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PubMed2006

The physiology and potential clinical applications of ghrelin, a novel peptide hormone.

Ghrelin, a peptide hormone originally identified as the endogenous ligand of the growth hormone secretagogue receptor, is secreted primarily from the stomach and secondarily from the small intestine and colon. Ghrelin may also be expressed in the pancreatic islets, hypothalamus, pituitary, and several tissues in the periphery. The growth hormone secretagogue receptor is widely expressed, suggesting diverse physiologic roles for ghrelin. A growing body of evidence suggests that, in addition to its predictable effect on growth hormone secretion, ghrelin has an important role in the short-term regulation of appetite and the long-term regulation of energy balance and glucose homeostasis. Recent studies have implicated ghrelin in the regulation of gastrointestinal, cardiovascular, and immune function and have suggested a role for ghrelin in bone physiology. The identification of obestatin, a novel peptide hormone derived from the same gene as ghrelin, has recently added further complexity to ghrelin physiology. Obestatin appears to have actions opposite of ghrelin on energy homeostasis and gastrointestinal function. Despite the rapid progress, many questions remain unanswered, including the regulation of ghrelin and obestatin secretion, the downstream pathways that mediate their effects, and their precise physiologic endocrine and paracrine roles. This review presents data on ghrelin structure, expression, and function, with emphasis placed on human studies, highlighting areas that require future investigation and providing speculation about potential clinical applications of ghrelin agonists or antagonists.

Appetite Regulation↗
PubMed2001

Management of anorexia in the cat.

One of the most frequent motivations for seeking veterinary attention for a cat is when the owner recognises a loss of normal appetite in his pet. The medical term for a lack of appetite for food is 'anorexia', and it may be partial or complete. While anorexia is a common manifestation of disease, the mechanisms underlying decreased food intake are complex and not completely understood. The regulation of appetite involves interaction of external stimuli with signals from the gastrointestinal tract and central nervous system. Aberrations in any of the internal control systems for hunger and satiety, or changes in external factors such as diet or feeding environment, can result in partial or total anorexia. The challenge for the practitioner is not only to diagnose and treat the underlying condition, but to recognise at what point inadequate food intake has or will impinge on the patient's nutritional status to the extent that it might deleteriously affect clinical outcome. It is also important to bear in mind the significance that the patient's appetite and food intake has for the cat owner in his overall perception of his pet's condition and quality of life.

Animals↗
PubMed1990

A re-assessment of the regulation of adiposity and appetite by the brain insulin system.

We have provided strong support for the hypothesis that the pancreatic hormone, insulin, provides a signal to the brain indicating the level of adiposity. Because insulin is found in the cerebrospinal fluid (CSF) in direct proportion to plasma levels, and because changes of plasma insulin result in subsequent changes of CSF insulin, we previously hypothesized that the blood-borne insulin signal enters the central nervous system by initially entering the CSF and then diffuses into the brain. Such a route explained the time lag for influences of insulin upon food intake and body weight. Recent evidence suggests that insulin may enter the brain directly through brain capillaries, raising the possibility that what is measured in the CSF may not be indicative of insulin on its way into critical brain areas. Implications of this change of route of entry of insulin into the brain for the regulation of food intake and body weight are discussed.

Adipose Tissue↗
PubMed1999

Mechanisms of uremic suppression of appetite.

Food intake is regulated by short-term satiety factors (gastric distension, amino acids, peptide hormones), as well as factors involved in long-term appetite regulation (leptin, insulin). Integration of the various signals takes place in the central nervous system (CNS). Appetite suppression in uremia is multifactorial and may include effects of uremia per se and of various comorbidity and psychosocial factors. Uremic anorexia is associated with elevated levels in plasma and CNS of short-term satiety factors (cholecystokinine, glucagon, serotonin, middle molecules) and factors that influence long-range regulation of appetite (leptin, insulin), but it is still unsettled to what extent these factors cause or contribute to appetite loss in uremic patients. Proinflammatory cytokines most probably also have a role in appetite suppression and malnutrition in patients with chronic renal failure.

Appetite↗
PubMed1981

Cholecystokinin as satiety signal.

Already in 1910 Pavlov suggested that appetite was regulated by signals from the gut to hypothalamus. Since Gibbs et al. in 1973 demonstrated that cholecystokinin (CCK) - in contrast to other gut hormones - decreased food intake in rats, great interest has focused upon this substance. A major question now is the significance in man of large doses of CCK administered intraperitoneally in rats. We now know that CCK can act as a signal both via blood (as hormone) or via nerves ( as transmitter). We have recently shown that CCK in man and pig circulates in low concentrations (a few pmol) making blood-borne CCK an unlikely satiety signal. However, we have also shown that CCK nerves are abundant in the gut. This observation raises the possibility that afferent CCK nerves from the gut may transfer satiety signals to the hypothalamus. The recent demonstration that gastric vagotomy abolishes the satiety effect of CCK may support the idea that afferent vagal nerves containing CCK or the related peptide, gastrin, are crucial in appetite regulation.

Animals↗
PubMed2005

The effect of low carbohydrate on energy metabolism.

OBJECTIVE: To investigate whether low-carbohydrate diets are efficient for reduction of body weight and through which mechanism. DESIGN: A couple of studies using low-carbohydrate diets in the treatment of obesity are reviewed. Mechanisms for explaining the reduced appetite are described in relation to knowledge on regulation of appetite for fat and carbohydrate. RESULTS: Studies with low-carbohydrate diets demonstrate a rapid weight loss, being more pronounced after 3 and 6 months compared to low-fat diets. After 12 months there is no difference between the low-carbohydrate and the conventional low-fat diet on weight loss. Both diets lead to improvements in risk factors for coronary heart disease, the low-carbohydrate diet leading to a greater decrease in serum triglycerides and increase in HDL cholesterol compared to the low-fat diet. Blood pressure, insulin sensitivity and LDL cholesterol were improved to a similar degree by the two diets. The mechanism for the rapid weight loss with the low-carbohydrate diet is a suppressed appetite, first through the high-protein content of the diet, second through the ketogenic nature of the diet with satiety signals for fat being active and third through the absence of hunger-promoting carbohydrate components like sucrose and/or fructose. CONCLUSION: A rapid initial weight loss occurs with a low-carbohydrate diet due to a suppressed appetite. There is as yet no indication of an increased metabolic rate and an increased thermogenesis by the low-carbohydrate diet. The safety and efficacy of low-carbohydrate diets have to await further studies.

Appetite Regulation↗
PubMed2004

Genetic deletion of ghrelin does not decrease food intake but influences metabolic fuel preference.

Ghrelin is a recently identified growth hormone (GH) secretogogue whose administration not only induces GH release but also stimulates food intake, increases adiposity, and reduces fat utilization in mice. The effect on food intake appears to be independent of GH release and instead due to direct activation of orexigenic neurons in the arcuate nucleus of the hypothalamus. The effects of ghrelin administration on food intake have led to the suggestion that inhibitors of endogenous ghrelin could be useful in curbing appetite and combating obesity. To further study the role of endogenous ghrelin in appetite and body weight regulation, we generated ghrelin-deficient (ghrl(-/-)) mice, in which the ghrelin gene was precisely replaced with a lacZ reporter gene. ghrl(-/-) mice were viable and exhibited normal growth rates as well as normal spontaneous food intake patterns, normal basal levels of hypothalamic orexigenic and anorexigenic neuropeptides, and no impairment of reflexive hyperphagia after fasting. These results indicate that endogenous ghrelin is not an essential regulator of food intake and has, at most, a redundant role in the regulation of appetite. However, analyses of ghrl(-/-) mice demonstrate that endogenous ghrelin plays a prominent role in determining the type of metabolic substrate (i.e., fat vs. carbohydrate) that is used for maintenance of energy balance, particularly under conditions of high fat intake.

Animals↗
PubMed1990

The clinical efficacy of a 5-HT1A agonist, SM-3997, in the treatment of bulimia.

Psychotherapeutic and pharmacological treatment of bulimia and vomiting require long duration and frequently entail considerable obstacles in patience compliance, making such regimens difficult to pursue. The regulating mechanism of the appetite center is recognized to be complex and recently an important role of serotonin (5-HT), a neurotransmitter, has been shown in rats. In the present study a newly developed 5-HT1A agonist, SM-3997, was administered to 12 patients with bulimia and its clinical efficacy was evaluated. The patients were treated on an open basis with SM-3997, 30-40 mg/day, for 6-15 weeks. Bulimic behavior stopped completely in 4 patients, was improved in 4 others and was unchanged in the remaining 4. These results suggest that the administration of a 5-HT1A agonist, SM-3997, may be effective in the treatment of bulimia and vomiting and that further investigation is warranted.

Administration, Oral↗
PubMed1999

Effect of nitric oxide synthase inhibitors on short-term appetite and food intake in humans.

Animal studies suggest that nitric oxide (NO) may be a physiological regulator of appetite; NO synthase (NOS) inhibition suppresses food intake in rats, mice, and chickens. It is not known whether NO has any effect on appetite in humans. We have used NG-monomethyl-L-arginine (L-NMMA) and NG-nitro-L-arginine methyl ester (L-NAME), both competitive, nonselective inhibitors of NOS, in two separate studies to evaluate the role of NO in the short-term regulation of appetite in humans. In study I, 13 men (18-25 yr) underwent paired studies, in randomized, double-blind fashion, after an overnight fast. L-NMMA (4 mg. kg-1. h-1) or saline (0.9%) was infused intravenously at a rate of 40 ml/h for 1.5 h. In study II, eight men (18-26 yr) underwent three randomized, double-blind studies after an overnight fast. L-NAME (75 or 180 micrograms . kg-1. h-1) or saline (0.9%) was infused intravenously at a rate of 20 ml/h for 120 min. Hunger and fullness were measured using visual analog scales; blood pressure and heart rate were monitored, and 30 min before the end of the infusion, subjects were offered a cold buffet meal. Total caloric intake and the macronutrient composition of the meal were determined. Both L-NMMA (P = 0.052) and L-NAME (P < 0.05; both doses) decreased heart rate, L-NMMA increased diastolic blood pressure (P < 0.01), and L-NAME increased systolic blood pressure (P = 0.052). Neither drug had any effect on caloric intake or sensations of hunger or fullness. Despite having significant effects on cardiovascular function in the doses used, neither L-NMMA nor L-NAME had any effect on feeding, suggesting that NO does not affect short-term appetite or food intake in humans.

Adolescent↗
PubMed2005

Dissecting the role of cocaine- and amphetamine-regulated transcript (CART) in the control of appetite.

Cocaine- and amphetamine-regulated transcript (CART) codes for a neuropeptide system with a number of biological roles. The high conservation of CART across species suggests that it has an important role in mammalian physiology. CART is widely expressed in the central nervous system and the periphery, but is particularly concentrated in the hypothalamus. CART peptides, particularly CART (55-102), appear to have an important function in the regulation of energy homeostasis. This review aims to dissect the role of CART in appetite and energy expenditure. CART interacts with a number of central appetite circuits. Hypothalamic CART expression is regulated by a number of peripheral factors, including the adipose hormone leptin. Intracerebroventricular administration of CART (55-102) reduces appetite and stimulates energy expenditure. Hypothalamic CART may also play an orexigenic role under specific circumstances, however, as injection of CART (55-102) into specific hypothalamic nuclei increases food intake.

Amino Acid Sequence↗
PubMed2002

The role of hypocretins (orexins) in sleep regulation and narcolepsy.

The hypocretins (orexins) are two novel neuropeptides (Hcrt-1 and Hcrt-2), derived from the same precursor gene, that are synthesized by neurons located exclusively in the lateral, posterior, and perifornical hypothalamus. Hypocretin-containing neurons have widespread projections throughout the CNS with particularly dense excitatory projections to monoaminergic centers such as the noradrenergic locus coeruleus, histaminergic tuberomammillary nucleus, serotoninergic raphe nucleus, and dopaminergic ventral tegmental area. The hypocretins were originally believed to be primarily important in the regulation of appetite; however, a major function emerging from research on these neuropeptides is the regulation of sleep and wakefulness. Deficiency in hypocretin neurotransmission results in the sleep disorder narcolepsy in mice, dogs, and humans. The hypocretins are also uniquely positioned to link sleep, appetite, and neuroendocrine control. The aim of this review is to describe and discuss the current knowledge regarding the hypocretin neurotransmitter system in narcolepsy and normal sleep.

Animals↗
PubMed1999

Feeding and body-weight regulation by hypothalamic neuropeptides--mediation of the actions of leptin.

Neuropeptides are essential for the regulation of appetite and body weight within the hypothalamus. The understanding of the neuropeptide regulation of energy homeostasis has been greatly advanced by the recent discovery of leptin, the protein product of the obese gene (ob). Significant new insights into the relationship between peripheral adiposity signals and their impact on the hypothalamic neuropeptide signaling circuitry have provided some crucial missing links in the negative-feedback regulation of appetite and body weight. The neuropeptide Y orexigenic network is a final common pathway for this signaling cascade and, along with feeding-inhibitory neuropeptides such as melanocortin, corticotropin-releasing factor and glucagon-like peptide 1, it is a major target through which leptin exerts a regulatory tonic restraint on body adiposity.

Animals↗
PubMed2003

Hypothalamic neuronal networks and feeding-related peptides involved in the regulation of feeding.

The hypothalamus is a region of the brain that plays a critical role in feeding regulation. It has been revealed by various physiological experiments that the feeding-regulating center is confined to the ventromedial hypothalamus, lateral hypothalamus (LH) and arcuate nucleus (ARC). Many kinds of neurons in these areas of the hypothalamus express factors such as melanin-concentrating hormone (MCH), neuropeptide Y (NPY), proopiomelanocortin (POMC), orexin (OX) and ghrelin, which have been implicated in feeding regulation. In tissues of the periphery, two critical factors involved in feeding regulation, leptin and ghrelin, have been identified. Both hormone peptides are secreted mainly from adipose and stomach tissue, respectively, and are considered to function via their receptors mainly through several hypothalamic nuclei that play important roles in the regulation of appetite. The present review looks mainly at the functional significance of feeding-regulation factors, such as those described above, and the humoral and neuronal interactions among these compounds in the hypothalamus by drawing on published reports of morphological and physiological analyses. Immunohistochemical and in situ hybridization experiments indicate that both leptin and ghrelin receptors are distributed in the hypothalamus and that there are reciprocal interactions between MCH and OX neurons in the LH. Morphological and physiological studies on single living cells isolated from fresh rat hypothalamus or with receptor agonist and antagonist combined with immunohistochemisry clearly demonstrate that both leptin and OX reciprocally regulate NPY- and POMC-containing neurons in the ARC and that ghrelin may regulate feeding status independently through direct OX and NPY pathways. In this way, cross-talking systems in the hypothalamus play a role in determining feeding states.

Animals↗
PubMed2001

Role of various types of serotonin receptors in regulation of drinking behavior and salt appetite in vasopressin-deficient brattleboro rats.

Serotonin 5-HT(1A)receptor agonist 8-OH DPAT suppressed drinking behavior in Brattleboro and Wistar rats. 5-HT(1B)agonist CGS-12066A and 5-HT(2A)antagonist ketanserin did not affect drinking behavior in Brattleboro rats; 5-HT(3)antagonist ondansetron suppressed water consumption and 5-HT(1A)agonist stimulated salt appetite in Brattleboro, but not in Wistar rats. Presumably, vasopressin regulates thirst and salt appetite by modulating sensitivity/density of various types of 5-HT receptors.

8-Hydroxy-2-(di-n-propylamino)tetralin↗