Peripheral regulation of food intake in chickens: adiposity signals, satiety signals and others

An overview is presented of those signals generated by the gastrointestinal (GI) tract during meals that interact with the central nervous system to create a sensation of fullness and satiety. Although dozens of enzymes, hormones, and other factors are secreted by the GI tract in response to food in the lumen, only a handful are able to influence food intake directly. Most of these cause meals to terminate and hence are called satiety signals, with CCK being the most investigated. Only one GI signal, ghrelin, that increases meal size has been identified. The administration of exogenous CCK or other satiety signals causes smaller meals to be consumed, whereas blocking the action of endogenous CCK or other satiety signals causes larger meals to be consumed. Satiety signals are relayed to the hindbrain, either indirectly via nerves such as the vagus from the GI tract or else directly via the blood. Most factors that influence how much food is eaten during individual meals act by changing the sensitivity to satiety signals. This includes adiposity signals as well as habits and learning, the social situation, and stressors.

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IL CONTROLLO NEUROENDOCRINO DEL COMPORTAMENTO ALIMENTARE

Istituto Lombardo - Accademia di Scienze e Lettere - Incontri di Studio ◽

10.4081/incontri.2020.625 ◽

2020 ◽

Author(s):

Francesco Cavagnini

Keyword(s):

Gastrointestinal Tract ◽

Food Intake ◽

Nutritional Status ◽

Eating Behavior ◽

Nucleus Tractus Solitarius ◽

Peptide Yy ◽

Releasing Hormone ◽

Fat Depots ◽

Adiposity Signals ◽

The Brain

Appetite is regulated by a complex system of central and peripheral signals that interact in order to modulate eating behavior according the individual needs, i.e. the fasting or fed condition and the general nutritional status. Peripheral regulation includes adiposity signals and satiety signals, while central control is accomplished by several effectors, including the neuropeptidergic, monoaminergic and endocannabinoid systems. Adiposity signals inform the brain of the general nutritional status of the subject as indicated by the extent of fat depots. Indeed, leptin produced by the adipose tissue and insulin, whose pancreatic secretion tends to increase with the increase of fat mass, convey to the brain an anorexigenic message. Satiety signals, including cholecystokinin (CCK), glucagon-like peptide-1 (GLP-1) and peptide YY (PYY), originate from the gastrointestinal tract during a meal and, through the vagus nerve, reach the nucleus tractus solitarius (NTS) in the caudal brainstem. From NTS afferents fibers project to the arcuate nucleus (ARC) of the hypothalamus, where satiety signals are integrated with adiposity signals and with several hypothalamic and supra-hypothalamic inputs, thus creating a complex network of neural circuits that finally elaborate the most appropriate response, in terms of eating behavior. In more detail, ARC neurons secrete a number of neuropeptides with orexigenic properties, such as neuropeptide Y (NPY) and agouti-related peptide (AGRP), or anorexigenic effects such as pro-opiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART). Other brain areas involved in the control of food intake are located downstream the ARC: among these, the paraventricular nucleus (PVN), which produces anorexigenic peptides such as thyrotropin releasing hormone (TRH), corticotrophin releasing hormone (CRH) and oxytocin, the lateral hypothalamus (LHA) and perifornical area (PFA), secreting the orexigenic substances orexin-A (OXA) and melanin concentrating hormone (MCH). Recently, a great interest has developed for endogenous cannabinoids, important players in the regulation of food intake and energy metabolism. In the same context, increasing evidence is accumulating for a role played by the microbiota, the trillion of microorganism populating the human gastrointestinal tract. The complex interaction between the peripheral organs and the central nervous system has generated the concept of gut-brain axis, now incorporated into the physiology. A better understanding of the mechanisms governing the eating behavior will allow the development of drugs capable of reducing or enhancing food consumption.

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Central and peripheral control of food intake

Endocrine Regulations ◽

10.1515/enr-2017-0006 ◽

2017 ◽

Vol 51 (1) ◽

pp. 52-70 ◽

Cited By ~ 19

Author(s):

M. M. I. Abdalla

Keyword(s):

Body Weight ◽

Food Intake ◽

Energy Expenditure ◽

Current Knowledge ◽

The Body ◽

Therapeutic Implications ◽

New Therapeutic Approaches ◽

Control Food ◽

Adiposity Signals ◽

Control Food Intake

Abstract The maintenance of the body weight at a stable level is a major determinant in keeping the higher animals and mammals survive. Th e body weight depends on the balance between the energy intake and energy expenditure. Increased food intake over the energy expenditure of prolonged time period results in an obesity. Th e obesity has become an important worldwide health problem, even at low levels. The obesity has an evil effect on the health and is associated with a shorter life expectancy. A complex of central and peripheral physiological signals is involved in the control of the food intake. Centrally, the food intake is controlled by the hypothalamus, the brainstem, and endocannabinoids and peripherally by the satiety and adiposity signals. Comprehension of the signals that control food intake and energy balance may open a new therapeutic approaches directed against the obesity and its associated complications, as is the insulin resistance and others. In conclusion, the present review summarizes the current knowledge about the complex system of the peripheral and central regulatory mechanisms of food intake and their potential therapeutic implications in the treatment of obesity.

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Obesity and Appetite Control

Experimental Diabetes Research ◽

10.1155/2012/824305 ◽

2012 ◽

Vol 2012 ◽

pp. 1-19 ◽

Cited By ~ 104

Author(s):

Keisuke Suzuki ◽

Channa N. Jayasena ◽

Stephen R. Bloom

Keyword(s):

Food Intake ◽

Energy Homeostasis ◽

Peptide Yy ◽

Gut Hormones ◽

Appetite Control ◽

Control Food ◽

Adiposity Signals ◽

Term Energy ◽

Glucagon Like Peptide 1 ◽

Control Food Intake

Obesity is one of the major challenges to human health worldwide; however, there are currently no effective pharmacological interventions for obesity. Recent studies have improved our understanding of energy homeostasis by identifying sophisticated neurohumoral networks which convey signals between the brain and gut in order to control food intake. The hypothalamus is a key region which possesses reciprocal connections between the higher cortical centres such as reward-related limbic pathways, and the brainstem. Furthermore, the hypothalamus integrates a number of peripheral signals which modulate food intake and energy expenditure. Gut hormones, such as peptide YY, pancreatic polypeptide, glucagon-like peptide-1, oxyntomodulin, and ghrelin, are modulated by acute food ingestion. In contrast, adiposity signals such as leptin and insulin are implicated in both short- and long-term energy homeostasis. In this paper, we focus on the role of gut hormones and their related neuronal networks (the gut-brain axis) in appetite control, and their potentials as novel therapies for obesity.

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Insulin and leptin: dual adiposity signals to the brain for the regulation of food intake and body weight

Brain Research ◽

10.1016/s0006-8993(99)01974-5 ◽

1999 ◽

Vol 848 (1-2) ◽

pp. 114-123 ◽

Cited By ~ 269

Author(s):

Denis G. Baskin ◽

Dianne Figlewicz Lattemann ◽

Randy J. Seeley ◽

Stephen C. Woods ◽

Daniel Porte ◽

...

Keyword(s):

Body Weight ◽

Food Intake ◽

Adiposity Signals ◽

The Brain

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Central Control of Body Weight and Appetite

The Journal of Clinical Endocrinology & Metabolism ◽

10.1210/jc.2008-1630 ◽

2008 ◽

Vol 93 (11_supplement_1) ◽

pp. s37-s50 ◽

Cited By ~ 264

Author(s):

Stephen C. Woods ◽

David A. D'Alessio

Keyword(s):

Food Intake ◽

Body Fat ◽

Energy Homeostasis ◽

Evidence Synthesis ◽

Treatment Options ◽

Meal Size ◽

Reduce Food Intake ◽

Therapeutic Goals ◽

Therapeutic Implications ◽

Adiposity Signals

ABSTRACT Context Energy balance is critical for survival and health, and control of food intake is an integral part of this process. This report reviews hormonal signals that influence food intake and their clinical applications. Evidence Acquisition A relatively novel insight is that satiation signals that control meal size and adiposity signals that signify the amount of body fat are distinct and interact in the hypothalamus and elsewhere to control energy homeostasis. This review focuses upon recent literature addressing the integration of satiation and adiposity signals and therapeutic implications for treatment of obesity. Evidence Synthesis During meals, signals such as cholecystokinin arise primarily from the GI tract to cause satiation and meal termination; signals secreted in proportion to body fat such as insulin and leptin interact with satiation signals and provide effective regulation by dictating meal size to amounts that are appropriate for body fatness, or stored energy. Although satiation and adiposity signals are myriad and redundant and reduce food intake, there are few known orexigenic signals; thus, initiation of meals is not subject to the degree of homeostatic regulation that cessation of eating is. There are now drugs available that act through receptors for satiation factors and which cause weight loss, demonstrating that this system is amenable to manipulation for therapeutic goals. Conclusions Although progress on effective medical therapies for obesity has been relatively slow in coming, advances in understanding the central regulation of food intake may ultimately be turned into useful treatment options.

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Obesity and adiposity: the culprit of dietary protein efficacy

Clinical Science ◽

10.1042/cs20190583 ◽

2020 ◽

Vol 134 (4) ◽

pp. 389-401

Author(s):

Carla El-Mallah ◽

Omar Obeid

Keyword(s):

Food Intake ◽

Behavioural Change ◽

Physiological Mechanism ◽

Short Term ◽

The Past ◽

Body Adiposity ◽

Reduce Sugar ◽

Eye Opening ◽

Potential Strategy ◽

Limitations And Exceptions

Abstract Obesity and increased body adiposity have been alarmingly increasing over the past decades and have been linked to a rise in food intake. Many dietary restrictive approaches aiming at reducing weight have resulted in contradictory results. Additionally, some policies to reduce sugar or fat intake were not able to decrease the surge of obesity. This suggests that food intake is controlled by a physiological mechanism and that any behavioural change only leads to a short-term success. Several hypotheses have been postulated, and many of them have been rejected due to some limitations and exceptions. The present review aims at presenting a new theory behind the regulation of energy intake, therefore providing an eye-opening field for energy balance and a potential strategy for obesity management.

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