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      Peptides and Food Intake

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          Abstract

          The mechanisms for controlling food intake involve mainly an interplay between gut, brain, and adipose tissue (AT), among the major organs. Parasympathetic, sympathetic, and other systems are required for communication between the brain satiety center, gut, and AT. These neuronal circuits include a variety of peptides and hormones, being ghrelin the only orexigenic molecule known, whereas the plethora of other factors are inhibitors of appetite, suggesting its physiological relevance in the regulation of food intake and energy homeostasis. Nutrients generated by food digestion have been proposed to activate G-protein-coupled receptors on the luminal side of enteroendocrine cells, e.g., the L-cells. This stimulates the release of gut hormones into the circulation such as glucagon-like peptide-1 (GLP-1), oxyntomodulin, pancreatic polypeptides, peptide tyrosine tyrosine, and cholecystokinin, which inhibit appetite. Ghrelin is a peptide secreted from the stomach and, in contrast to other gut hormones, plasma levels decrease after a meal and potently stimulate food intake. Other circulating factors such as insulin and leptin relay information regarding long-term energy stores. Both hormones circulate at proportional levels to body fat content, enter the CNS proportionally to their plasma levels, and reduce food intake. Circulating hormones can influence the activity of the arcuate nucleus (ARC) neurons of the hypothalamus, after passing across the median eminence. Circulating factors such as gut hormones may also influence the nucleus of the tractus solitarius (NTS) through the adjacent circumventricular organ. On the other hand, gastrointestinal vagal afferents converge in the NTS of the brainstem. Neural projections from the NTS, in turn, carry signals to the hypothalamus. The ARC acts as an integrative center, with two major subpopulations of neurons influencing appetite, one of them coexpressing neuropeptide Y and agouti-related protein (AgRP) that increases food intake, whereas the other subpopulation coexpresses pro-opiomelanocortin (POMC) and cocaine and amphetamine-regulated transcript that inhibits food intake. AgRP antagonizes the effects of the POMC product, α-melanocyte-stimulating hormone (α-MSH). Both populations project to areas important in the regulation of food intake, including the hypothalamic paraventricular nucleus, which also receives important inputs from other hypothalamic nuclei.

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          Environmental contributions to the obesity epidemic.

          The current epidemic of obesity is caused largely by an environment that promotes excessive food intake and discourages physical activity. Although humans have evolved excellent physiological mechanisms to defend against body weight loss, they have only weak physiological mechanisms to defend against body weight gain when food is abundant. Control of portion size, consumption of a diet low in fat and energy density, and regular physical activity are behaviors that protect against obesity, but it is becoming difficult to adopt and maintain these behaviors in the current environment. Because obesity is difficult to treat, public health efforts need to be directed toward prevention.
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            Effects of the obese gene product on body weight regulation in ob/ob mice.

            C57BL/6J mice with a mutation in the obese (ob) gene are obese, diabetic, and exhibit reduced activity, metabolism, and body temperature. Daily intraperitoneal injection of these mice with recombinant OB protein lowered their body weight, percent body fat, food intake, and serum concentrations of glucose and insulin. In addition, metabolic rate, body temperature, and activity levels were increased by this treatment. None of these parameters was altered beyond the level observed in lean controls, suggesting that the OB protein normalized the metabolic status of the ob/ob mice. Lean animals injected with OB protein maintained a smaller weight loss throughout the 28-day study and showed no changes in any of the metabolic parameters. These data suggest that the OB protein regulates body weight and fat deposition through effects on metabolism and appetite.
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              Gut hormones and the regulation of energy homeostasis.

              Food intake, energy expenditure and body adiposity are homeostatically regulated. Central and peripheral signals communicate information about the current state of energy balance to key brain regions, including the hypothalamus and brainstem. Hunger and satiety represent coordinated responses to these signals, which include neural and hormonal messages from the gut. In recent years our understanding of how neural and hormonal brain-gut signalling regulates energy homeostasis has advanced considerably. Gut hormones have various physiological functions that include specifically targeting the brain to regulate appetite. New research suggests that gut hormones can be used to specifically regulate energy homeostasis in humans, and offer a target for anti-obesity drugs.
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                Author and article information

                Contributors
                URI : http://frontiersin.org/people/u/72437
                URI : http://frontiersin.org/people/u/100219
                Journal
                Front Endocrinol (Lausanne)
                Front Endocrinol (Lausanne)
                Front. Endocrinol.
                Frontiers in Endocrinology
                Frontiers Media S.A.
                1664-2392
                24 April 2014
                2014
                : 5
                : 58
                Affiliations
                [1] 1Biochemistry and Molecular Biology Unit, Department of Systems Biology, Faculty of Medicine, University of Alcalá , Alcalá de Henares, Spain
                [2] 2Department of Endocrinology, Hospital Infantil Universitario Niño Jesús, Instituto de Investigación La Princesa , Madrid, Spain
                [3] 3Centro de Investigación Biomédica en Red Fisiopatología Obesidad y Nutrición, Instituto de Salud Carlos III , Madrid, Spain
                Author notes

                Edited by: Anca Dana Dobrian, Eastern Virginia Medical School, USA

                Reviewed by: Subrata Chakrabarti, The University of Western Ontario, Canada; Brian M. Shewchuk, Brody School of Medicine at East Carolina University, USA

                *Correspondence: Eduardo Arilla Ferreiro, Biochemistry and Molecular Biology Unit, Department of Systems Biology, Faculty of Medicine, University of Alcalá, Alcalá de Henares, Madrid E-28871, Spain e-mail: eduardo.arilla@ 123456uah.es

                This article was submitted to Diabetes, a section of the journal Frontiers in Endocrinology.

                Article
                10.3389/fendo.2014.00058
                4005944
                24795698
                ff4242f9-c666-4afc-bd00-0d69d3a20d5d
                Copyright © 2014 Sobrino Crespo, Perianes Cachero, Puebla Jiménez, Barrios and Arilla Ferreiro.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 06 January 2014
                : 09 April 2014
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 203, Pages: 13, Words: 13193
                Categories
                Endocrinology
                Review Article

                Endocrinology & Diabetes
                peptides,orexigenic,ghrelin,anorexigenic,insulin
                Endocrinology & Diabetes
                peptides, orexigenic, ghrelin, anorexigenic, insulin

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