scholarly journals Glucagon, GLP-1 and Thermogenesis

2019 ◽  
Vol 20 (14) ◽  
pp. 3445 ◽  
Author(s):  
Ismael González-García ◽  
Edward Milbank ◽  
Carlos Diéguez ◽  
Miguel López ◽  
Cristina Contreras
Keyword(s):  
Energy Expenditure ◽  
Direct Action ◽  
Short Review ◽  
Obesity And Diabetes ◽  
Promising Target ◽  
Brown Adipose ◽  
Endocrine Factors ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Maintain Body Temperature

Brown adipose tissue (BAT) thermogenesis is a conserved mechanism to maintain body temperature in mammals. However, since BAT contribution to energy expenditure can represent a relevant modulator of metabolic homeostasis, many studies have focused on the nervous system and endocrine factors that control the activity of this tissue. There is long-established evidence that the counter-regulatory hormone glucagon negatively influences energy balance, enhances satiety, and increases energy expenditure. Despite compelling evidence showing that glucagon has direct action on BAT thermogenesis, recent findings are questioning this conventional attribute of glucagon action. Glucagon like peptide-1 (GLP-1) is an incretin secreted by the intestinal tract which strongly decreases feeding, and, furthermore, improves metabolic parameters associated with obesity and diabetes. Therefore, GLP-1 receptors (GLP-1-R) have emerged as a promising target in the treatment of metabolic disorders. In this short review, we will summarize the latest evidence in this regard, as well as the current therapeutic glucagon- and GLP-1-based approaches to treating obesity.

scholarly journals Energy Expenditure, Satiety, and Plasma Ghrelin, Glucagon-Like Peptide 1, and Peptide Tyrosine-Tyrosine Concentrations following a Single High-Protein Lunch

2008 ◽  
Vol 138 (4) ◽  
pp. 698-702 ◽  
Author(s):  
Astrid J. Smeets ◽  
Stijn Soenen ◽  
Natalie D. Luscombe-Marsh ◽  
Øydis Ueland ◽  
Margriet S. Westerterp-Plantenga
Keyword(s):  
Energy Expenditure ◽  
High Protein ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

scholarly journals Oleoylethanolamide modulates glucagon-like peptide-1 receptor agonist signaling and enhances exendin-4-mediated weight loss in obese mice

2018 ◽  
Vol 315 (4) ◽  
pp. R595-R608 ◽  
Author(s):  
Jacob D. Brown ◽  
Danielle McAnally ◽  
Jennifer E. Ayala ◽  
Melissa A. Burmeister ◽  
Camilo Morfa ◽  
...  
Keyword(s):  
Weight Loss ◽  
Energy Expenditure ◽  
Receptor Agonist ◽  
Day Treatment ◽  
Mtor Pathway ◽  
Obese Mice ◽  
Promote Weight Loss ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Long Acting

Long-acting glucagon-like peptide-1 (GLP-1) receptor (GLP-1R) agonists (GLP-1RA), such as exendin-4 (Ex4), promote weight loss. On the basis of a newly discovered interaction between GLP-1 and oleoylethanolamide (OEA), we tested whether OEA enhances GLP-1RA-mediated anorectic signaling and weight loss. We analyzed the effect of GLP-1+OEA and Ex4+OEA on canonical GLP-1R signaling and other proteins/pathways that contribute to the hypophagic action of GLP-1RA (AMPK, Akt, mTOR, and glycolysis). We demonstrate that OEA enhances canonical GLP-1R signaling when combined with GLP-1 but not with Ex4. GLP-1 and Ex4 promote phosphorylation of mTOR pathway components, but OEA does not enhance this effect. OEA synergistically enhanced GLP-1- and Ex4-stimulated glycolysis but did not augment the hypophagic action of GLP-1 or Ex4 in lean or diet-induced obese (DIO) mice. However, the combination of Ex4+OEA promoted greater weight loss in DIO mice than Ex4 or OEA alone during a 7-day treatment. This was due in part to transient hypophagia and increased energy expenditure, phenotypes also observed in Ex4-treated DIO mice. Thus, OEA augments specific GLP-1RA-stimulated signaling but appears to work in parallel with Ex4 to promote weight loss in DIO mice. Elucidating cooperative mechanisms underlying Ex4+OEA-mediated weight loss could, therefore, be leveraged toward more effective obesity therapies.

Liraglutide for psychiatric disorders: clinical evidence and challenges

2018 ◽  
Vol 36 (2) ◽  
Author(s):  
Mehmet Akif Camkurt ◽  
Luca Lavagnino ◽  
Xiang Y. Zhang ◽  
Antonio L Teixeira
Keyword(s):  
Risk Factors ◽  
Psychiatric Disorders ◽  
Clinical Evidence ◽  
Preclinical Studies ◽  
Potential Candidate ◽  
Obesity And Diabetes ◽  
Treatment Of Diabetes ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Diabetes And Obesity

Abstract Obesity and diabetes are both risk factors and consequences of psychiatric disorders. Glucagon like peptide 1 (GLP-1) receptor agonists such as liraglutide are widely used in the treatment of diabetes and obesity. There are considerable amounts of preclinical studies showing the effects of liraglutide on promotion of neurogenesis, while preventing apoptosis and oxidation. Preliminary clinical evidence has suggested that liraglutide could decrease weight gain, improve cognition and prevent cognitive decline. Accordingly, liraglutide has been regarded as a potential candidate for the management of psychiatric disorders. Herein, we will discuss the association between obesity/diabetes and psychiatric disorders, and the emerging use of liraglutide in psychiatry.

The effect of glucagon-like peptide 1 and glucagon-like peptide 1 receptor agonists on energy expenditure: A systematic review and meta-analysis

2018 ◽  
Vol 142 ◽  
pp. 222-235 ◽  
Author(s):  
Michel Garcia Maciel ◽  
Bruna Teles Soares Beserra ◽  
Fernanda Cerqueira Barroso Oliveira ◽  
Carolina Martins Ribeiro ◽  
Michella Soares Coelho ◽  
...  
Keyword(s):  
Systematic Review ◽  
Energy Expenditure ◽  
Meta Analysis ◽  
Receptor Agonists ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Incretins: pathophysiological and therapeutic implications of glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1

2008 ◽  
Vol 61 (4) ◽  
pp. 401-409 ◽  
Author(s):  
L R Ranganath
Keyword(s):  
B Cell ◽  
Cell Mass ◽  
Therapeutic Agents ◽  
Glycosidase Inhibitors ◽  
Therapeutic Implications ◽  
Obesity And Diabetes ◽  
Control Of Diabetes ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
High Doses

Incretins such as glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are intestinal postprandial hormones that stimulate insulin release from the pancreas as long as circulating glucose concentrations are raised. In addition to their effect on insulin secretion and consequent glucose lowering, GIP and GLP-1, especially the latter, have a number of physiological effects such as inhibition of glucagon release, gastric emptying and food intake, as well as a tropic action on pancreatic B-cell mass. There is currently a pandemic of obesity and diabetes, and existing treatments are largely inadequate both in regard to efficacy as well as their ability to tackle important factors in the pathogenesis of type 2 diabetes (T2D). There is increasing evidence that current treatments do not address the issue of progressive B-cell failure in T2D. Since obesity is the engine that is driving the epidemic of diabetes, it is disappointing that most treatments that succeed in lowering plasma glucose are also associated with weight gain. It is now well established that intensively treated T2D has a better outcome than standard treatment. Consequently, achieving better control of diabetes with lower HbA1c is the goal of optimal treatment. Despite the use of usual therapeutic agents in T2D, often in high doses and as combinations, such as metformin, sulphonylurea, α-glycosidase inhibitors, thiazolidinediones and a number of animal and human insulin preparations, optimal control of glycaemia is not achieved. The use of incretins as therapeutic agents offers a new approach to the treatment of T2D.

scholarly journals Energy compensation in response to aerobic exercise training in overweight adults

2018 ◽  
Vol 315 (4) ◽  
pp. R619-R626 ◽  
Author(s):  
Kyle D. Flack ◽  
Kelsey Ufholz ◽  
LuAnn Johnson ◽  
John S. Fitzgerald ◽  
James N. Roemmich
Keyword(s):  
Energy Expenditure ◽  
Food Reinforcement ◽  
Resting Metabolic Rate ◽  
Acylated Ghrelin ◽  
Compensatory Responses ◽  
Energy Stores ◽  
Energy Compensation ◽  
Exercise Energy Expenditure ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Weight loss from exercise is often less than expected. Putative compensatory mechanisms may limit exercise-induced reductions in body fat and might be proportional to exercise energy expenditure (ExEE). This study was conducted to determine compensation for (the difference between accumulated exercise energy expenditure and changes in body tissue energy stores) and compensatory responses to 1,500 or 3,000 kcal/wk of ExEE. Overweight-to-obese ( n = 36) sedentary men and women were randomized to groups expending 300 or 600 kcal/exercise session, 5 days/wk, for 12 wk. Fourteen participants in the 300-kcal group and 15 in the 600-kcal group completed the study. The primary outcome was energy compensation assessed through changes in body tissue energy stores. Secondary outcomes were putative compensatory responses of resting metabolic rate, food reinforcement, dietary intake, and serum acylated ghrelin and glucagon-like peptide-1. All measures were determined pre- and posttraining. The 3,000 kcal/wk group decreased ( P < 0.01) percentage and kilograms of body fat, while the 1,500 kcal/wk group did not. The 1,500 and 3,000 kcal/wk groups compensated for 943 (−164 to 2,050) and 1,007 (32 to 1,982) kcal/wk (mean, 95% CI, P ≥ 0.93), or 62.9% and 33.6% of ExEE, respectively. Resting metabolic rate and energy intake did not change. Food reinforcement and glucagon-like peptide-1 decreased ( P < 0.02), whereas acylated ghrelin increased ( P ≤ 0.02). Compensation is not proportional to ExEE. Similar energy compensation occurred in response to1,500 and 3,000 kcal/wk of ExEE. ExEE of 3,000 kcal/wk is sufficient to exceed compensatory responses and reduce fat mass.

Sign in / Sign up

Export Citation Format

Share Document