin effect was numerically impaired. Patients co-treated with pegvisomant (SSA+PEG, N=4) had a numerically increased secretion of insulin and glucagon compared to patients on SSA (N=11) during OGTT (insulin AUC mean (SEM), SSA+PEG 49 nmol/l*min (8.3) vs SSA 25 (3.4), P&gt;0.05) [healthy controls 62 (13.6)]; glucagon AUC, SSA+PEG 823 pmol/l*min (194) vs SSA 332 (69), P&gt;0.05) [healthy controls 946 (233)]). GIP secretion remained significantly impaired, whereas GLP1 secretion was numerically increased with PEG (SSA+PEG 3088 pmol/l*min (366) vs SSA 2401 (239), P&gt;0.05) [healthy controls 3972 (451)] but remained without a glucose-dependant increase as in SSA. The incretin effect numerically increased in SSA+PEG compared to SSA (SSA+PEG 49.9% (13.9) vs SSA 33.6% (47.4), P&gt;0.05) [healthy controls 55.5% (7.7)]. Conclusion: Somatostatin analogues impaired the secretion of both insulin, glucagon and incretin hormones secretion. Co-treatment with pegvisomant seemed to counteract the somatostatinergic inhibition of the glucagon secretion and improved the insulin response to OGTT. We speculate that pegvisomant exerts its action via GH-receptors on pancreatic δ-cells.

scholarly journals Antidepressant Effects on Insulin Sensitivity and Proinflammatory Cytokines in the Depressed Males

2010 ◽  
Vol 2010 ◽  
pp. 1-7 ◽  
Author(s):  
Yi-Chyan Chen ◽  
Wei-Win Lin ◽  
Yu-Jung Chen ◽  
Wei-Chung Mao ◽  
Yi-Jen Hung
Keyword(s):  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Rating Scale ◽  
Glucose Tolerance Test ◽  
Antidepressant Treatment ◽  
Insulin Response ◽  
Tolerance Test ◽  
Oral Glucose ◽  
Intravenous Glucose ◽  
Testing Procedures

Growing evidence suggests that mood disorder is associated with insulin resistance and inflammation. Thus the effects of antidepressants on insulin sensitivity and proinflammatory responses will be a crucial issue for depression treatment. In this study, we enrolled 43 non-diabetic young depressed males and adapted standard testing procedures to assess glucose metabolism during 4-week hospitalization. Before and after the 4-week antidepressant treatment, participants underwent oral glucose tolerance test (OGTT) and frequently sampled intravenous glucose tolerance test (FSIGT). Insulin sensitivity (SI), glucose effectiveness (SG), acute insulin response, and disposition index (DI) were estimated using the minimal model method. The plasma levels of C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor-α(TNF-α), and adiponectin were measured. The Hamilton depression rating scale (HAM-D) total scores were reduced significantly during the course of treatment. There were no significant changes in the parameters ofSI,SG, and DI. Compared to drug naïve status, the level of plasma IL-6 was significantly elevated (0.77to1.30 pg/ml;P=.001) after antidepressant therapy. However, the concentrations of CRP, TNF-α, and adiponectin showed no differences during the course of treatment. The results suggest that antidepressants may promote stimulatory effect on the IL-6 production in the early stage of antidepressant treatment.

scholarly journals The augmenting effect on insulin secretion by oral versus intravenous glucose is exaggerated by high-fat diet in mice

2008 ◽  
Vol 197 (1) ◽  
pp. 181-187 ◽  
Author(s):  
Bo Ahrén ◽  
Maria Sörhede Winzell ◽  
Giovanni Pacini
Keyword(s):  
Insulin Secretion ◽  
High Fat Diet ◽  
Insulin Response ◽  
Area Under The Curve ◽  
Oral Glucose ◽  
Incretin Effect ◽  
High Fat ◽  
Intravenous Glucose ◽  
Insulin Resistant ◽  
Glucose Levels

To study whether the incretin effect is involved in adaptively increased insulin secretion in insulin resistance, glucose was infused at a variable rate to match glucose levels after oral glucose (25 mg) in normal anesthetized C57BL/6J female mice or in mice rendered insulin resistant by 8 weeks of high-fat feeding. Insulin response was markedly higher after oral than i.v. glucose in both groups, and this augmentation was even higher in high-fat fed than normal mice. In normal mice, the area under the curve (AUCinsulin) was augmented from 4.0±0.8 to 8.0±1.8 nmol/l×60 min by the oral glucose, i.e. by a factor of 2 (P=0.023), whereas in the high-fat fed mice, AUCinsulin was augmented from 0.70±0.4 to 12.4±2.5 nmol/l×60 min, i.e. by a factor of 17 (P<0.001). To examine whether the incretin hormone glucagon-like peptide-1 (GLP-1) is responsible for this difference, the effect of i.v. GLP-1 was compared in normal and high-fat fed mice. The sensitivity to i.v. GLP-1 in stimulating insulin secretion was increased in the high-fat diet fed mice: the lowest effective dose of GLP-1 was 650 pmol/kg in normal mice and 13 pmol/kg in the high-fat diet fed mice. We conclude that 1) the incretin effect contributes by ∼50% to insulin secretion by the oral glucose in normal mice, 2) this effect is markedly exaggerated in insulin-resistant mice fed a high-fat diet, and 3) this augmented incretin contribution in the high-fat fed mice may partially be explained by GLP-1.

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