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Appetite Regulation (appetite + regulation)
Selected AbstractsHow Palatable Food Disrupts Appetite RegulationBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 2 2005Charlotte Erlanson-Albertsson Hunger signals may be generated in peripheral organs (e.g. ghrelin) but most of them are expressed in the hypothalamus (neuropeptide Y, orexins, agouti-related peptide, melanin concentrating hormone, endogenous opiates and dopamine) and are expressed during situations of energy deficiency. Some satiety signals, such as cholecystokinin, glucagon-like peptide 1, peptide YY and enterostatin are released from the digestive tract in response to food intake. Others, such as leptin and insulin, are mobilized in response to perturbations in the nutritional state. Still others are generated in neurones of the hypothalamus (,-melanocyte-stimulating hormone and serotonin). Satiety signals act by inhibiting the expression of hunger signals and/or by blunting their effect. Palatable food, i.e. food rich in fat and sugar, up-regulates the expression of hunger signals and satiety signals, at the same time blunting the response to satiety signals and activating the reward system. Hence, palatable food offsets normal appetite regulation, which may explain the increasing problem of obesity worldwide. [source] Neurohormonal regulation of feed intake and response to nutrients in fish: aspects of feeding rhythm and stressAQUACULTURE RESEARCH, Issue 5 2010Ewa Kulczykowska Abstract The regulation of feed intake is very complex and involves interaction among the circadian and homeostatic control systems within the central nervous system, the gastrointestinal tract and the environment. The hypothalamus, which receives, integrates and transmits relevant internal and external signals, is recognized as the primary centre of regulation of feed intake. The neuroendocrine factors that originate from the hypothalamus either stimulate or inhibit feed intake so that nutritional demands of the organism can be fulfilled and energy balance can be achieved. Appetite regulation is a physiological mechanism in which a variety of neurohormones interact and fish show different feeding behaviour (e.g. diurnal, nocturnal). This complicated system is very sensitive to any disturbance. Fish in farms and fish in a natural environment are equipped with the same combination of neurohormones to regulate feed intake, but they meet different challenges, particularly with regard to the type of feed and feeding schedule. In this review, the neurohormonal regulation of feed intake is analysed in fish in terms of entrainment of their circadian feeding rhythms and while exposed to different stressors in captivity. [source] RD Lawrence Lecture 2008 Targeting GLP-1 release as a potential strategy for the therapy of Type 2 diabetesDIABETIC MEDICINE, Issue 8 2008F. M. Gribble Abstract Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are gastrointestinal hormones that play an important role in stimulating postprandial insulin release from pancreatic ,-cells. Agents that either mimic GLP-1 or prevent its degradation are now available for the treatment of Type 2 diabetes, and strategies to enhance endogenous GLP-1 release are under assessment. As intestinal peptides have a range of actions, including appetite regulation and coordination of fat metabolism, harnessing the enteric endocrine system is a promising new field for drug development. [source] PRECLINICAL STUDY: Changes in leptin, ghrelin, growth hormone and neuropeptide-Y after an acute model of MDMA and methamphetamine exposure in ratsADDICTION BIOLOGY, Issue 1 2008Firas H. Kobeissy ABSTRACT Club drug abuse is a growing problem in the United States. Beyond addiction and toxicity are endocrine effects which are not well characterized. Specifically, the changes in appetite following exposure to drugs of abuse are an interesting but poorly understood phenomenon. Serum hormones such as leptin, ghrelin, growth hormone (GH), and neuropeptide-Y (NP-Y) are known to affect appetite, but have not been studied extensively with drugs of abuse. In this work, we examine the effects of club drugs 3,4-methylenedioxymethamphetamine (MDMA) (ecstasy) and methamphetamine (METH) (doses of 5, 20 and 40 mg/kg) on serum concentrations of these hormones in adult male Sprague-Dawley rats 6, 12, 24 and 48 hours after drug administration. In a dose-dependent manner, MDMA was shown to cause transient significant decreases in serum leptin and GH followed by a base line recovery after 24 hours. Conversely, serum ghrelin increased and normalized after 24 hours. Interestingly, serum NP-Y showed a steady decrease in both treatment of MDMA and METH at different time points and dosages. In humans, abuse of these drugs reduces eating. As evident from these data, acute administration of METH and MDMA had significant effects on different serum hormone levels involved in appetite regulation. Future studies should be performed to see how chronic, low dose drug administration would affect hormone levels and try to answer questions about the physiological mechanisms involved in the anorexic paradigm observed in drug use. [source] Peptide dynamic fingerprints: a tool for investigating the role of conformational flexibility for GLP-1 analogs affinityJOURNAL OF PEPTIDE SCIENCE, Issue 8 2005Dr M. Adenot Abstract Glucagon-like peptide-1 (GLP-1) is a 30-residue peptide implicated in short-term appetite regulation. Its analogs are presumed to be potential drugs against obesity and non-insulin dependent diabetes mellitus (NIDDM or type 2 diabetes). This study examined how the dynamic fingerprints can be used for establishing dynamics,activity relationships in a series of peptides for which the mechanism of action is unknown and in which mutations can cause an increase or decrease in biological activity. The 3D autocorrelation method was used to generate maps of both active and inactive analogs. As the active conformation of GLP-1 is not yet clearly defined, the dynamic fingerprints of peptides in an aqueous environment were compared to explain the high affinity of the peptide for its receptor. The suggestion that the peptide could bind to the receptor in a folded conformation has been examined. In the case of the GLP-1 analogs, it was shown that the folding tendency cannot be directly related to affinity values and the results do not favor a folded active conformation model of GLP-1. Copyright © 2005 European Peptide Society and John Wiley & Sons, Ltd. [source] Cerebral activation by fasting induces lactate accumulation in the hypothalamusMAGNETIC RESONANCE IN MEDICINE, Issue 2 2009Inês R. Violante Abstract Carbon-13 (13C) high-resolution magic angle spinning (HR-MAS) spectroscopy was used to investigate the neuroglial coupling mechanisms underlying appetite regulation in the brain of C57BL/6J mice metabolizing [1- 13C]glucose. Control fed or overnight fasted mice received [1- 13C]glucose (20 ,mol/g intraperitoneally [i.p.]), 15 min prior to brain fixation by focused microwaves. The hypothalamic region was dissected from the rest of the brain and 13C HR-MAS spectra were obtained from both biopsies. Fasting resulted in a significant increase in hypothalamic [3- 13C]lactate and [2- 13C],-aminobutyric acid (GABA) relative to the remaining brain. Administration of the orexigenic peptide ghrelin (0.3 nmol/g i.p.) did not increase hypothalamic [3- 13C]lactate or [2- 13C]GABA, suggesting that ghrelin signaling is not sufficient to elicit all the metabolic consequences of hypothalamic activation by fasting. Our results indicate that the hypothalamic regulation of appetite involves, in addition to the well-known neuropeptide signaling, increased neuroglial lactate shuttling and augmented GABA concentrations. Magn Reson Med, 2009. © 2009 Wiley-Liss, Inc. [source] Prebiotic inulin-type fructans: nutritional benefits beyond dietary fibre sourceNUTRITION BULLETIN, Issue 3 2008H. Alexiou Summary For several years, there has been an increasing awareness of the fundamental role that the complex bacterial ecosystem plays in our health. Inulin and oligofructose are prebiotic dietary fibres naturally present in the chicory root. They escape metabolism in the small intestine, and their selective fermentation by the human colonic microflora leads to a shift in the composition of the indigenous bacterial ecosystem, in favour of health-promoting bifidobacteria. In addition to their dietary fibre effects on improved bowel regularity, several physiological advantages are linked to their specific pattern of fermentation in the colon, including improved mineral absorption, enhanced natural host defences and colonic protection, improved gut health, and beneficial influence on appetite regulation. The aim of the present review was to highlight the nutritional benefits of inulin-type fructans, focusing on key physiological functions. [source] Obesity is Associated with Genetic Variants That Alter Dopamine AvailabilityANNALS OF HUMAN GENETICS, Issue 3 2006A. C. Need Summary Human and animal studies have implicated dopamine in appetite regulation, and family studies have shown that BMI has a strong genetic component. Dopamine availability is controlled largely by three enzymes: COMT, MAOA and MAOB, and by the dopamine transporter SLC6A3, and each gene has a well-characterized functional variant. Here we look at these four functional polymorphisms together, to investigate how heritable variation in dopamine levels influences the risk of obesity in a cohort of 1150, including 240 defined as obese (BMI , 30). The COMT and SLC6A3 polymorphisms showed no association with either weight, BMI or obesity risk. We found, however, that both MAOA and MAOB show an excess of the low-activity genotypes in obese individuals (MAOA:,2= 15.45, p = 0.004; MAOB:,2= 8.05, p = 0.018). Additionally, the MAOA genotype was significantly associated with both weight (p = 0.0005) and BMI (p = 0.001). When considered together, the ,at risk genotype' - low activity genotypes at both the MAOA and MAOB loci - shows a relative risk for obesity of 5.01. These results have not been replicated and, given the experience of complex trait genetics, warrant caution in interpretation. In implicating both the MAOA and MOAB variants, however, this study provides the first indication that dopamine availability (as opposed to other effects of MAOA) is involved in human obesity. It is therefore a priority to assess the associations in replication datasets. [source] Weight gain and lipid deposition in Atlantic salmon, Salmo salar, during compensatory growth: evidence for lipostatic regulation?AQUACULTURE RESEARCH, Issue 12 2001S J S Johansen Abstract Feed-restricted fish gain less body mass and storage reserves than well-fed fish, and reduced rates of gain often trigger compensatory responses, characterized by increased appetite (hyperphagia) and growth rate. The results of previous investigations have introduced a hypothesis in which adipose tissue (fat stores) had a regulatory role in governing appetite. An extension of this suggests that hyperphagia may relate to the severity of the feed restriction, and that the compensatory responses will cease once fat reserves are restored relative to body size. This was tested in two trials in which feed-restricted or -deprived postsmolt Atlantic salmon, Salmo salar, became hyperphagic after transfer to excess feeding. At the end of the first trial, previously feed-restricted fish had fully compensated for their lost weight gain compared to continuously fed control fish, but had a leaner body composition (i.e. reduced energy stores) and were still showing signs of compensatory growth. In the second trial, feed deprivation drained body lipids and caused a stronger hyperphagic response than restrictive feeding, although it took longer to develop. Feed intake became coincident when fish had a similar body composition for size, but this occurred at different times. Hence, the fish that had been deprived of feed were smaller than the restricted fish at the end of the trial. The results of the present study demonstrate a link between the magnitude of lipid stores, feed intake and weight gain, and provide some evidence for lipostatic appetite regulation in fish. [source] How Palatable Food Disrupts Appetite RegulationBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 2 2005Charlotte Erlanson-Albertsson Hunger signals may be generated in peripheral organs (e.g. ghrelin) but most of them are expressed in the hypothalamus (neuropeptide Y, orexins, agouti-related peptide, melanin concentrating hormone, endogenous opiates and dopamine) and are expressed during situations of energy deficiency. Some satiety signals, such as cholecystokinin, glucagon-like peptide 1, peptide YY and enterostatin are released from the digestive tract in response to food intake. Others, such as leptin and insulin, are mobilized in response to perturbations in the nutritional state. Still others are generated in neurones of the hypothalamus (,-melanocyte-stimulating hormone and serotonin). Satiety signals act by inhibiting the expression of hunger signals and/or by blunting their effect. Palatable food, i.e. food rich in fat and sugar, up-regulates the expression of hunger signals and satiety signals, at the same time blunting the response to satiety signals and activating the reward system. Hence, palatable food offsets normal appetite regulation, which may explain the increasing problem of obesity worldwide. [source] | |||||||||||||