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Results for “Appetite Regulation”

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At least 181 records · Page 10Linked to original sources
PubMed1993

Serotonergic neurotransmission in the regulation of appetite: a receptor approach.

Neurochemical research on brain 5-hydroxytryptamine (5-HT; serotonin) and feeding shows that rat brain serotonin metabolism is increased following ingestion of a carbohydrate rich diet to generate a neurochemical signal for the termination of meal. Increased metabolism may not necessarily enhance postsynaptic function; neuropharmacological studies therefore gained attention. Drugs which mimick 5-HT function at the post synaptic sites have been shown to decrease feeding in experimental animals. Moreover some 5-HTergic drugs are potent anorectic agents. Multiple receptors for 5-HT exist in the central nervous system. Drugs with selectivity towards 5-HT-1B/ 5-HT-1C sites produced hypophagia, while 5-HT-1A selective drugs increased food intake. Studies designed to investigate sensitivity of these receptors following starvation or satiety may prove useful to develop drugs for therapeutic purposes.

Journal Article↗
PubMedDate not supplied

Effect of total amygdalectomy upon regulation of salt intake in rats.

Sodium appetite was studied in rats with lesions destroying the entire amygdaloid nuclear complex. The rats were totally aphagic and adipsic for several days following lesioning but regained nearly normal levels of food and water intake about 2 to 3 weeks postoperatively. Intake of 3% saline was observed after induction of sodium appetite by treatment with a mineralocorticoid and a natriuretic agent. Rats with amygdaloid lesions generally manifested severe but not total loss of sodium appetite. Regulation of water intake was also moderately to severely impaired. Suggestive evidence was obtained that recovery of sodium appetite in amygdalectomized rats can be enhanced by postoperative experience with sodium appetite and saline reinforcement.

Amygdala↗
PubMed2006

Gut hormones and the regulation of energy homeostasis.

Food intake, energy expenditure and body adiposity are homeostatically regulated. Central and peripheral signals communicate information about the current state of energy balance to key brain regions, including the hypothalamus and brainstem. Hunger and satiety represent coordinated responses to these signals, which include neural and hormonal messages from the gut. In recent years our understanding of how neural and hormonal brain-gut signalling regulates energy homeostasis has advanced considerably. Gut hormones have various physiological functions that include specifically targeting the brain to regulate appetite. New research suggests that gut hormones can be used to specifically regulate energy homeostasis in humans, and offer a target for anti-obesity drugs.

Animals↗
PubMed2005

Neuropeptide Y2 receptors as drug targets for the central regulation of body weight.

During the past decade, a detailed understanding has emerged of the aminergic and peptidergic neural pathways present within the brain that regulate appetite. Central among the peptide regulators is neuropeptide Y (NPY), a potent orexigenic agent that acts through five different receptor subtypes. Efforts to find novel appetite suppressant drugs that inhibit the interaction of NPY with either the NPY Y1 or NPY Y5 receptor subtypes have proven disappointing. Attempts have now been made to identify an NPY Y2 stimulator that will suppress appetite. Within the hypothalamus, NPY Y2 receptors have a predominantly presynaptic location where they act to inhibit NPY release. Stimulation of NPY Y2 receptors with synthetic peptide ligands or the gut derived peptide PY3-36 has been shown to reduce food intake. The NPY Y2 receptor has a wide distribution both within the brain and in the periphery. Stimulation of the NPY Y2 subtype at these sites produces a wide array of effects unrelated to changes in food intake. In consequence, the administration of both endogenous and exogenous agonists of the NPY Y2 receptor is likely to cause side effects, particularly regarding pituitary hormone release, as well as on the cardiovascular and gastrointestinal systems. The possibility that long-term NPY Y2 agonism could cause bone thinning and retinal angiogenesis are of particular concern and will need to be investigated as drug discovery moves forward.

Animals↗
PubMed2005

[Ghrelin and obesity].

Ghrelin is a peptide hormone secreted by the stomach. It was initially described as a stimulant of growth hormone secretion. Soon, however, it was discovered to play an important role in feeding behaviour in animals and in appetite regulation in man: ghrelin stimulates appetite, and as such is an orexigenic peptide implicated in energy balance mechanisms and weight gain. Abnormal ghrelin activity leads to over- or underweight. Additionally, the efficacy of different treatment strategies against obesity seems to be related to modifications in plasma ghrelin levels. This review summarizes the current knowledge about ghrelin and its implications in obesity medicine.

Ghrelin↗
PubMed2005

The brain-adipose axis: a review of involvement of molecules.

Many molecules are involved in the regulation of feeding behavior, and they and their receptors are located in the brain hypothalamus and adipocytes. On the basis of evidence suggesting an association between the brain and adipose tissue, we propose the concept of the brain-adipose axis. This model consists of (l) the expression of endogenous molecules and/or their receptors in the hypothalamus and peripheral adipose tissue, (2) the function of these molecules as appetite regulators in the brain, (3) their existence in the general circulation as secreted proteins and (4) the physiological affects of these molecules on fat cell size and number. These molecules can be divided into two anorexigenic and orexigenic classes. In adipose tissue, all orexigenic molecules possess adipogenic activity, and almost all anorexigenic molecules suppress fat cell proliferation. Although the manner, in which they present in the circulating blood connect the brain and peripheral adipocytes, remains to be well-organized, these observations suggest the positive feedback axis affecting molecules in the hypothalamus and adipose tissue. Analysis of the disturbance and dysregulation of this axis might promote the development of new anti-obesity drugs useful in treating the metabolic syndrome.

Adipose Tissue↗
PubMed2000

Anorexigenic cocaine- and amphetamine-regulated transcript peptide intensifies fear reactions in rats.

An increasing number of appetite-regulating peptides are being discovered. The list of regulators inhibiting food intake is considerably longer than that of appetite stimulators. In many cases, the peptides inhibiting food intake facilitate fear reactions, whereas the majority of the agents reducing anxiety responses stimulate appetite. Cocaine- and amphetamine-regulated transcript (CART) cDNA was isolated from hypothalamic libraries and CART was reported to inhibit food intake and to mediate the anorectic effects of leptin. Here, we show that the active core fragment of CART (CART(89-103), 0.04-5.0 nmol) injected into lateral cerebral ventricle not only inhibits food intake, but also causes a dose-dependent increase in anxiety-like reactions in elevated plus-maze test. Intracerebroventricular administration of CART(82-103) (0.04-5.0 nmol) did not inhibit water intake and did not affect spontaneous locomotor activity in the open field test ruling out unspecific effects of the peptide. Our results suggest that CART could be an endogenous factor in the brain mediating the effects of stress on appetite.

Animals↗
PubMedDate not supplied

Neuropharmacology of paradoxic weight gain with selective serotonin reuptake inhibitors.

It has been suggested that weight gain associated with tricyclic antidepressants (TCA) reflect actions on dopamine (DA) and histamine receptors. However, a definitive cause is purely assumptive given the nonselective pharmacology of these agents. The selective serotonin reuptake inhibitors (SSRIs), as well as agents like dexfenfluramine (DFF), have emphasized the pivotal role of serotonin (5HT) in reducing carbohydrate (CHO) intake, and have provided a more selective tool with which to study appetite regulation. It would be expected that all SSRIs should exert a similar anorectic action. However, recent reports provide evidence to the contrary. Despite their claimed selectivity, SSRIs still interact, either directly or indirectly, with various critical neurotransmitter systems. In addition, although the anorectic action of fluoxetine (FLX) is well recognized, long-term follow-up studies in depressed patients and in obese nondepressed patients reveal that its weight-reducing effects are transient, even leading to a gain in body weight. Similarly, paroxetine (PRX) and citalopram (CTP) have also been associated with weight gain. These latter observations are unexpected because PRX and CTP are highly potent and selective SSRIs. A neuropharmacologic rationale for the apparent paradoxic effects of SSRIs on appetite not a review of neuronal regulation of appetite is presented in this article. As with the regulation of feeding, paradoxic weight gain observed with SSRIs appears to rest on the interaction of 5HT with multiple mechanisms, with the extent of weight gain observed being dependent on subtle, yet important pharmacologic differences within the group. Finally, the neurobiology of depressive illness itself, and of recovery from it, is a major contributing factor to individual response to these drugs.

Appetite↗
PubMed1999

Comparison of the effects of a high-fat and high-carbohydrate soup delivered orally and intragastrically on gastric emptying, appetite, and eating behaviour.

To investigate the effects of fat and carbohydrate on appetite, food intake and gastric emptying with and without the influence of orosensory factors, a group of nine healthy, fasted male subjects took part in two separate paired experiments involving high-fat and high-carbohydrate radiolabelled soup preloads. In the first experiment subjects received direct intragastric isocaloric infusions of either a high-fat tomato soup or a high-carbohydrate tomato soup (400 kcal in 425 mL) over 15 min, on two occasions. In the second paired experiment subjects ingested the same high-fat and high-carbohydrate soup over 15 min. In both experiments ratings of hunger and fullness were recorded over a period of 135 min and gastric emptying was measured by scintigraphy. Food intake was evaluated from a test meal (yoghurt drink) given 2 h after the end of the soup infusion/ingestion. When soup was administered intragastrically (Experiment 1) both the high-fat and high-carbohydrate soup preloads suppressed appetite ratings from baseline, but there were no differences in ratings of hunger and fullness, food intake from the test meal, or rate of gastric emptying between the two soup preloads. When the same soups were ingested (Experiment 2), the high-fat soup suppressed hunger, induced fullness, and slowed gastric emptying more than the high-carbohydrate soup and also tended to be more effective at reducing energy intake from the test meal. The results of these studies demonstrate that orosensory stimulation plays an important role in appetite regulation, and also indicate that subtle differences in orosensory stimulation produced by particular nutrients may profoundly influence appetite and gastrointestinal responses.

Adult↗
PubMed2001

[Physiology of appetite and feeding behavior: introduction].

Food intake is regulated by the central nervous system depending on macronutrients and environmental changes. The hypothalamus is the target of hunger and satiety signals arising from the peripheral organs and the brain. Noradrenaline-neuropeptide Y and opioid-galanine are involved in carbohydrate and fat intake, respectively, while serotonin-CCK-insulin and dopamine-cyclic dipeptides systems inhibit them. Histamine and proinflammatory cytokines are involved in stress- and sickness-induced anorexia. Leptin accelerated intrahypothalamic anorexic mechanisms executed by POMC/CART and CRH but suppresses orexigenic mechanisms promoted by NPY and orexin. Although these mechanisms elegantly regulate appetite and feeding behavior, disruption of weight control has been accelerated and the incidence of obesity and eating disorder are dramatically increasing recent years in our modern society. New approach may be necessary to solve the problems of weight control.

Appetite↗
PubMed2005

Macronutrients as sources of food energy.

This background paper considers the extent to which the development of new recommendations for dietary energy requirements needs to account for the macronutrient (fat, carbohydrate, protein and alcohol) profiles of different diets. The issues are discussed from the dual perspectives of avoiding under-nutrition and obesity. It is shown that, in practice, human metabolic processes can adapt to a wide range of fuel supply by altering fuel selection. It is concluded that, at the metabolic level, only diets with the most extreme macronutrient composition would have any consequences by exceeding the natural ability to modify fuel selection. However, diets of different macronutrient composition and energy density can have profound implications for innate appetite regulation and hence overall energy consumption.

Adaptation, Physiological↗
PubMed2006

Glucose sensing by hypothalamic neurones and pancreatic islet cells: AMPle evidence for common mechanisms?

A fuller understanding of the central mechanisms involved in controlling food intake and metabolism is likely to be crucial for developing treatments to combat the growing problem of obesity in Westernised societies. Within the hypothalamus, specialized neurones respond to both appetite-regulating hormones and circulating metabolites to regulate feeding behaviour accordingly. Thus, the activity of hypothalamic glucose-excited and glucose-inhibited neurones is increased or decreased, respectively, by an increase in local glucose concentration. These 'glucose-sensing' neurones may therefore play a key role in the central regulation of food intake and potentially in the regulation of blood glucose concentrations. Whilst the intracellular signalling mechanisms through which glucose-sensing neurones detect changes in the concentration of the sugar have been investigated quite extensively, many elements remain poorly understood. Furthermore, the similarities, or otherwise, with other nutrient-sensing cells, including pancreatic islet cells, are not completely resolved. In this review, we discuss recent advances in this field and explore the potential involvement of AMP-activated protein kinase and other nutrient-regulated protein kinases.

AMP-Activated Protein Kinases↗