scholarly journals Neuropeptides and intestinal tract in the control of glucose Homeostasis Hypothalamic regulatory peptides and the regulation of food intake and energy balance: signals or noise?

1991 ◽  
Vol 50 (3) ◽  
pp. 527-544 ◽  
Author(s):  
Gareth Williams ◽  
Pauline E. McKibbin ◽  
H. David McCarthy
Keyword(s):  
Energy Balance ◽  
Food Intake ◽  
Glucose Homeostasis ◽  
Intestinal Tract ◽  
Regulatory Peptides

scholarly journals The CNS glucagon-like peptide-2 receptor in the control of energy balance and glucose homeostasis

2014 ◽  
Vol 307 (6) ◽  
pp. R585-R596 ◽  
Author(s):  
Xinfu Guan
Keyword(s):  
Energy Balance ◽  
Food Intake ◽  
Signaling Pathway ◽  
Glucose Homeostasis ◽  
Hepatic Glucose Production ◽  
Physiological Role ◽  
Glucose Production ◽  
Short Chain Fatty Acids ◽  
Hepatic Insulin Resistance ◽  
Membrane Excitability

The gut-brain axis plays a key role in the control of energy balance and glucose homeostasis. In response to luminal stimulation of macronutrients and microbiota-derived metabolites (secondary bile acids and short chain fatty acids), glucagon-like peptides (GLP-1 and -2) are cosecreted from endocrine L cells in the gut and coreleased from preproglucagonergic neurons in the brain stem. Glucagon-like peptides are proposed as key mediators for bariatric surgery-improved glycemic control and energy balance. Little is known about the GLP-2 receptor (Glp2r)-mediated physiological roles in the control of food intake and glucose homeostasis, yet Glp1r has been studied extensively. This review will highlight the physiological relevance of the central nervous system (CNS) Glp2r in the control of energy balance and glucose homeostasis and focuses on cellular mechanisms underlying the CNS Glp2r-mediated neural circuitry and intracellular PI3K signaling pathway. New evidence (obtained from Glp2r tissue-specific KO mice) indicates that the Glp2r in POMC neurons is essential for suppressing feeding behavior, gastrointestinal motility, and hepatic glucose production. Mice with Glp2r deletion selectively in POMC neurons exhibit hyperphagic behavior, accelerated gastric emptying, glucose intolerance, and hepatic insulin resistance. GLP-2 differentially modulates postsynaptic membrane excitability of hypothalamic POMC neurons in Glp2r- and PI3K-dependent manners. GLP-2 activates the PI3K-Akt-FoxO1 signaling pathway in POMC neurons by Glp2r-p85α interaction. Intracerebroventricular GLP-2 augments glucose tolerance, suppresses glucose production, and enhances insulin sensitivity, which require PI3K (p110α) activation in POMC neurons. Thus, the CNS Glp2r plays a physiological role in the control of food intake and glucose homeostasis. This review will also discuss key questions for future studies.

196-LB: Synergetic and Distinct Roles in the Control of Food Intake and Energy Balance for Subpopulations of NTS Neurons

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 196-LB
Author(s):  
WENWEN C. CHENG ◽  
ERMELINDA NDOKA ◽  
BASMA MAERZ ◽  
KAREN J. ROELOFS ◽  
CHRISTOPHER J. RHODES ◽  
...  
Keyword(s):  
Energy Balance ◽  
Food Intake

Regulation of energy balance and controls of food intake in humans

Appetite ◽  
1990 ◽  
Vol 14 (1) ◽  
pp. 67-69 ◽  
Author(s):  
Theresa A. Spiegel
Keyword(s):  
Energy Balance ◽  
Food Intake

Secretin as a satiation whisperer with the potential to turn into an obesity-curbing knight

Endocrinology ◽  
2021 ◽  
Author(s):  
Katharina Schnabl ◽  
Yongguo Li ◽  
Mueez U-Din ◽  
Martin Klingenspor
Keyword(s):  
Bariatric Surgery ◽  
Body Weight ◽  
Energy Balance ◽  
Food Intake ◽  
Weight Control ◽  
Therapeutic Potential ◽  
Physiological Mechanism ◽  
Gut Hormones ◽  
Metabolic Effects ◽  
Beneficial Effects

Abstract The obesity pandemic requires effective preventative and therapeutic intervention strategies. Successful and sustained obesity treatment is currently limited to bariatric surgery. Modulating the release of gut hormones is considered promising to mimic bariatric surgery with its beneficial effects on food intake, body weight and blood glucose levels. The gut peptide secretin was the first molecule to be termed a hormone; nevertheless, it only recently has been established as a legitimate anorexigenic peptide. In contrast to gut hormones that crosstalk with the brain either directly or by afferent neuronal projections, secretin mediates meal-associated brown fat thermogenesis to induce meal termination, thereby qualifying this physiological mechanism as an attractive, peripheral target for the treatment of obesity. In this perspective, it is of pivotal interest to deepen our yet superficial knowledge on the physiological roles of secretin as well as meal-associated thermogenesis in energy balance and body weight regulation. Of note, the emerging differences between meal-associated thermogenesis and cold-induced thermogenesis must be taken into account. In fact, there is no correlation between these two entities. In addition, the investigation of potential effects of secretin in hedonic-driven food intake, bariatric surgery as well as chronic treatment using suitable application strategies to overcome pharmacokinetic limitations will provide further insight into its potential to influence energy balance. The aim of this article is to review the facts on secretin’s metabolic effects, address prevailing gaps in our knowledge, and provide an overview on the opportunities and challenges of the therapeutic potential of secretin in body weight control.

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