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Results for “Appetite Regulation”

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PubMed2006

Role of endogenous ghrelin in growth hormone secretion, appetite regulation and metabolism.

Ghrelin, a 28-amino acid hormone that is acylated post-translation, is the endogenous ligand for the growth hormone (GH) secretagogue (GHS) receptor (GHS-R). The highest concentrations of ghrelin are found in the stomach; however ghrelin peptide is also present in hypothalamic nuclei known to be important in the control of GH and feeding behavior. Exogenous ghrelin potently stimulates pituitary GH release through a mechanism that is dependent, in part, on endogenous GH-releasing hormone. Whether endogenous ghrelin plays a role in the control of GH secretion and growth is not clear and ghrelin deficient animals appear to grow normally. In contrast, experimental animal and clinical data suggest that abnormalities in GHS-R signaling could impact growth. Ghrelin or other GHS are clinically useful for GH-testing and limited data suggest that they might be useful in the treatment of some patients with GH deficiency. Substantial data have implicated ghrelin as an important regulator of feeding behavior and energy equilibrium. Ghrelin has a potent orexigenic effect in both animals and humans and this effect is mediated through hypothalamic neuropeptide Y (NPY) and Agouti-related peptide (AgRP). Appetite simulation coupled with other metabolic effects promotes weight gain during chronic treatment with ghrelin. These metabolic effects are in part mediated through an increase in respiratory quotient (VQ). Presence of ghrelin appears to be necessary for the development of obesity in some animal models. Whether abnormalities in ghrelin signaling are involved in human obesity is not yet known.

Agouti-Related Protein↗
PubMed2004

The role of melanocortin-3 and -4 receptor in regulating appetite, energy homeostasis and neuroendocrine function in the pig.

A recently discovered class of receptors, melanocortin-3 and -4 receptor (MC3/4-R), are located within the brain and modulate feed intake in rodents. Stimulation of the receptor (agonist) inhibits feed intake whereas blockade (antagonist) of the receptor increases intake. Our knowledge of factors regulating voluntary feed intake in humans and domestic animals is very limited. i.c.v. administration of an MC3/4-R agonist, NDP-MSH, suppressed (P<0.05) feed intake compared with controls at 12, 24, 48 and 72 h after treatment in growing pigs. Fed pigs were more responsive to the MC3/4-R agonist then fasted animals. However, i.c.v. treatment with MC3/4-R antagonist, SHU9119, failed to stimulate intake. The failure of MC3/4-R antagonist to stimulate feed intake suggests involvement of other brain hormone(s) which antagonize the action of SHU9119 at the MC3/4-R, blocking its stimulatory effect on intake. Treatment with NDP-MSH or SHU9119, across a wide dose range, failed to affect LH and GH secretion, except for the 10 micro g dose of NDP-MSH, which exhibited both a stimulatory and an inhibitory effect on GH secretion in fasted animals. Treatment with agouti-related peptide, a natural brain hormone that blocks the MC3/4R, failed to stimulate feed intake. These results do not support the idea that endogenous melanocortin pays a critical role in regulating feed intake and pituitary hormone secretion in the pig. SHU9119 blocked the NDP-MSH-induced increase in cAMP in HEK293 cells expressing the porcine MC4-R sequence without the missense mutation. The EC(50) and IC(50) values were similar to the human MC4-R, confirming that SHU9119 is a pig MC4-R antagonist. However, pigs were heterozygous for an MC4-R gene missense mutation. It is possible that the MC4-R mutation alters function and this may explain the failure to demonstrate MC3/4-R involvement in modulating feeding behavior and LH and GH secretion in the pig.

Animals↗
PubMed2006

Possible role of creatine concentrations in the brain in regulating appetite and weight.

Cobaltic protoporphyrin IX (CoPP) is a synthetic heme analog which can elicit profound and prolonged decreases in appetite and body weight in several different animal species. Intracerebroventricular administration of CoPP in rats was found, by differential display and confirmed by Real-Time PCR, to result in an increase in expression of the creatine transporter when compared to vehicle-treated fed or vehicle-treated fasted control animals. In situ hybridization studies showed that creatine transporter mRNA concentrations were increased in several areas of the brain involved in the regulation of food intake, but creatine concentrations were decreased in hypothalamic homogenates in CoPP-treated animals compared to controls. Intracerebroventricular administration of beta-guanidinopropionic acid, a compound known to decrease intracellular creatine concentration by competition for uptake, resulted in decreased food intake and body weight and increased Fos expression in the hypothalamus. Taken together, these findings suggest that creatine concentrations in the brain may play a role in regulating food intake and body weight.

Analysis of Variance↗
PubMed2005

Novel therapeutic targets for appetite regulation.

Obesity is currently the major cause of premature death in the UK, killing almost 1000 individuals per week, and worldwide, its prevalence is accelerating. Many peptides are synthesized and released from the gastrointestinal tract and, while their roles in the regulation of gastrointestinal function have been known for some time, it is now evident that they also physiologically influence eating behavior. Therefore, manipulation of gastrointestinal hormones provides the prospect of an effective and well-tolerated treatment for obesity. Whereas drugs targeting appetite-signaling neuropeptides in the brain may also affect other aspects of the central nervous system, agents based on gut hormones themselves have the advantage of targeting specific appetite circuits within the brain without producing any unacceptable side effects.

Appetite Regulation↗
PubMed1984

Plasma cholecystokinin (CCK) before and after a jejunoileal bypass operation in obese patients with reference to appetite regulation.

Plasma cholecystokinin (CCK) rose significantly after a 15-min liquid test meal in six normal controls and six obese patients, both before and after a jejunoileal bypass operation. Post-prandial rises in the obese patients were virtually unaffected by the operation, and tended to be higher in the obese patients than in the normal controls. It is therefore concluded that hormonal CCK is unlikely to be a mediator of satiety signals from the digestive tract in obese persons.

Adult↗
PubMed1990

Appetite regulation by gut peptides.

A number of gastrointestinal hormones that are released from the gut in response to intraluminal food stuffs have been shown to play a role in producing satiety. Some of these hormones apparently activate ascending vagal fibers that send messages to the nucleus tractus solitarius, and perhaps from there messages are sent to the paraventricular nucleus of the hypothalamus. Not only do gastrointestinal hormones play a role in the termination of a meal but they also appear to modulate energy metabolism (at least in rodents) through the activation of brown adipose tissue.

Animals↗
PubMed1983

The role of CCK-like peptides in appetite regulation.

The physiological dose levels for the classically defined functions of CCK peptides, i.e., their effect on gall bladder contraction and release of pancreatic enzymes, are well established. However, the reported effects of peripheral administration of these peptides on regulation of satiety are achieved only at levels greatly in excess of the physiological range achieved in response to feeding. Thus, endogenous peripheral CCK alone would appear not to be the physiological satiety factor. The observations by Della-Fera et al. (1981) that lateral ventricular infusion into sheep of antibody to CCK results in increased feeding, if confirmed by other investigators and in other species, is the strongest evidence for a CSF-mediated role for CCK peptides in the regulation of satiety. However, numerous reports now delineate a variety of other CNS functions for these peptides. With so many effects reported, it is difficult at present to be certain which are real, which are direct or acting indirectly through another system, or which are the physiologically important functions. It can be expected that another decade will be required to sort out and define fully the multiple roles of CCK peptides that are synthesized independently in mucosal and in neuronal tissues.

Animals↗
PubMed1988

A possible physiological function of pancreatic pro-colipase activation peptide in appetite regulation.

Pancreatic pro-colipase activation peptide, a pentapeptide with the sequence VPDPR was found to significantly suppress food intake of 20 h fasted Sprague-Dawley rats in a dose-dependent way. A rat treated with pro-colipase-enriched pellets for 26 days showed decreased daily food intake and retarded growth, which were restored during a following period of regular feeding. Genetically obese Zucker rats (fa/fa) were found to contain a reduced content of pancreatic pro-colipase (60% reduction), whereas the pancreatic lipase content was normal. A physiological function of pancreatic pro-colipase activation peptide as an endogenous satiety signal is suggested.

Animals↗
PubMed2001

Hypothalamic appetite-regulating neuropeptide mRNA levels in cachectic nude mice bearing human tumor cells.

We previously reported that the human melanoma cell line, SEKI, induces severe weight loss in nude mice. In the present study, we examined the expression of weight-regulating neuropeptide mRNAs in the hypothalamus of this cancer cachectic model by using a sensitive quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) method and in situ hybridization. mRNA levels of neuropeptide Y (NPY) and corticotropin-releasing hormone (CRH) in the whole hypothalamus were elevated significantly in the SEKI mice as compared with control mice. In situ hybridization showed that NPY and CRH mRNA were upregulated in the arcuate nucleus and the paraventricular nucleus, respectively. There were no significant differences in melanin-concentrating hormone (MCH), orexin (OX), and cholecystokinin mRNA levels between the SEKI and control mice. These results suggest that the NPYergic system is functioning in the rodent model of cancer cachexia; however, the role of the CRHergic system in energy homeostasis remains to be elucidated. This is the first report of the hypothalamic neuropeptide response to cachexia-inducing human cells.

Animals↗
PubMed2003

The NMR-derived conformation of orexin-A: an orphan G-protein coupled receptor agonist involved in appetite regulation and sleep.

The conformation of orexin-A, an orphan G-protein coupled receptor agonist has been determined when bound to sodium dodecylsulphate-d(25) (SDS) micelles by (1)H and (13)C NMR and molecular modeling. Orexin-A has been implicated in sleep-wakefulness and feeding regulation. The conformational preference of orexin-A consists of a short helical section, involving Asp(5) to Gln(9) that makes up helix I, followed by a bend from Lys(10) to Ser(13). Residues Leu(16) to Gly(22) make up helix II. The conformation of orexin-A can now be used to explain the results of earlier Ala substitution mutagenesis experiments (J. G. Darker et al., Bioorg. Med. Chem. Lett. 11, 737-740 (2001); S. Ammoun, et al., J. Pharmacol. Expt. Ther. 305, 507-514 (2003)). Darker et al., working with orexin-A (15-33) amide, observed a significant drop in functional potency at the OX(1)R receptor when Leu(16), Leu(19), Leu(20), His(26), Gly(29), Ile(30), Leu(31), Thr(32), and Leu(33) were replaced by Ala. Ammoun et al. identified three areas of interest, which were the same for OX(1)R and OX(2)R receptors, as amino acids 15-17, 20 and 25-26 with the most marked reduction in activity being produced by the replacement of Leu(20) by Ala. We suggest that Leu(16), Leu(19), and Leu(20), which are in helix II, are likely responsible for binding orexin-A to the surface of the micelle.

Amino Acid Sequence↗
PubMed2004

Inulin-type fructans modulate gastrointestinal peptides involved in appetite regulation (glucagon-like peptide-1 and ghrelin) in rats.

The hypothesis tested in the present study is that dietary fructans are able to modulate gastrointestinal peptides involved in the control of food intake, namely glucagon-like peptide (GLP)-1 (7-36) amide and ghrelin. After 3 weeks of treatment with a standard diet (control) or the same diet enriched with 100 g fructans varying in their degrees of polymerization (oligofructose (OFS), Synergy 1 (Syn) or long chain inulin)/kg, male Wistar rats were deprived of food for 8 h before sample collection. Dietary energy intake throughout the experiment was significantly lower (P<0.05) in fructans-fed rats than in control rats, leading to a significant decrease (P<0.01) in epidydimal fat mass at the end of the treatment in OFS- and Syn-treated rats. GLP-1 (7-36) amide concentration in portal vein serum was higher in OFS- and Syn-fed than in control rats. Both GLP-1 (7-36) amide concentration and proglucagon mRNA concentrations were significantly greater (P<0.05) in the proximal colonic mucosa of fructans-fed rats v. controls. Normally active ghrelin concentration in plasma increases during food deprivation and rapidly falls during a meal. In the present study, after 8 h of food deprivation, active ghrelin in the plasma remained significantly lower (P<0.05) in OFS and Syn-fed than in control rats. These results are in accordance with the modifications of dietary intake and fat-mass development in short-chain fructans-treated rats and demonstrate the potential modulation of GLP-1 (7-36) amide and ghrelin by fermentable fibres such as fructans, which are rapidly and extensively fermented in the proximal part of the colon.

Animals↗
PubMed2006

The regulation of appetite.

The worsening global obesity epidemic, particularly the increase in childhood obesity, has prompted research into the mechanisms of appetite regulation. Complex pathways modulate energy balance, involving appetite centres in the hypothalamus and brain stem, and hormonal signals of energy status released by the gut and by the periphery. Better understanding of appetite regulation improves understanding of the aetiology of obesity. Manipulation of this homoeostatic system offers potentially useful treatments for obesity.

Adult↗
PubMed1999

Interacting appetite-regulating pathways in the hypothalamic regulation of body weight.

Various aspects of the complex spatio-temporal patterning of hypothalamic signaling that leads to the development of synchronized nocturnal feeding in the rat are critically examined. Undoubtedly, as depicted in Fig. 7, a distinct ARN in the hypothalamus is involved in the control of nocturnal appetite. At least four basic elements operate within this ARN. These are: 1) A discrete appetite-driving or orexigenic network of NPY, NE, GABA, GAL, EOP, and orexin transduces and releases appetite-stimulating signals. 2) Similarly, anorexigenic signal-producing pathways (e.g., CRH, GLP-1, alpha MSH, and CART) orchestrate neural events for dissipation of appetite and to terminate feeding, possibly by interrupting NPY efflux and action at a postsynaptic level within the hypothalamus. It is possible that some of these may represent the physiologically relevant "off" switches under the influence of GABA alone, or AgrP alone, or in combination with NPY released from the NPY-, GABA-, and AgrP-coproducing neurons. 3) Recent evidence shows that neural elements in the VMN-DMN complex tonically restrain the orexigenic signals during the intermeal interval; the restraint is greatly aided by leptin's action via diminution of orexigenic (NPY) and augmentation of anorexigenic (GLP-1, alpha MSH, and CART) signals. Since interruption of neurotransmission in the VMN resulted in hyperphagia and development of leptin resistance, it seems likely that the VMN is an effector site for the restraint exercised by leptin. The daily rhythms in leptin synthesis and release are temporally dissociable because the onset of daily rise in leptin gene expression in adipocytes precedes that in leptin secretion. Nevertheless, these rhythms are in phase with daily ingestive behavior because the peak in circulating leptin levels occurs during the middle of the feeding period. These observations, coupled with the fact that circulating levels of leptin are directly related to adiposity, pose a new challenge for elucidating the precise role of leptin in daily patterning of feeding in the rat. 4) A neural timing mechanism also operates upstream from the ARN in the daily management of energy homeostasis. Although the precise anatomical boundaries are not clearly defined, this device is likely to be composed of a group of neurons that integrate incoming internal and external information for the timely onset of the drive to eat. Evidently, this network operates independently in primates, but it is entrained to the circadian time keeper in the SCN of rodents. Apart from its role in the onset of drive to eat, the circadian patterns of gene expression of NPY, GAL, and POMC denote independent control of the timing device on the synthesis and availability for release of orexigenic signals. The VMN-DMN-PVN complex is apparently an integrated constituent of the timing mechanism in this context, because lesions in each of these sites result in loss of regulated feeding. The accumulated evidence points to the PVN and surrounding neural sites within this framework as the primary sites of release and action of various orexigenic and anorexigenic signals. A novel finding is the identification of the interconnected wiring of the DMN-mPVN axis that may mediate leptin restraint on NPY-induced feeding. The chemical phenotypes of leptin and NPY target neurons in this axis remain to be identified. These multiple orexigenic and anorexigenic pathways in the hypothalamic ARN appear to represent redundancy, a characteristic of regulated biological systems to provide a "fail-safe" neural mechanism to meet an organism's constant energy needs for growth and maintenance. Within this formulation, the coexisting orexigenic signals (NPY, NE, GAL, GABA, and AgrP) represent either another level of redundancy or it is possible that these signals operate within the ARN as reinforcing agents to varying degrees under different circumstances. (ABSTRACT TRUNCATED)

Animals↗