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At least 649 records · Page 36Linked to original sources
PubMed2005

Neuroendocrine control of food intake.

PURPOSE OF REVIEW: Obesity is a major public health problem and substantially increases the risk of type 2 diabetes, hypertension, stroke, cardiovascular, respiratory problems, gall bladder disease, osteoarthritis and sleep apnoea, as well as certain cancers. The prevalence of obesity is rapidly increasing worldwide. However, for individuals weight is regulated within a narrow range. This regulation depends on energy intake (in the form of food) and energy expenditure. Recently, there has been a remarkable increase in our understanding of the homeostatic mechanisms that control food intake and energy homeostasis. RECENT FINDINGS: There is increased understanding of the central regulation of appetite. In particular, this includes new knowledge about the hypothalamus and brainstem and their relation to food intake regulation. Peripheral hormones (notably adipostat factors and gut hormones) have now been found to be important in food intake regulation. SUMMARY: Complex central circuitry controls food intake. Circulating hormones, in particular the gut hormones have unexpectedly been found to be very important in appetite control. The gut hormones are thus new and exciting targets for future obesity therapies.

Animals↗
PubMed1985

Autoradiographic localization of kappa opiate receptors in CNS taste and feeding areas.

Recent evidence suggests that kappa opiate receptors may play a key role in the regulation of appetite. Such evidence implies that kappa receptors might be localized within specific brain areas known to regulate ingestive behaviors. On the basis of this implication we employed an in vitro film autoradiographic technique using 3H-ethylketocyclazozine as ligand to identify putative kappa receptors within CNS "taste" nuclei and surrounding areas. Coronal cryostat sections of rat brain were incubated with ligand in the presence of D-Ala2, D-Leu5-enkephalin (DADLE) and morphine, apposed to LKB Ultrofilm for 60 days, processed and kappa receptor densities evaluated with the aid of a hand held photometer and video image analyzer. Highest kappa receptor densities were found within various gustatory and feeding sites including the rostral pole of the nucleus of the solitary tract, parabrachial nuclei, ventral posterior and medial portions of the thalamus, medial hypothalamus, medial nuclei of the amygdala and bed nucleus of the stria terminalis. Various other midline and medial limbic areas also showed significant kappa densities.

Animals↗
PubMed1996

Glucagon-like peptide I receptors in the subfornical organ and the area postrema are accessible to circulating glucagon-like peptide I.

The intestinal incretin hormone glucagon-like peptide I (GLP-I) inhibits gastric motility and secretion in normal, but not in vagotomized subjects, pointing to a centrally mediated effect. Therefore, our aim was to study the availability of rat brain GLP-I receptors to peripherally injected 125I-labeled GLP-I. The specificity of the binding was tested by co-injection of excess amounts of unlabeled GLP-I. Using light microscopical autoradiography of rat brain sections, we found specific 125I-GLP-I binding exclusively in the subfornical organ and the area postrema. This binding was abolished when an excess amount of unlabeled GLP-I was co-injected with the labeled GLP-I. We conclude that cells in the subfornical organ and the area postrema could be responsive to blood-borne GLP-I. The observed binding of peripherally administered GLP-I to the subfornical organ and the area postrema, which both have close neuroanatomical connections with hypothalamic areas involved in water and appetite homeostasis, is consistent with the potential roles of circulating GLP-I in the central regulation of appetite and autonomic functions.

Animals↗
PubMed1995

Effects of restricted feeding on the light-induced body weight change and locomotor activity in the Djungarian hamster.

To investigate the role of food intake in seasonal body weight changes in the Djungarian hamster, we divided animals, which had minimum body weights after 18 wk in SD, into ad-lib feeding and restricted feeding groups under a long day (LD) and a short day (SD) photoperiods. In the ad-lib feeding groups, body weight and food intake increased in parallel after 3 wk under LD and after 6-7 wk in SD because of photorefractoriness. In the restricted feeding groups, almost all animals moved around furiously (food-seeking activity) when they came to consume all the food provided at 2-3 wk of the treatment in LD and after several weeks in SD with the initiation of photorefractoriness, and ended up with death. In the restricted feeding groups, body weight increase was not observed. The furious food-seeking activity in the restricted groups and the increase of body weight specific food intake (food intake/body weight) in the ad-lib feeding groups might reflect the increased requirement for food. This increase of requirement for food seems to be one of the critical factors regulating the seasonal body weight change.

Animals↗
PubMed1975

Involvement of food intake in the lysine-arginine antagonism in chicks.

Studies were conducted to evaluate the involvement of food intake in the lysine-arginine antagonism. Diets were formulated to compensate for the metabolic consequences of excess dietary lysine; induction of renal arginase activity, depression of heptic glycine transamidinase, and urinary losses of arginine. This was accomplished by inclusion of creatine in the basal diet, use of a moderate excess of lysine that did not increase urinary arginine excretion, and addition of the arginase depressors, alpha-aminoisobutyric acid (AIB) and L-threonine, to diets containing excess lysine. When chicks were fed diets containing excess lysine ad libitum, growth and efficiency of arginine retention were reduced. Supplementation of the diets with AIB and threonine markedly reduced the growth depression and restored efficiency of arginine utilization. When chicks were force-fed the diet containing excess lysine, growth was depressed, and body composition was altered. Inclusion of AIB and threonine in the diet containing excess lysine resulted in growth and body composition equivalent to levels of force-fed controls. In a second experiment the basal diet and basal supplemented with AIB and threonine were pair-fed to lysine-supplemented diets containing AIB and threonine. Body weight gains and body composition of all groups were similar. In other experiments, food intake increased within 24 hours (P less than 0.05) and probably within 12 hours (P less than 0.10) after removal of excess lysine from the diet. It is concluded that a portion of the lysine-arginine antagonism is due to a primary effect of lysine on regulation of food intake.

Animals↗
PubMedDate not supplied

Interactions of glucagon-like peptide-1 (GLP-1) with the blood-brain barrier.

Glucagon-like peptide-1 (GLP-1) reduces insulin requirement in diabetes mellitus and promotes satiety. GLP-1 in the periphery (outside the CNS) has been shown to act on the brain to reduce food ingestion. As GLP-1 is readily degraded in blood, we focused on the interactions of [Ser8]GLP-1, an analog with similar biological effects and greater stability, with the blood-brain barrier (BBB). The influx of radiolabeled [Ser8]GLP-1 into brain has several distinctive characteristics: 1. A rapid influx rate of 8.867 +/- 0.798 x 10(4) mL/g-min as measured by multiple-time regression analysis after iv injection in mice. 2. Lack of self-inhibition by excess doses of the unlabeled [Ser8]GLP-1 either iv or by in situ brain perfusion, indicating the absence of a saturable transport system at the BBB. 3. Lack of modulation by short-term fasting and some other ingestive peptides that may interact with GLP-1, including leptin, glucagon, insulin, neuropeptide Y, and melanin-concentrating hormone. 4. No inhibition of influx by the selective GLP-1 receptor antagonist exendin(9-39), suggesting that the GLP-1 receptor is not involved in the rapid entry into brain. Similarly, there was no efflux system for [Ser8]GLP-1 to exit the brain other than following the reabsorption of cerebrospinal fluid (CSF). The fast influx was not associated with high lipid solubility. Upon reaching the brain compartment, substantial amounts of [Ser8]GLP-1 entered the brain parenchyma, but a large proportion was loosely associated with the vasculature at the BBB. Finally, the influx rate of [Ser8]GLP-1 was compared with that of GLP-1 in a blood-free brain perfusion system; radiolabeled GLP-1 had a more rapid influx than its analog and neither peptide showed the self-inhibition indicative of a saturable transport system. Therefore, we conclude that [Ser8]GLP-1 and the endogenous peptide GLP-1 can gain access to the brain from the periphery by simple diffusion and thus contribute to the regulation of feeding.

Animals↗
PubMed2002

[Leptin and psychiatric disorders].

As early as the beginning of the 20th century, changes in appetite and weight were recognized as important symptoms of severe psychiatric disorders. Particularly in the last decade, understanding of the regulation of appetite and weight has made major progress. In this context, the discovery of the adipose tissue hormone leptin, which signals the size of the peripheral fat stores to the CNS, was crucial. In addition, leptin is also involved in a number of CNS networks regulating behavior and thus of great importance for the pathophysiology of psychiatric disorders. Apart from sexual behavior, those networks include motor activity, sleep, and cognition. Moreover, leptin seems to be involved in the development and maturation of the brain. The present paper summarizes current studies which suggest that, in psychiatric disorders, leptin could be of importance not only for disease-associated or drug-related changes in appetite and weight but also for alterations in behavior and cognition.

Alcoholism↗
PubMed2005

Molecular and anatomical determinants of central leptin resistance.

The increasing incidence of obesity in developed nations is an ever-growing challenge to health care, promoting diabetes and other diseases. The hormone leptin, which is derived from adipose tissue, regulates feeding and energy expenditure. Most forms of obesity are associated with diminished responsiveness to the appetite-suppressing effects of leptin. Here we review the mechanisms by which leptin activates intracellular signals, the roles of these signals in leptin action in vivo, and mechanisms that may attenuate leptin signaling, limiting its action in obese individuals. We highlight data regarding the expression of SOCS3 (a potential mediator of leptin resistance) in the arcuate nucleus of the hypothalamus.

Adipose Tissue↗
PubMed2001

The differential regulation of CART gene expression in a pituitary cell line and primary cell cultures of ovine pars tuberalis cells.

The cocaine-amphetamine regulated transcript (CART) encodes for a protein which has an important role in the regulation of appetite and body weight. To date, no details of the molecular events and signal transduction pathways which regulate this gene are available. We report the identification of CART gene expression in the GH3 pituitary cell line. We have used activators of the cAMP or protein kinase C (PKC) signal transduction pathways to show that, in GH3 cells, CART is transcriptionally up-regulated by activators of the cAMP signal transduction pathway. We also identify CART gene expression in ovine pars tuberalis (PT) tissue and primary cell cultures. In PT cells in contrast to GH3 cells, CART gene expression is upregulated by activators of the PKC signal transduction pathway. Cultured cells have provided a valuable resource for the detailed analysis of specific regulatory mechanisms underlying transcriptional or translational regulation of genes, signal transduction events and many other cellular processes. GH3 and PT cells may therefore provide a resource for the further detailed molecular analysis of the events regulating CART gene expression and processing.

Animals↗
PubMed2005

The hypothalamic neuropeptide melanin-concentrating hormone acts in the nucleus accumbens to modulate feeding behavior and forced-swim performance.

Melanin-concentrating hormone (MCH) is a hypothalamic neuropeptide with a prominent role in feeding and energy homeostasis. The rodent MCH receptor (MCH1R) is highly expressed in the nucleus accumbens shell (AcSh), a region that is important in the regulation of appetitive behavior. Here we establish a role for MCH and MCH1R in mediating a hypothalamic-limbic circuit that regulates feeding and related behaviors. Direct delivery of an MCH1R receptor antagonist to the AcSh blocked feeding and produced an antidepressant-like effect in the forced swim test, whereas intra-AcSh injection of MCH had the opposite effect. Expression studies demonstrated that MCH1R is present in both the enkephalin- and dynorphin-positive medium spiny neurons of the AcSh. Biochemical analysis in AcSh explants showed that MCH signaling blocks dopamine-induced phosphorylation of the AMPA glutamate receptor subunit GluR1 at Ser845. Finally, food deprivation, but not other stressors, stimulated cAMP response element-binding protein-dependent pathways selectively in MCH neurons of the hypothalamus, suggesting that these neurons are responsive to a specific set of physiologically relevant conditions. This work identifies a novel hypothalamic-AcSh circuit that influences appetitive behavior and mediates the antidepressant activity of MCH1R antagonists.

Analysis of Variance↗
PubMed2005

Anatomy and regulation of the central melanocortin system.

The central melanocortin system is perhaps the best-characterized neuronal pathway involved in the regulation of energy homeostasis. This collection of circuits is unique in having the capability of sensing signals from a staggering array of hormones, nutrients and afferent neural inputs. It is likely to be involved in integrating long-term adipostatic signals from leptin and insulin, primarily received by the hypothalamus, with acute signals regulating hunger and satiety, primarily received by the brainstem. The system is also unique from a regulatory point of view in that it is composed of fibers expressing both agonists and antagonists of melanocortin receptors. Given that the central melanocortin system is an active target for development of drugs for the treatment of obesity, diabetes and cachexia, it is important to understand the system in its full complexity, including the likelihood that the system also regulates the cardiovascular and reproductive systems.

Adipose Tissue↗
PubMed2001

[Distorted control of feeding behavior induced by abnormally regulated peripheral energy metabolism].

To regulate feeding behavior and energy metabolism, a variety of neuronal and hormonal messages are integrated by glucose sensing system located in peripheral organ and central nervous system. Among them, a hepatoportal glucose sensor plays a major role in perception of peripheral humoral information such as brain-gut peptides and cytokines. These signals are transmitted to the hypothalamus through the hepatic afferent vagus nerve and the nucleus of the solitary tract. Recent molecular approaches using knock out or transgenic mice have indicated important effects of peripheral energy metabolism on feeding control. Particularly, fatty acid metabolism in the liver and functions of uncoupling protein family in the brown adipose tissue and the muscle play an essential role as detector for energy storage, and in turn may be contributable to regulation of feeding behavior.

Adipose Tissue, Brown↗