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Results for “Appetite Regulation”

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PubMed2001

A role of ghrelin in neuroendocrine and behavioral responses to stress in mice.

Ghrelin, an endogenous ligand of the growth hormone secretagogue receptor, was recently identified in the rat stomach. Previous studies have shown that ghrelin potently increases growth hormone release and food intake. We examined the effects of the gastric peptide ghrelin on anxiety-like behavior in association with the hypothalamic-pituitary-adrenal axis in mice. Both intra-third cerebroventricular and intraperitoneal administration of ghrelin potently and significantly induced anxiogenic activities in the elevated plus maze test. Ghrelin gene expression in the stomach was increased by tail pinch stress as well as by starvation stress. Administration of a corticotropin-releasing hormone (CRH) receptor antagonist significantly inhibited ghrelin-induced anxiogenic effects. Peripherally administered ghrelin significantly increased CRH mRNA, but not urocortin mRNA expression in the hypothalamus. Furthermore, intraperitoneal injection of ghrelin produced a significant dose- dependent increase in serum corticosterone levels. These findings suggest that ghrelin may have a role in mediating neuroendocrine and behavioral responses to stressors and that the stomach could play an important role, not only in the regulation of appetite, but also in the regulation of anxiety.

Animals↗
PubMed2006

Genetic polymorphisms and weight loss in obesity: a randomised trial of hypo-energetic high- versus low-fat diets.

OBJECTIVES: To study if genes with common single nucleotide polymorphisms (SNPs) associated with obesity-related phenotypes influence weight loss (WL) in obese individuals treated by a hypo-energetic low-fat or high-fat diet. DESIGN: Randomised, parallel, two-arm, open-label multi-centre trial. SETTING: Eight clinical centres in seven European countries. PARTICIPANTS: 771 obese adult individuals. INTERVENTIONS: 10-wk dietary intervention to hypo-energetic (-600 kcal/d) diets with a targeted fat energy of 20%-25% or 40%-45%, completed in 648 participants. OUTCOME MEASURES: WL during the 10 wk in relation to genotypes of 42 SNPs in 26 candidate genes, probably associated with hypothalamic regulation of appetite, efficiency of energy expenditure, regulation of adipocyte differentiation and function, lipid and glucose metabolism, or production of adipocytokines, determined in 642 participants. RESULTS: Compared with the noncarriers of each of the SNPs, and after adjusting for gender, age, baseline weight and centre, heterozygotes showed WL differences that ranged from -0.6 to 0.8 kg, and homozygotes, from -0.7 to 3.1 kg. Genotype-dependent additional WL on low-fat diet ranged from 1.9 to -1.6 kg in heterozygotes, and from 3.8 kg to -2.1 kg in homozygotes relative to the noncarriers. Considering the multiple testing conducted, none of the associations was statistically significant. CONCLUSIONS: Polymorphisms in a panel of obesity-related candidate genes play a minor role, if any, in modulating weight changes induced by a moderate hypo-energetic low-fat or high-fat diet.

Journal Article↗
PubMed2001

Effects of abomasal infusion of long-chain fatty acids on intake, feeding behavior and milk production in dairy cows.

Fat is often fed to dairy cows to increase the energy concentration of their diet; however, feeding fat often reduces dry matter intake (DMI), which limits its impact on metabolizable energy (ME) intake. To investigate the effects of postruminal fat infusion on intake, feeding behavior, and milk production of dairy cows at two stages of lactation (55 and 111 d postpartum), six Holstein x British Friesian cows were infused into the abomasum, with a mixture of rapeseed and sunflower oils supplying predominantly unsaturated long-chain fatty acids (LCFA). Dry matter intake was significantly depressed by oil infusion, but estimated ME intake was unchanged, and thus there was no effect of oil infusion on milk yield. There was no effect of stage of lactation on the DM or ME intake response to oil infusion. Milk fat concentration was increased by oil infusion in mid-lactation but not in early lactation, suggesting that the infused LCFA were utilized differently in early compared with midlactation. Cows spent an average of 654 min idling, 462 min ruminating, and 248 min eating during the last 22.8 h of each infusion. There were no significant effects of oil infusion or stage of lactation on the total time spent engaged in these activities. An assessment of the circadian pattern of feeding behavior suggested that the depression in DMI in response to oil infusion occurred after the 1630 and 2230 h feeding times. This may reflect differences in mechanisms regulating feed intake behavior and appetite during the day. Comparison of the results of the present study with the results of other trials involving postruminal fat infusion suggests that polyunsaturated nonesterified fatty acids have the most potent effect on DMI intake.

Abomasum↗
PubMed1999

Effects of food deprivation and metabolic fuel utilization on food hoarding by jirds (Meriones shawi).

Food hoarding plays an important role in the energetic repertoire of a variety of mammalian species. Both food hoarding and food intake have been examined in rodents using several energetic challenges including food deprivation, treatment with metabolic fuel blockers, and enhancement of fuel storage. In the present experiment, we examined food hoarding by female jirds (Meriones shawi), a desert rodent species occupying the arid steppes and desert regions of Egypt. Jirds are prodigious hoarders in the field; however, virtually nothing is known about their hoarding within controlled laboratory settings. In the present study, the effects of food deprivation as well as alterations in metabolic fuel utilization (i.e., 2-deoxy-D-glucose and isophane insulin) on food hoarding and food intake were tested in female jirds using a simulated burrow system. Jirds decreased body mass and increased food consumption following either 32 or 56-h food deprivation. Food hoarding, however, was virtually abolished after food deprivation and treatment with 2-DG. In contrast, isophane insulin treatment had no effect on food consumption or hoarding in this species. Taken together, the present results suggest that total body mass (fat), rather than short-term metabolic fuel utilization, regulates both food consumption and hoarding in female jirds. In addition, these results provide a novel set of appetitive responses to these energetic challenges in small mammals.

Analysis of Variance↗
PubMed2005

Brain regulation of food intake and appetite: molecules and networks.

In the clinic, obesity and anorexia constitute prevalent problems whose manifestations are encountered in virtually every field of medicine. However, as the command centre for regulating food intake and energy metabolism is located in the brain, the basic neuroscientist sees in the same disorders malfunctions of a model network for how integration of diverse sensory inputs leads to a coordinated behavioural, endocrine and autonomic response. The two approaches are not mutually exclusive; rather, much can be gained by combining both perspectives to understand the pathophysiology of over- and underweight. The present review summarizes recent advances in this field including the characterization of peripheral metabolic signals to the brain such as leptin, insulin, peptide YY, ghrelin and lipid mediators as well as the vagus nerve; signalling of the metabolic sensors in the brainstem and hypothalamus via, e.g. neuropeptide Y and melanocortin peptides; integration and coordination of brain-mediated responses to nutritional challenges; the organization of food intake in simple model organisms; the mechanisms underlying food reward and processing of the sensory and metabolic properties of food in the cerebral cortex; and the development of the central metabolic system, as well as its pathological regulation in cancer and infections. Finally, recent findings on the genetics of human obesity are summarized, as well as the potential for novel treatments of body weight disorders.

Animals↗
PubMed2007

Regulation of hypothalamic NPY by diet and smoking.

Appetite is regulated by a number of hypothalamic neuropeptides including neuropeptide Y (NPY), a powerful feeding stimulator that responds to feeding status, and drugs such as nicotine and cannabis. There is debate regarding the extent of the influence of obesity on hypothalamic NPY. We measured hypothalamic NPY in male Sprague-Dawley rats after short or long term exposure to cafeteria-style high fat diet (32% energy as fat) or laboratory chow (12% fat). Caloric intake and body weight were increased in the high fat diet group, and brown fat and white fat masses were significantly increased after 2 weeks. Hypothalamic NPY concentration was only significantly decreased after long term consumption of the high fat diet. Nicotine decreases food intake and body weight, with conflicting effects on hypothalamic NPY reported. Body weight, plasma hormones and brain NPY were investigated in male Balb/c mice exposed to cigarette smoke for 4 days, 4 and 12 weeks. Food intake was significantly decreased by smoke exposure (2.32+/-0.03g/24h versus 2.71+/-0.04g/24h in control mice (non-smoke exposed) at 12 weeks). Relative to control mice, smoke exposure led to greater weight loss, while pair-feeding the equivalent amount of chow caused an intermediate weight loss. Chronic smoke exposure, but not pair-feeding, was associated with decreased hypothalamic NPY concentration, suggesting an inhibitory effect of cigarette smoking on brain NPY levels. Thus, consumption of a high fat diet and smoke exposure reprogram hypothalamic NPY. Reduced NPY may contribute to the anorexic effect of smoke exposure.

Animals↗
PubMed1996

Substitution and caloric regulation in a closed economy.

Three experiments were conducted to study the effect of an imperfect substitute for food on demand for food in a closed economy. In Experiments 1 and 2, rats pressed a lever for their entire daily food ration, and a fixed ratio of presses was required for each food pellet. In both experiments, the fixed ratio was held constant during a daily session but was increased between sessions. The fixed ratio was increased over a series of daily sessions once in the absence of concurrently available sucrose and again when sucrose pellets were freely available. For both series, increases in the fixed ratio reduced food intake, but body weight was reduced only in the no-sucrose condition. In the sucrose condition, body weight and total caloric intake (sucrose plus food) were relatively unaffected by increases in the fixed ratio. At all fixed ratios, food intake was proportionally reduced by the intake of sucrose. In Experiment 3, monkeys obtained food or saccharin by pressing keys; the fixed ratio of presses per food pellet was increased once when tap water was each monkey's only source of fluid, again when each monkey's water was sweetened with saccharin, and a third time when each monkey had concurrent access to the saccharin solution and plain water. Increases in the fixed ratio, but not the intake of the saccharin solution, reduced each monkey's food intake. Because neither rats' sucrose nor monkeys' saccharin intakes affected the slope of the respective demand curves for food, monkeys and rats increased their daily output of presses and thereby defended their daily intake of those complementary elements of food. However, sucrose reduced rats' food intake. The relative constancy of body weight and total caloric intake in the sucrose condition is consistent with the possibility that rats tended to regulate caloric intake.

Animals↗
PubMed2005

Stimulation of appetite by ghrelin is regulated by leptin restraint: peripheral and central sites of action.

A reciprocal rhythmic pattern of 2 afferent hormonal signals, anorexigenic leptin and orexigenic ghrelin, imparts rhythmicity to the neuropeptide Y (NPY) system, the final common pathway for appetite expression in the hypothalamus. We now show that leptin inhibits both the secretion of gastric ghrelin and the stimulation of feeding by ghrelin. We propose that this dual leptin restraint is the major regulatory arm of the feedback communication between the periphery and the hypothalamus for weight homeostasis, and disruption in the rhythmic communication at any locus in the leptin-ghrelin-NPY feedback loop impels loss of hypothalamic control, leading to abnormal weight gain and obesity.

Afferent Pathways↗
PubMed2004

AMP-activated protein kinase plays a role in the control of food intake.

AMP-activated protein kinase (AMPK) is the downstream component of a protein kinase cascade that acts as an intracellular energy sensor maintaining the energy balance within the cell. The finding that leptin and adiponectin activate AMPK to alter metabolic pathways in muscle and liver provides direct evidence for this role in peripheral tissues. The hypothalamus is a key regulator of food intake and energy balance, coordinating body adiposity and nutritional state in response to peripheral hormones, such as leptin, peptide YY-(3-36), and ghrelin. To date the hormonal regulation of AMPK in the hypothalamus, or its potential role in the control of food intake, have not been reported. Here we demonstrate that counter-regulatory hormones involved in appetite control regulate AMPK activity and that pharmacological activation of AMPK in the hypothalamus increases food intake. In vivo administration of leptin, which leads to a reduction in food intake, decreases hypothalamic AMPK activity. By contrast, injection of ghrelin in vivo, which increases food intake, stimulates AMPK activity in the hypothalamus. Consistent with the effect of ghrelin, injection of 5-amino-4-imidazole carboxamide riboside, a pharmacological activator of AMPK, into either the third cerebral ventricle or directly into the paraventricular nucleus of the hypothalamus significantly increased food intake. These results suggest that AMPK is regulated in the hypothalamus by hormones which regulate food intake. Furthermore, direct pharmacological activation of AMPK in the hypothalamus is sufficient to increase food intake. These findings demonstrate that AMPK plays a role in the regulation of feeding and identify AMPK as a novel target for anti-obesity drugs.

AMP-Activated Protein Kinases↗
PubMed1997

Menstrual cycle and appetite control: implications for weight regulation.

Hormonal fluctuations associated with the menstrual cycle influence appetite control and eating behaviour. Energy intake varies during the reproductive cycle in humans and animals, with a periovulatory nadir and a luteal phase peak. Patterns of macronutrient selection show less consistency but a number of studies report carbohydrate cravings in the premenstrual phase, particularly in women with premenstrual syndrome. The cyclical nature of food cravings are frequently, but not invariably, associated with depression. Fluctuations in appetite, cravings and energy intake during the menstrual cycle may occur in parallel with cyclical rhythms in serotonin, which can be accompanied by affective symptoms. The premenstrual phase can be considered as a time when women are especially vulnerable to overconsumption, food craving and depression; this is often associated with low serotonin activity.

Affect↗
PubMed2000

Central bombesin inhibits food intake and the orexigenic effect of neuropeptide Y in the neonatal chick.

It is well known that central injection of bombesin (BN) suppresses feeding in mammalian and avian species, but the anorexigenic effect of central BN are still open with special reference to the chick. The dose response (0, 0.1 and 0.5 microg) of intracerebroventricular (ICV) injection of BN was examined in Experiment 1. ICV injection of BN inhibited food intake in a dose-dependent manner. Experiment 2 was done to determine whether BN interacts with the orexigenic effect of neuropeptide Y (NPY) in the neonatal chick. Central administration of NPY (2.5 microg) greatly enhanced food intake, but co-injection of BN (0.5 microg) suppressed food intake. The dose response of NPY (2.5 microg) co-injected with three levels of BN (0, 0.1 and 0.5 microg) was examined in Experiment 3. ICV injection of BN attenuated the hyperphagia by NPY in a dose-related fashion. It is suggested that central BN may interact with NPY for the regulation of feeding in the neonatal chick.

Animals↗
PubMed1993

Forebrain lesions that disrupt water homeostasis do not eliminate the sodium appetite of sodium deficiency in sheep.

Brain structures located within the anterior wall of the third brain ventricle (subfornical organ, median preoptic nucleus and organum vasculosum of the lamina terminalis) are known to be involved in thirst as well as other aspects of body fluid and electrolyte balance. The present studies evaluated the role of these structures in the Na appetite of mildly or moderately Na-depleted sheep (sheep with a parotid fistula deprived of Na solution for 22 or 46 h). In addition, the role of these structures was tested in mildly Na-depleted sheep in which the Na appetite was enhanced by decreasing cerebrospinal fluid and brain extracellular fluid Na concentration (i.e., i.c.v. infusion of hypertonic saccharide solution) or was decreased by systemic infusion of hypertonic saline. The results indicated that sheep with lesions which reduced or eliminated daily water intake or water intake in response to hypertonicity of body fluids had, in all situations tested, appropriate changes in Na appetite (i.e., similar to their prelesion changes). Thus, the present experiments demonstrated that the brain areas involved in thirst as well as other aspects of body fluid and electrolyte balance are anatomically different from those involved in regulating Na appetite.

Animals↗
PubMed2003

Distribution, function, and properties of leptin receptors in the brain.

Leptin, a peptide hormone, is implicated in the modulation of food intake and maintenance of energy balance in many vertebrates including humans. It is considered to act via its receptor mainly through several hypothalamic nuclei that play critical roles in the regulation of appetite. This article looks mainly at the functional significance of leptin in rat brain by drawing on published reports of morphological and physiological analyses. Our immunohistochemical observations indicate that the leptin receptor is distributed throughout the brain, including the hypothalamus, and interestingly, is found in the hippocampus and neocortex. Physiological experiments with single living cells isolated from fresh rat hypothalamus clearly demonstrate that leptin has a significant effect on feeding-regulating neurons in the hypothalamus. Studies to date support a role for leptin not only in modulating food intake and appetite in rats and humans, but also in relation to learning and memory processes.

Animals↗
PubMed2005

[Genetic causes of obesity].

BACKGROUND: Overweight and obesity represent an increasing health problem. Both genetic and environmental factors contribute to the development of obesity. This article summarises the genetic aspects of these conditions. MATERIAL AND METHODS: A literature search was conducted using PubMed and OMIM. Both original and review articles were included. RESULTS AND INTERPRETATION: The genetic influence on body weight is shown by twin and family studies. Environmental changes in recent decades have promoted the development of obesity in individuals at risk because of their genetic composition. Our understanding of the molecular pathways underlying common obesity is limited. During the last decade a handful of monogenic disorders leading to early, severe obesity in humans have been identified. All affect the central regulation of appetite. These conditions are rare, except for mutations in the melanocortin 4 receptor that account for about 5% of morbidly obese patients (BMI > 40 kg/m). The identification of monogenic forms of obesity has contributed valuable insight into the regulation of appetite and development of obesity, although causal treatment only exists for leptin deficiency. In addition, several well defined Mendelian syndromes are associated with overweight and obesity. The molecular genetic cause is known for some of these syndromes, but how appetite and energy balance are affected is still unclear.

Adult↗
PubMed1999

The relation between meal size and the time between meals: effects of cage complexity and food cost.

Certain popular models of the regulation of food intake predict a positive correlation between the size of a meal and the preceding and/or following intermeal interval. However, the reported strength of these prandial correlations has varied widely in the literature. To determine what factors may influence the strength of these relationships, we measured the timing of and amount consumed in meals of laboratory rats as a function of 1) whether they were housed in isolation or with partial access to peers or a running wheel, 2) whether they were disturbed daily or weekly for maintenance procedures, and 3) whether food was free or contingent on operant responding. We also compared two definitions of "meal" and "intermeal interval." Strong prandial correlations were found only occasionally. Caging, food cost, and maintenance frequency did not affect the size of the correlations, although these factors did influence the rats' meal patterns. We conclude the regulation of food intake cannot be explained by models relying on a regular relationship between meal size and intermeal interval.

Analysis of Variance↗
PubMed2006

Altered brain activity in women recovered from bulimic-type eating disorders after a glucose challenge: a pilot study.

OBJECTIVE: It is not known whether individuals with bulimic-type eating disorders have a dysregulation of brain pathways that modulate appetite. Taste plays a role in the regulation of appetite and the purpose of the current study was to determine whether bulimic women have alterations in the physiologic response to the blind administration of glucose. METHOD: To avoid the confounding effects of a current eating disorder, and to assess possibly trait-related disturbances, we studied 10 subjects recovered (> or = 1 year) from a bulimic-type eating disorder and 6 control women. Subjects were administered a solution of glucose or artificial saliva (control solution) in alternating blocks during a functional magnet resonance imaging scan. RESULTS: Individuals who recovered from a bulimic-type eating disorder had significantly lower activation in the right anterior cingulate cortex (ACC; Montreal Neurological Institute [MNI] coordinates x = 8, y = 22, z = 28; cluster size = 18 voxels, T = 5.11, Z-score = 3.78) and in the left cuneus (occipital cortex; MNI coordinates x = -12, y = -78, z = 10; cluster size = 21 voxels, T = 4.27, Z-score = 3.36), when glucose was compared with artificial saliva. CONCLUSION: The ACC plays a role in the anticipation of reward. Individuals with bulimic-type eating disorders may have a reduced reward response to nutrients, and thus may be vulnerable to overeating. However, this is a small sample and the current study will need replication in a larger sample size with investigation of additional regions of interest.

Adult↗