Neuroendocrine Regulation Of Food Intake Research Articles

Neuroendocrine Regulation of Food Intake in Polycystic Ovary Syndrome.

Several peripheral and central signals are involved in the sophisticated regulation of food intake. Women with polycystic ovary syndrome (PCOS) are prone to consume a diet higher in saturated fat and foods with high glycemic index and show impaired appetite regulation and measures of satiety. As a consequence, obesity, mostly of the central type, is prevalent in the syndrome and worsens the endocrine and metabolic profile of the affected patients. This review article briefly analyzes the current knowledge about the neuroendocrine mechanisms underlying the interplay between feeding behavior, obesity, and reproductive abnormalities in PCOS.

Growth hormone treatment modulates active ghrelin levels in rats

Introduction: Impairments in neuroendocrine regulation of food intake and postprandial satiety are leading causes to obesity. Ghrelin peptide is a GI hormone known to increase food intake partly through induction of growth hormone. The regulation of ghrelin production is still unknown. Objective: The aim of the current study is to investigate the influence of growth hormone (Genotropin) treatment on active ghrelin levels in plasma, stomach, pancreas and kidney in rats. Material/methods: Male Sprague-Dawley rats, randomly allocated into control and three treatment groups, received daily subcutaneous injections of Genotropin at 2, 20 and 100 µg/rat/day for 5 consecutive days. Active ghrelin levels were quantified per tissue mass or tissue protein. Results: In control groups, the highest active ghrelin concentration in pmol/g tissue was found in the stomach (15.5 ± 0.21) followed by the pancreas (1.96 ± 0.066) and the kidney (1.36 ± 0.037). Genotropin treatment caused a dose dependent decrease in active ghrelin concentration in stomach, kidney and pancreas with a concomitant increase in plasma, and reaching significance at 20 and 100 µg/rat/day doses. However, the treatment caused variable effect on total protein concentrations, with a decrease in pancreas and an increase in stomach and kidney supernatants. Consequently, under such treatment, determination of active ghrelin concentration per tissue mass rather than per tissue protein is favored. Conclusions: The present study suggests a direct correlation between Genotropin treatment and active ghrelin secretion into the rat plasma via modulating its stores in stomach, kidney and pancreas.

Neuroendocrine regulation of food intake

Despite a global obesity epidemic suggesting that human physiology is unable to prevent unhealthy gains in body weight, ample evidence indicates that weight can be tightly regulated. Food intake regulation is complex and in this article we will present a basic endocrine feedback loop model of energy homeostasis. Next, integration of long-term regulation with short-term, meal specific regulation and satiety will be discussed. Finally, the role of adiposity signals in modulation of food reward will be highlighted. A basic understanding of the structure-function of these systems will inform the challenges of clinical care for those with disorders of energy balance.

Neuroendocrine Regulation of Food Intake During Acute Stress in the Tilapia

Event Abstract Back to Event Neuroendocrine Regulation of Food Intake During Acute Stress in the Tilapia Larry Riley1* and Kelli Upton1 1 California State University at Fresno, Biology, United States The general stress response principally results in the release of cortisol, with the overall effect of mobilizing metabolic energy and redirecting it towards homeostatic maintenance. Consequently, an important factor by stress is food intake. In several teleosts species, a decrease in food intake following stress has been observed, though the neuroendocrine mechanism controlling the reduction in food intake during stress has yet to be determined. These studies were designed to investigate the effect of an acute stress on food intake and brian expression of corticotropin-releasing hormone (CRH), neuropeptide Y (NPY), and ghrelin and whether these effects are mediated cortisol. Therefore, metyrapone, a cortisol synthesis inhibitor, was administered via feed in three doses of 10,25, and 50 mg/kg body weight for 1 wk prior to a 30 min crowding and handling stress. Following the stressor, fish were allowed to feed for 1 h. Stress reduced food intake, while elevating mRNA levels of CRH, an appetite suppressor. Additionally, metyrapone treatment dose-dependently blocked the stress-reduction in food intake. The elevation of CRH mRNA levels was also reveresed with metyrapone treatment, suggesting cortisol and CRH play a role in mediating reduction of food intake during stress in tilapia Acknowledgements This project was supported by Agriculture and Food Research Initiative Competitive Grant no. 2010-65206-20615 from the USDA National Institute of Food and Agriculture to LGR. Keywords: Corticotropin-Releasing Hormone, food intake, Neuropeptide Y, stress, Tilapia Conference: NASCE 2011: The inaugural meeting of the North American Society for Comparative Endocrinology, Ann Arbor, United States, 13 Jul - 16 Jul, 2011. Presentation Type: Poster Topic: Metabolism and feeding Citation: Riley L and Upton K (2011). Neuroendocrine Regulation of Food Intake During Acute Stress in the Tilapia. Front. Endocrinol. Conference Abstract: NASCE 2011: The inaugural meeting of the North American Society for Comparative Endocrinology. doi: 10.3389/conf.fendo.2011.04.00075 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 22 Jul 2011; Published Online: 09 Aug 2011. * Correspondence: Prof. Larry Riley, California State University at Fresno, Biology, Fresno, CA, 93740, United States, lriley@csufresno.edu Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Larry Riley Kelli Upton Google Larry Riley Kelli Upton Google Scholar Larry Riley Kelli Upton PubMed Larry Riley Kelli Upton Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

The Brain Renin-Angiotensin System Controls Divergent Efferent Mechanisms to Regulate Fluid and Energy Balance

The renin-angiotensin system (RAS), in addition to its endocrine functions, plays a role within individual tissues such as the brain. The brain RAS is thought to control blood pressure through effects on fluid intake, vasopressin release, and sympathetic nerve activity (SNA), and may regulate metabolism through mechanisms which remain undefined. We used a double-transgenic mouse model that exhibits brain-specific RAS activity to examine mechanisms contributing to fluid and energy homeostasis. The mice exhibit high fluid turnover through increased adrenal steroids, which is corrected by adrenalectomy and attenuated by mineralocorticoid receptor blockade. They are also hyperphagic but lean because of a marked increase in body temperature and metabolic rate, mediated by increased SNA and suppression of the circulating RAS. β-adrenergic blockade or restoration of circulating angiotensin-II, but not adrenalectomy, normalized metabolic rate. Our data point to contrasting mechanisms by which the brain RAS regulates fluid intake and energy expenditure.

Changes in gut hormones after bariatric surgery

Bariatric surgery is one of the most effective treatments for achieving long-term weight loss in morbidly obese patients. Bariatric surgery causes weight loss through substantial decline of hunger and increased satiety. Recently our understanding of neuroendocrine regulation of food intake and weight gain, especially regarding the role of gut hormones, has significantly increased. The changes in these hormones following bariatric surgery can partly explain the mechanism behind weight loss achieved through these procedures. In this paper, we review the effect bariatric procedures have on different gut hormone levels and how they in turn can alter the complex neuroendocrine regulation of energy homeostasis.

The satiety hormone peptide YY as a regulator of appetite

Obesity is a major cause of premature death in the UK, and may contribute to as many as 30 000 deaths a year in the UK. Although effective treatment for...

Neuroendocrine regulation of food intake

The majority of adults in many developed countries are overweight or obese. The obesity epidemic is also affecting children worldwide. Obesity increases the risk of several diseases leading to life-threatening complications. Weight regulation depends on food intake (energy intake) and energy expenditure. The purpose of this review is to provide updated information on the neuroendocrine regulation of food intake and energy homeostasis. New knowledge about the role of the prefrontal cortex in the regulation of food intake has emerged. The pathways responsible for energy homeostasis are now increasingly being understood, and as a consequence, an increasing number of pharmacologic agents targeting these pathways are being actively developed. Emphasis on the concept of long-term (as opposed to short-term) homeostasis has guided the search for therapeutic molecules or combination of molecules that would inhibit food intake constantly and thus lead to maintained weight loss. Complex and intricate neuroendocrine pathways control food intake and energy homeostasis. The increasing understanding of the different components orchestrating the regulation of food intake provides new and exciting targets for much needed pharmacotherapy for obesity.

Gastrointestinal regulation of food intake

Despite substantial fluctuations in daily food intake, animals maintain a remarkably stable body weight, because overall caloric ingestion and expenditure are exquisitely matched over long periods of time, through the process of energy homeostasis. The brain receives hormonal, neural, and metabolic signals pertaining to body-energy status and, in response to these inputs, coordinates adaptive alterations of energy intake and expenditure. To regulate food consumption, the brain must modulate appetite, and the core of appetite regulation lies in the gut-brain axis. This Review summarizes current knowledge regarding the neuroendocrine regulation of food intake by the gastrointestinal system, focusing on gastric distention, intestinal and pancreatic satiation peptides, and the orexigenic gastric hormone ghrelin. We highlight mechanisms governing nutrient sensing and peptide secretion by enteroendocrine cells, including novel taste-like pathways. The increasingly nuanced understanding of the mechanisms mediating gut-peptide regulation and action provides promising targets for new strategies to combat obesity and diabetes.

Transcriptomes of purified gastric ECL and parietal cells: identification of a novel pathway regulating acid secretion

The gastric entero-chromaffin-like (ECL) cell plays a key regulatory role in peripheral regulation of acid secretion due to the release of histamine that stimulates acid secretion by the parietal cell. Studies in intact animals, gastric glands, and isolated cells after short-term culture have shown expression of stimulatory CCK2 and PAC1 and inhibitory SST2 and Gal1 receptors as well as histidine decarboxylase. However, the pattern of its gene expression as a neuroendocrine cell has not been explored. Comparison of gene expression by 95% pure ECL cells obtained by density gradient, elutriation, and fluorescence-assisted cell sorting with isolates of the intact fundic gastric epithelium (i.e., "subtractive hybridization") identified a variety of additional expressed gene families characteristic of this neuroendocrine cell. These include genes 1) involved in neuropeptide synthesis and secretory vesicle exocytosis, 2) involved in control of inflammation, 3) implicated in healing of the epithelium, 4) encoding inhibitory Gi protein-coupled receptors, 5) playing a role in neuroendocrine regulation of food intake, and 6) encoding proteins likely involved in maintenance of circadian rhythm, in addition to the ECL cell-specific genes histidine decarboxylase and monoamine transporter. Particularly, the inhibitory apelin receptor gene, APJ, was highly expressed in the ECL cell preparation. Because parietal cells express apelin, immunohistochemical and functional studies showed that there is an inhibitory feed back loop between the parietal and ECL cell during gastrin stimulation, providing evidence for a novel pathway of downregulation of acid secretion due to interaction between these two cell types.

The Hypothalamic-Pituitary-Adrenal Axis in the Neuroendocrine Regulation of Food Intake and Obesity: The Role of Corticotropin Releasing Hormone

The aim of this paper is to review the present knowledge on the role of the hypothalamic-pituitary-adrenal axis in the control of food intake and the pathogenesis of obesity and to discuss, on the basis of available literature, the interactions between other neurosystems and this hormonal axis. Food intake is influenced by a system of physiologic signals and behavioral controls consisting of positive and negative sensory feedback mechanisms. It is regulated by a complex neuroendocrine system consisting of peripheral signals (cortisol, leptin) in constant interplay with central neurosystems such as the cocaine-amfetamine-regulated transcript system. In these neurosystems, corticotropin-releasing hormone, pro-opiomelanocortin, melanin-concentrating hormone and neuropeptide Y are actively involved. The corticotropin-releasing hormone system is widely distributed throughout the brain, but it is particularly abundant in the medial parvocellular division of the paraventricular nucleus. Within the brain corticotropin-releasing hormone with its two receptor types, its binding protein and its closely related peptide urocortin forms a network of neuronal pathways capable of interacting with other circuitries controlling food intake and sympathetically-mediated thermogenesis. A defect in the synthesis and release of corticotropin-releasing hormone has been implicated in the development of obesity in laboratory animals. This condition is alleviated by exogenous corticotropin-releasing hormone treatment. The relationship between the neuropeptide Y system and the hypothalamic-pituitary-adrenal axis is complex and seems to include positive feedback between neuropeptide Y and corticosteroids and negative feedback between corticotropin-releasing hormone and neuropeptide Y. Leptin is involved in the regulation of energy balance by interacting with the hypothalamic-pituitary-adrenal axis. In the past, we have shown by cross-correlation analysis, that under physiological conditions cortisol and plasma leptin levels are related to each other in a time-related negative and positive fashion over 24 h.

Secretory, Endocrine and Autocrine/Paracrine Function of the Adipocyte

Obesity is a major public health problem in Western countries, and >55% of adult Americans are overweight or obese. A major contributor to the epidemic of obesity is the current environment, which is characterized by increased availability of high energy foods and decreased physical activity. Several studies also demonstrated that genetic susceptibility contributes to obesity in some populations. Obesity research has focused primarily on the role of the hypothalamus in neuroendocrine regulation of food intake. However, a growing number of studies support a potential contribution of adipose tissue, via its newly discovered secretory function, to the pathogenesis of obesity and co-morbid conditions including cardiovascular disease, diabetes and hypertension. This paper will review the role of four factors secreted by adipose tissue (leptin, agouti, angiotensin II and prostaglandins) and their functions in the regulation of energy balance and whole-body homeostasis. Several other peptide and nonpeptide substances are secreted from adipose tissue; their function and regulation have been documented extensively.

Neuroendocrine regulation of food intake.

Maintenance of appropriate stores of metabolic fuels depends on carefully matching caloric intake to caloric expenditure. Achieving such 'energy balance' is a product of complex interactions of peripheral hormones with effector systems in the central nervous system (CNS) that regulate food intake and energy expenditure. Leptin is a hormone that is made in the adipocytes, circulates in the blood and interacts with receptors in the CNS. These receptors can be found in two different types of systems. One effector system is termed 'anabolic' and is activated by low levels of leptin during negative energy balance. This system (exemplified by the hypothalamic neuropeptide Y system) increases food intake and decreases energy expenditure to facilitate the regaining of lost energy stores. The other effector system is termed 'catabolic' and is activated by high levels of leptin during positive energy balance. This system (exemplified by the hypothalamic melanocortin and corticotrophin-releasing hormone systems) decreases food intake and increases energy expenditure to facilitate the loss of excess energy stores. Further understanding of these systems is necessary to develop adequate treatments for disorders of energy balance, such as obesity and wasting.

Neuroendocrine regulation of food intake and body weight

This paper reviews the effects of peptide hormones upon food intake. These effects are seen as falling into one of two categories depending upon whether the hormone in question is affected by the degree of adiposity. Many gut peptides, such as CCK and somatostatin, influence the size of individual meals and presumably reflect only the calories involved with that meal. Other peptides, especially insulin as it acts at the CNS, influence the size of all meals by indicating the current degree of adiposity. Such signals reflect not only single meal calories but also calories stored in the adipose beds and are therefore often called “long-term” signals.