scholarly journals Brain glucagon-like peptide-1 increases insulin secretion and muscle insulin resistance to favor hepatic glycogen storage

2005 ◽  
Vol 115 (12) ◽  
pp. 3554-3563 ◽  
Author(s):  
C. Knauf
Keyword(s):  
Insulin Resistance ◽  
Insulin Secretion ◽  
Glycogen Storage ◽  
Hepatic Glycogen ◽  
Muscle Insulin Resistance ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

GLP-1 response to sequential mixed meals: influence of insulin resistance

2017 ◽  
Vol 131 (24) ◽  
pp. 2901-2910 ◽  
Author(s):  
Eleni Rebelos ◽  
Brenno Astiarraga ◽  
Roberto Bizzotto ◽  
Andrea Mari ◽  
Maria Laura Manca ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Release ◽  
Cell Function ◽  
Fasting Glucose ◽  
Insulin Resistant ◽  
Esterified Fatty Acids ◽  
Β Cell Function ◽  
Glucose Sensitivity ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Previous work has shown that potentiation of insulin release is impaired in non-diabetic insulin resistance; we tested the hypothesis that this defect may be related to altered glucagon-like peptide-1 (GLP-1) release. On consecutive days, 82 non-diabetic individuals, classified as insulin sensitive (IS, n=41) or insulin resistant (IR, n=41) by the euglycaemic clamp, were given two sequential mixed meals with standard (75 g, LCD) or double (150 g, HCD) carbohydrate content. Plasma glucose, insulin, C-peptide, non-esterified fatty acids (NEFA) and GLP-1 concentrations were measured; β-cell function (glucose sensitivity and potentiation) was resolved by mathematical modelling. Fasting GLP-1 levels were higher in IR than IS (by 15%, P=0.006), and reciprocally related to insulin sensitivity after adjustment for sex, age, fat mass, fasting glucose or insulin concentrations. Mean postprandial GLP-1 responses were tightly correlated with fasting GLP-1, were higher for the second than the first meal, and higher in IR than IS subjects but only with LCD. In contrast, incremental GLP-1 responses were higher during (i) the second than the first meal, (ii) on HCD than LCD, and (iii) significantly smaller in IR than IS independently of meal and load. Potentiation of insulin release was markedly reduced in IR vs IS across meal and carbohydrate loading. In the whole dataset, incremental GLP-1 was directly related to potentiation, and both were inversely related to mean NEFA concentrations. We conclude that (a) raised GLP-1 tone may be inherently linked with a reduced GLP-1 response and (b) defective post-meal GLP-1 response may be one mechanism for impaired potentiation of insulin release in insulin resistance.

The Effect of Zinc-Crystallized Glucagon-Like Peptide-1 on Insulin Secretion of Macroencapsulated Pancreatic Islets

2001 ◽  
Vol 7 (1) ◽  
pp. 35-44 ◽  
Author(s):  
Heather Gappa ◽  
Miroslav Baudyš ◽  
Jae Joon Koh ◽  
Sung Wan Kim ◽  
You Han Bae
Keyword(s):  
Insulin Secretion ◽  
Pancreatic Islets ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

scholarly journals Subthreshold α2-Adrenergic Activation Counteracts Glucagon-Like Peptide-1 Potentiation of Glucose-Stimulated Insulin Secretion

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Minglin Pan ◽  
Guang Yang ◽  
Xiuli Cui ◽  
Shao-Nian Yang
Keyword(s):  
Insulin Secretion ◽  
Insulin Release ◽  
Adrenergic Agonist ◽  
Signaling Systems ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Glucose Stimulated Insulin Secretion ◽  
Insulin Secretory Response ◽  
Adrenergic Activation ◽  
Gi Proteins

The pancreatic β cell harbors α2-adrenergic and glucagon-like peptide-1 (GLP-1) receptors on its plasma membrane to sense the corresponding ligands adrenaline/noradrenaline and GLP-1 to govern glucose-stimulated insulin secretion. However, it is not known whether these two signaling systems interact to gain the adequate and timely control of insulin release in response to glucose. The present work shows that the α2-adrenergic agonist clonidine concentration-dependently depresses glucose-stimulated insulin secretion from INS-1 cells. On the contrary, GLP-1 concentration-dependently potentiates insulin secretory response to glucose. Importantly, the present work reveals that subthreshold α2-adrenergic activation with clonidine counteracts GLP-1 potentiation of glucose-induced insulin secretion. This counteractory process relies on pertussis toxin- (PTX-) sensitive Gi proteins since it no longer occurs following PTX-mediated inactivation of Gi proteins. The counteraction of GLP-1 potentiation of glucose-stimulated insulin secretion by subthreshold α2-adrenergic activation is likely to serve as a molecular mechanism for the delicate regulation of insulin release.

scholarly journals Glucagon-Like Peptide-1 as Predictor of Body Mass Index and Dentate Gyrus Neurogenesis: Neuroplasticity and the Metabolic Milieu

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Jeremy D. Coplan ◽  
Shariful Syed ◽  
Tarique D. Perera ◽  
Sasha L. Fulton ◽  
Mary Ann Banerji ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Body Mass Index ◽  
Body Weight ◽  
Dentate Gyrus ◽  
Body Mass ◽  
Adult Neurogenesis ◽  
Plasma Lipids ◽  
High Plasma ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Glucagon-like peptide-1 (GLP-1) regulates carbohydrate metabolism and promotes neurogenesis. We reported an inverse correlation between adult body mass and neurogenesis in nonhuman primates. Here we examine relationships between physiological levels of the neurotrophic incretin, plasma GLP-1 (pGLP-1), and body mass index (BMI) in adolescence to adult neurogenesis and associations with a diabesity diathesis and infant stress. Morphometry, fasting pGLP-1, insulin resistance, and lipid profiles were measured in early adolescence in 10 stressed and 4 unstressed male bonnet macaques. As adults, dentate gyrus neurogenesis was assessed by doublecortin staining. High pGLP-1, low body weight, and low central adiposity, yet peripheral insulin resistance and high plasma lipids, during adolescence were associated with relatively high adult neurogenesis rates. High pGLP-1 also predicted low body weight with, paradoxically, insulin resistance and high plasma lipids. No rearing effects for neurogenesis rates were observed. We replicated an inverse relationship between BMI and neurogenesis. Adolescent pGLP-1 directly predicted adult neurogenesis. Two divergent processes relevant to human diabesity emerge—high BMI, low pGLP-1, and low neurogenesis and low BMI, high pGLP-1, high neurogenesis, insulin resistance, and lipid elevations. Diabesity markers putatively reflect high nutrient levels necessary for neurogenesis at the expense of peripheral tissues.

Self-inducible secretion of glucagon-like peptide-1 (GLP-1) that allows MIN6 cells to maintain insulin secretion and insure cell survival

2012 ◽  
Vol 349 (2) ◽  
pp. 281-288 ◽  
Author(s):  
Koji Nakashima ◽  
Masashi Shimoda ◽  
Sumiko Hamamoto ◽  
Fuminori Tatsumi ◽  
Hidenori Hirukawa ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Cell Survival ◽  
Min6 Cells ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

scholarly journals Differential effects of glucagon-like peptide-1 on microvascular recruitment and glucose metabolism in short- and long-term insulin resistance

2015 ◽  
Vol 593 (9) ◽  
pp. 2185-2198 ◽  
Author(s):  
Kim A. Sjøberg ◽  
Stephen Rattigan ◽  
Jacob F. Jeppesen ◽  
Anne-Marie Lundsgaard ◽  
Jens J. Holst ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Glucose Metabolism ◽  
Differential Effects ◽  
Short And Long Term ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Microvascular Recruitment
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