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Results for “Appetite Regulation”

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PubMed1980

Physiological control of energy balance.

Physiological control of energy balance is reviewed in terms of food seeking and enery (food) intake, utilization and storage. In particular the role of hormonal and metabolic signals, as clarified by whole-body calorimetry and cellular studies, and the interaction of energy expenditure with the mechanism regulating intake are outlined.

Adolescent↗
PubMed2006

Orexin A in the rostrolateral hypothalamic area induces feeding by modulating GABAergic transmission.

The neuromodulatory peptides orexin A and B are important central nervous system regulators of appetite. We previously identified the rostral lateral portion of the hypothalamus as an area important to orexin A feeding regulation. As gamma-aminobutyric-acid (GABA) within the lateral hypothalamus also mediates feeding, we sought to determine the relationship between orexin and GABA signaling within this site. Adult male Sprague-Dawley rats were implanted with cannulae directed to the rostral lateral hypothalamus and saclofen (GABA-B receptor antagonist), biccuculine (GABA-A receptor antagonist) or muscimol (GABA-A receptor agonist) were injected prior to orexin A. Both GABA antagonists failed to significantly affect orexin A-induced feeding, but muscimol significantly and dose dependently inhibited orexin A-induced feeding. Using in vivo microdialysis GABA release within this region significantly dropped during the first hour following orexin A administration, coinciding with orexin A-induced feeding. Together, these data indicate that orexin A may influence food intake by decreasing GABAergic tone within the rostral lateral hypothalamus.

Analysis of Variance↗
PubMed2006

High-fat hyperphagia in neurotrophin-4 deficient mice reveals potential role of vagal intestinal sensory innervation in long-term controls of food intake.

Neurotrophin-4 (NT-4) deficient mice exhibit substantial loss of intestinal vagal afferent innervation and short-term deficits in feeding behavior, suggesting reduced satiation. However, they do not show long-term changes in feeding or body weight because of compensatory behaviors. The present study examined whether high-fat hyperphagia induction would overcome compensation and reveal long-term effects associated with the reduced vagal sensory innervation of NT-4 mutants. First, modifications of a feeding schedule previously developed in rats were examined in wild-type mice to identify the regimen most effective at producing hyperphagia. The most successful schedule, which was run for 26 days, included access to a 43%-fat diet and pelleted chow every other day and access to only powdered chow on the alternate days. On high-fat access days mice consumed 25% more calories than mice with continuous daily access to the same high-fat diet and pelleted chow. This feeding regimen also induced hyperphagia in NT-4 deficient mice and their wild-type controls: on high-fat exposure days mutants consumed 35% more calories relative to continuous-access mutants, and wild types ate 25% more than continuous-access wild types. Moreover, on high-fat access days the alternating NT-4 mutants significantly increased caloric intake by 9% compared to alternating wild types. Thus, high-fat hyperphagia appeared to override compensation, permitting short-term changes in meal consumption by mutants that accrued into long-term changes in total daily food intake. This raises the possibility that intestinal vagal sensory innervation contributes to long-term, as well as to short-term regulation of food intake.

Adaptation, Physiological↗
PubMed2006

Thoughts for food: brain mechanisms and peripheral energy balance.

The past decade has witnessed dramatic advancements regarding the neuroendocrine control of food intake and energy homeostasis and the effects of peripheral metabolic signals on the brain. The development of molecular and genetic tools to visualize and selectively manipulate components of homeostatic systems, in combination with well-established neuroanatomical, electrophysiological, behavioral, and pharmacological techniques, are beginning to provide a clearer picture of the intricate circuits and mechanisms of these complex processes. In this review, we attempt to provide some highlights of these advancements and pinpoint some of the shortcomings of the current understanding of the brain's involvement in the regulation of daily energy homeostasis.

Animals↗
PubMed1967

Activity of single neurones in the hypothalamic feeding centres: effect of gastric distension.

1. Unit activity from neurones of hypothalamic ;feeding' and ;satiety' centres, and from adjacent hypothalmic regions, was recorded by means of steel micro-electrodes inserted by a stereotaxic method, under Dial anaesthesia.2. The spike frequency of these neurones was observed during inflation of the stomach with intragastrically placed balloons, and during electrical stimulation of the gastric branches of the vagus. As control measures, distension of the peritoneal cavity and stimulation of a sensory nerve were also carried out. These tests were repeated after severing the gastric vagal branches.3. In fasted animals the frequency of spontaneous discharge was slower in the units of the satiety centre as compared with those of the feeding centre. The spike frequency of neurones in these two hypothalamic regions maintained an inverse relationship in all experimental situations.4. Distension of the stomach and stimulation of the gastric vagal branches increased the spike frequency of satiety neurones, decreased the spike frequency of feeding neurones, and did not produce any change in spike frequency of adjacent hypothalamic neurones. A few units in the lateral mammillary region also changed their spike frequency on gastric distension. These responses were abolished after severing the gastric nerves.5. The results suggest that distension of the stomach brings about satiation through vagal afferents activating the hypothalamic satiety mechanism.6. The role of this in the nervous regulation of food intake is discussed.

Animals↗
PubMed2001

Recent insights into body weight control: from physiology to pathology.

Over the past several years, new modulators of feeding and body weight have been discovered, and our knowledge of the mechanisms and neurohumoral interactions between anorexigenic and orexigenic compounds has increased dramatically. This review aims to summarize the present knowledge of the role of leptin and several hypothalamic neuropeptides, such as neuropeptide Y (NPY), corticotropin-releasing hormone (CRH) and melanocortins, in the regulation of appetite and body weight. It also presents the progress made in the design of interactions between leptin and hypothalamic peptides in the regulation of feeding. The role of these compounds in the pathogenesis of obesity in animals and humans, and their potential usefulness in the treatment of this disorder, are discussed.

Animals↗
PubMed1977

Reduced food intake following cerebral intraventricular infusion of glucose in Gallus domesticus.

Unanaesthetized hens and cocks were infused into the cerebral lateral ventricle with 0.2 ml of a 6% glucose solution or equal volumes of isotonic saline following a 20-hr total food deprivation period. A more marked suppression of food intake occurred in the next 1-3 hr after glucose rather than after saline. The results provide new evidence that chickens possess central glucoreceptors involved in the regulation of their feeding behavior.

Animals↗
PubMed1984

Sodium appetite decreased by central angiotensin blockade.

Disturbances in body water and electrolytes that trigger sodium appetite, such as sodium depletion or hypovolemia, are potent activators of the renin-angiotensin system. In the absence of an actual deficit in body fluids, angiotensin injections are adequate to stimulate increased sodium ingestion. To assess whether angiotensin is a significant mediator of sodium appetite induced by acute alterations in body fluids, sodium intake was examined in rats during central or peripheral angiotensin blockade. Central blockade of angiotensin receptors by intracerebroventricular (ICVT) injection of the analogue antagonist saralasin decreased (but did not eliminate) sodium intake after polethylene glycol-induced hypovolemia or sodium depletion resulting from dialysis against glucose. Conversely, peripheral blockade of angiotensin converting enzyme with orally active captopril potentiated rather than decreased sodium appetite and stimulated water intake after sodium depletion. This increased water and salt intake after peripheral inhibition of converting enzyme was reversed, however, by concurrent central blockade of angiotensin receptors. These data support the hypothesis that angiotensin participates in sodium appetite associated with acute alteration in body fluids. Furthermore, the brain is the site at which angiotensin exerts its influence on sodium appetite. While the involvement of angiotensin of brain origin is not ruled out, the change in sodium appetite after peripheral blockade of converting enzyme suggests that circulating angiotensin derived from renal renin may interact with central angiotensin receptors regulating sodium appetite.

Angiotensin II↗
PubMed2000

Activation of hypothalamic insulin by serotonin is the primary event of the insulin-serotonin interaction involved in the control of feeding.

In previous experiments, we reported a close parallelism in the responses of both serotonin (5-HT) and insulin in the hypothalamic PVN-VMH region of freely-moving rats during feeding. Thus, hypothalamic 5-HT and insulin may participate, independently or in interaction, in the control of carbohydrate and fat ingestion. The precedence of the activation of one or the other substance remained to be investigated. In adult male Wistar rats, (a) dexfenfluramine was administered to the PVN-VMH region by reverse microdialysis (80 microM for 10 min) while local insulin was assessed; (b) insulin was locally infused (400 mU for 10 min) through the tip of the dialysis probe while 5-HT was measured. Dexfenfluramine immediately increased 5-HT release, and also extracellular insulin levels (+102%). This activation of insulin by serotonin is actually a central effect since neither insulinemia nor glycemia were affected. Conversely, insulin enhanced 5-HT release (+81%), but only 45 min after the beginning of its infusion. Noradrenaline, dopamine and metabolites were slightly or not at all modified by insulin. These data demonstrate that an interaction does exist between insulin and 5-HT in the VMH-PVN area. Because of the delay of 5-HT response to insulin, an activation of the serotonergic system would be the causal event acting immediately on insulin, and not the contrary. Whatever the exact mechanism of this interaction, it seems to be a link in a larger cascade of events involving numerous neurotransmitters and peptides leading to the regulation of feeding.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1982

Effect of exercise on spontaneous calorie intake in obesity.

The effect of increased physical activity on energy intake and balance was investigated in six obese women (mean 167% above ideal body weight) voluntarily hospitalized for metabolic balance studies. Three 19-day treatments-one sedentary and two with treadmill exercise which increased daily expenditure to 110% (mild) and 125% (moderate) of sedentary expenditure-were imposed on each subject. Individual daily expenditure and ad libitum intake were determined by activity diaries and covert monitoring, respectively. Subjects selected and did not not change an intake level which allowed for energy balance during the sedentary period only. Therefore, the difference between intake and expenditure between treatments was significantly different (sedentary 11, mild -114, and moderate -369 kcal/day). The negative balance observed with mild and moderate exercise was obtained because while expenditure was raised with exercise, no compensatory increase in intake occurred. Moderate, realistic levels of activity did not regulate intake.

Adult↗
PubMed2006

Developmental programming of hypothalamic feeding circuits.

The hypothalamus plays a critical role in the regulation of food intake and body weight, and recent work has defined a core circuitry in the hypothalamus that appears to mediate many of the effects of the adipocyte-derived hormone leptin on feeding and glucose homeostasis. However, until recently, little was known about the development of these critical pathways. This review summarizes recent advances regarding the post-natal development of 'metabolic' projections from the arcuate nucleus of the hypothalamus. Evidence accumulated primarily in mice indicates that these circuits develop after birth and remain both structurally and functionally immature until the second week of life. Recent studies have begun to identify cues governing development of these pathways, and leptin appears to play a crucial neurotrophic role in the development of the hypothalamic circuits regulating food intake and adiposity. The neurodevelopmental actions of leptin appear specifically to be restricted to a neonatal critical period that coincides with the naturally occurring surge in leptin. In addition, the timing and amplitude of the post-natal leptin surge has important consequences for normal body weight regulation and glucose homeostasis later in life. Ultimately, these data promise to provide new insight into the mechanisms by which alteration of perinatal nutrition may have long-term consequences on body weight regulation and adiposity in the offspring.

Adiposity↗
PubMed1999

Nutrient-specific preferences by lambs conditioned with intraruminal infusions of starch, casein, and water.

We hypothesized that lambs discriminate between postingestive effects of energy and protein and associate those effects with a food's flavor to modify food choices. Based on this hypothesis, we predicted that 1) lambs would acquire a preference for a poorly nutritious food (grape pomace) eaten during intraruminal infusions of energy (starch) or protein (casein) and that 2) shortly after an intraruminal infusion of energy or protein (preload), lambs would decrease their preferences for foods previously conditioned with starch or casein, respectively. Thirty lambs were allotted to three groups and conditioned as follows. On d 1, lambs in each group received grape pomace containing a different flavor and water was infused into their rumens as they ate the pomace. On d 2, the flavors were switched so each group received a new flavor and a suspension of starch (10% of the DE required per day) replaced the water infusion. On d 3, the flavors were switched again, and a suspension of casein (2.7 to 5.4% of the CP required per day) replaced the starch infusion. Conditioning was repeated during four consecutive trials. Lambs in Trial 1 had a basal diet of alfalfa pellets (e.g., free access from 1200 to 1700) and 400 g of rolled barley. Lambs in Trials 2, 3, and 4 received a restricted amount of alfalfa pellets (990 g/d) as their basal diet. After conditioning, all animals received an infusion of water, and, 30 min later, they were offered a choice of the three flavors previously paired with water, starch, or casein. On the ensuing days, the choice was repeated, but starch, casein, and barley replaced the water preload. The nutrient density of the infused preloads was increased during consecutive trials. Lambs preferred the flavors paired with starch > water > casein during Trial 1 (P < .05) and the flavors paired with starch > casein > water during Trials 2 (P < .05), 3 (P < .001), and 4 (P < .001). Preloads of casein decreased preferences for flavors previously paired with casein (P < .10 [Trial 2]; P < .001 [Trial 3], and increased preferences for flavors paired with starch (P < .05 [Trial 2]; P < .001 [Trial 3]). Preloads of energy (barley) had the opposite effect (P < .05 [Trial 3]). These results indicate that lambs discriminated between the postingestive effects of starch and casein and associated the effects with specific external cues (i.e., added flavors) to regulate macronutrient ingestion.

Animal Nutritional Physiological Phenomena↗
PubMed2006

The role of neuropeptide Y and interaction with leptin in regulating feed intake and luteinizing hormone and growth hormone secretion in the pig.

Two experiments (EXP) were conducted in ovariectomized prepubertal gilts to test the hypothesis that neuropeptide Y (NPY) stimulates appetite and modulates LH and GH secretion, and that leptin modifies such acute effects of NPY on feeding behavior and LH and GH secretion. In EXP I, gilts received intracerebroventricular (ICV) injections of 0.9% saline (saline; n = 6), or 10 microg (n = 7), 50 microg (n = 5) or 100 microg (n = 7) NPY in saline and blood samples were collected. In EXP II, gilts received ICV injections of S (n = 4), or 50 microg leptin (n = 4), or 100 microg NPY (n = 4) or 100 microg NPY +50 microg leptin (n = 4) in saline, and feed intake was measured at 4, 20 and 44 h after feed presentation and blood samples collected. In EXP I, NPY suppressed LH secretion and the 100 microg dose stimulated GH secretion. In EXP II, NPY reversed the inhibitory effect of leptin on feed intake and suppressed LH secretion, but serum GH concentrations were unaffected. These results support the hypothesis that NPY modulates feed intake, and LH and GH secretion and may serve as a neural link between metabolic state and the reproductive and growth axis in the pig.

Animals↗