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PubMed2006

Gut peptides and the regulation of appetite.

There is a growing worldwide epidemic of obesity. Obese people have a higher incidence of type 2 diabetes and cardiovascular disease, and hence present increasing social, financial and health burdens. Weight loss is always difficult to achieve through lifestyle changes alone, and currently licensed anti-obesity drug treatments, such as orlistat and sibutramine, if tolerated, only achieve modest weight loss. Therefore, there is a need to identify more potent pharmacological targets. In the last 10 years, discoveries of new hormones such as leptin and ghrelin, together with greater understanding of previously described hormones such as cholecystokinin (CCK), pancreatic polypeptide (PP), peptide YY (PYY) and glucagon-like peptide 1 (GLP-1), have led to a rapid increase in our knowledge of the regulation of energy balance. Among the most important factors, controlling appetite and satiety are peptide hormones released from the gut. In this paper, we provide a full up-to-date overview of the current state of knowledge of this field, together with the potential of these peptides as drugs, or as other therapeutic targets, in the treatment of obesity. Finally, we propose an integrated model to describe the complex interplay of these hormones in the broader physiology of energy balance.

Appetite Regulation↗
PubMed2001

[Appetite and regulation of food intake in uremia].

Anorexia, nausea and vomiting are common symptoms in patients with severe renal failure. Abnormalities in body fluids volume, serum electrolytes concentrations and acid-base balance and accumulations of uremic toxic substances might be primarily contributing to the suppression of appetite. However, the detailed mechanisms that cause appetite suppression in uremia are poorly understood. Impaired gastric emptying, constituents of peritoneal dialysate, plasma high leptin, high cholecystokinin and low neuropeptide Y are also considered to be contributing to appetite suppression in uremia.

Animals↗
PubMed2006

Regulation of appetite and insulin signaling in inflammatory states.

Inflammatory states are characterized by decreased food intake, hyperglycemia, and insulin resistance. The contribution of cytokines in this phenotype is important and is exerted through activation of SOCS proteins and inhibition of insulin signaling, as well as through direct stimulation of the ob gene. Obesity, a condition that has reached epidemic rates, is characterized by hyperglycemia, hyperlipidemia, insulin resistance and increased food intake, and body weight. In the following article we summarize the current views of the mechanisms underlying insulin resistance in obesity and the other inflammatory states. We also discuss the regulation of appetite in inflammatory states, and we provide evidence on the cytokine-independent induction of anorexia following immune activation in mice. Understanding of the exact mechanisms regulating these processes may provide important insights for the control of this group of diseases that compromise to a great extent the quality of life and are associated with high mortality.

Animals↗
PubMed2005

Programming of appetite and type 2 diabetes.

In the past decade, epidemiological findings and data from experimental studies in animals have shown that the structure and function of the organism can be programmed during critical periods of development which can lead to detrimental long-term consequences for the health of an individual. Low birth weight has been linked to many adult diseases in humans including type 2 diabetes. The full detrimental effects of early growth restriction are often accompanied by the presence of obesity, which itself might be a manifestation of programmed appetite regulation in fetal and neonatal life. The understanding of interactions between leptin and insulin and their roles in glucose and body weight regulation provides clues towards mechanisms underlying altered appetite regulation and increased risk of type 2 diabetes in low birth weight individuals. Molecular mechanisms involved might include epigenetic alteration of the fetal genome in response to maternal nutrition.

Animals↗
PubMed2002

Leptin regulates appetite-related neuropeptides in the hypothalamus of developing rats without affecting food intake.

Leptin regulates food intake in adult mammals by stimulating hypothalamic anorexigenic pathways and inhibiting orexigenic ones. In developing rodents, fat stores are low, yet circulating leptin levels are high and do not appear to regulate food intake. We determined whether two appetite-related neuropeptides [neuropeptide Y (NPY) and proopiomelanocortin (POMC)] and food intake behavior are sensitive to leptin [3 mg/kg body weight (BW), ip] in neonates. We measured the effects of 1) acute leptin administration (3 mg/kg BW, ip, 3 h before testing) on food intake on postnatal day (PND) 5, 8, and 10; and 2) chronic leptin treatment (3 mg/kg BW, ip, daily PND3-PND10) on BW gain and fat pads weight on PND10. In addition to hypothalamic POMC and NPY expression, we determined the expression of suppressor of cytokine signaling-3, all subtypes of leptin receptors, and corticotropin-releasing factor receptor-2 mRNA in PND10 pups receiving either an acute (PND10) or a chronic (PND 3-10) leptin (3 mg/kg BW, ip) or vehicle treatment. Brains were removed 30 or 120 min after the last injection. Acute leptin administration did not affect food intake at any age tested. Chronic leptin treatment did not change BW but decreased fat pad weight significantly. In the arcuate nucleus (ARC), acute leptin increased SOCS-3 and POMC mRNA levels, but decreased NPY mRNA levels in the rostral part of ARC. Chronic leptin down-regulated all subtypes of leptin receptors mRNA and decreased NPY mRNA levels in the caudal ARC but had no further effect on POMC expression. Chronic leptin increased corticotropin-releasing factor receptor-2 mRNA levels in the ventromedial hypothalamus. We conclude that despite adult-like effects of leptin on POMC, NPY, and CRFR-2 expression in neonates, leptin does not regulate food intake during early development.

Adipose Tissue↗
PubMed2000

Long-term alterations in adiposity affect the expression of melanin-concentrating hormone and enkephalin but not proopiomelanocortin in the hypothalamus of ovariectomized ewes.

We have developed a ruminant model to study long-term alterations in adiposity on the expression of appetite-regulating peptides in the hypothalamus. In this model endocrine and metabolic status are fully defined as well as body composition. The current study sought to define the effects of altered adiposity on the expression of genes for neuropeptide Y (NPY), POMC, enkephalin (ENK), and melanin-concentrating hormone (MCH). Ovariectomized ewes with high (60 +/- 1 kg) (FAT) or low (37 +/- 3 kg) body weights (THIN) were blood sampled every 10 min for 8 h to determine metabolic and endocrine status. The animals were then killed and the brains perfused for in situ hybridization. Body composition analysis was performed on the carcass using dual energy x-ray absorptiometry; this indicated that the FAT animals were 36 +/- 1% fat, whereas the THIN animals were 15 +/- 2% fat. The LH interpulse interval was lower and mean GH concentrations were higher in the THIN animals; cortisol and TSH levels were not different between the two groups but free T4 and free T3 levels were lower; the FT3:FT4 ratio was higher in THIN ewes. Levels of insulin, lactate, and nonesterified fatty acids were lower in the THIN group, and plasma glucose and urea concentrations were similar in THIN and FAT animals. Levels of gene expression of NPY and MCH were higher in THIN ewes. POMC expression was similar in the two groups. In the THIN animals, ENK expression was lower in the paraventricular and ventromedial nuclei but higher in the periventricular region. In conclusion, we have shown that alterations in adiposity influence the expression of appetite-regulating peptides in the absence of ovarian steroids. The appetite stimulators, NPY and MCH, appear to be involved in the metabolic response to altered adiposity, whereas ENK in the periventricular region may be linked to the secretion of GH and possibly LH. Our results suggest that altered expression of appetite- regulating peptides can be linked with the endocrine and metabolic adaptations that occur with long-term changes in adiposity.

Adipose Tissue↗
PubMed2006

Role of ghrelin in the regulation of appetite in children.

Ghrelin, the new recently discovered hormone, is a 28 amino-acid acylated peptide predominantly produced by the stomach characterized by a strong GH-releasing activity mediated by the hypothalamic-pituitary GH secretagogues (GHSs) receptors. Ghrelin and GHSs, acting on central and peripheral receptors, exert other actions such as stimulation of ACTH and prolactin secretion, influence on insulin secretion and glucose metabolism, orexigenic effect and modulatory activity on the neuroendocrine and metabolic response to starvation, influence on exocrine gastro-entero-pancreatic functions, cardiovascular activities and modulation of cell proliferation and apoptosis. The wide spectrum of ghrelin action requires further studies to provide critical information on the role of ghrelin and the potential perspectives of its analogues in the clinical practice. This point is of particular interest in the field of pediatric endocrinology and metabolism because the ghrelin story started focusing on GH deficiency and is now extending to aspects that once again are of major relevance such as obesity and eating disorders, regulation of the hypothalamus-pituitary-adrenal and gonadal axis. More studies are needed to evaluate the real impact of ghrelin in different non endocrine processes and the possible use of ghrelin analogues in different diseases condition.

Appetite↗
PubMed2004

Fat in the intestine as a regulator of appetite--role of CCK.

The present review summarizes the appetite-suppressing effects of intestinal fat in the regulation of food intake in humans, with a special focus on the role of cholecystokinin (CCK). Current evidence supports a role for intestinal fat (especially long-chain free fatty acids) acting via the peptide CCK as a physiological satiety pathway. The regulation of satiety is, however, complex and it is not surprising that multiple control systems exist. It is interesting to note that nutrients, such as hydrolysis products of fat in the small intestine, stimulate the release of satiety peptides, such as CCK or PYY, that serve as satiety signals. CCK, released from the gastrointestinal tract by the local action of digested food, exerts various functions: stimulation of gallbladder contraction and exocrine pancreatic secretion, inhibition of gastric emptying, and inhibition of appetite. CCK functions therefore (1) as a positive feedback signal to stimulate digestive processes and (2) as negative feedback signal to limit the amount of food consumed during an individual meal.

Appetite↗
PubMed1984

Neuropeptides and appetite: contribution of neuropharmacological modeling.

It is now clear that a variety of neuropeptides interact with the more classically defined neurotransmitters to stimulate or inhibit feeding. An extensive peripheral peptide satiety system has been identified. Peptides involved in this system include cholecystokinin, bombesin, gastrin-releasing peptide, glucagon, somatostatin, and possibly thyrotropin-releasing hormone and calcitonin. Some of these peptides appear to inhibit feeding by activating ascending fibers in the vagus, whereas others exert their actions independent of the vagus. In addition, neuropeptides appear to play a role in producing the neuromodulatory effects of taste on appetite, and hormones from the endocrine system modulate neuropeptide effects on feeding. The central appetite regulatory system appears to be arranged in a cascade, with an interaction between dynorphin and dopamine producing a part of the feeding drive. This drive is held in check by a variety of neuropeptides including calcitonin, corticotropin-releasing factor, and bombesin. In turn, these peptides are modulated by a norepinephrine-alpha-aminobutyric acid (GABA) system. Neurotensin, serotonin, cyclohistidyl proline diketopiperazine, and the peripheral satiety system appear to modulate the norepinephrine-GABA disinhibitory system. By the judicious use of neuropharmacological modeling we have developed a model of the neurotransmitter interactions involved in appetite regulation that can act as a springboard for the design of future experiments to unravel the mysteries of appetite regulation.

Animals↗
PubMedDate not supplied

Naltrexone in organic bulimia: a preliminary report.

Multiple lines of experimental evidence point to the involvement of endogenous opiates in appetite regulation. Post brain injury patients often exhibit driven eating behaviour. Since this problem fails to respond to behaviour modification, appetite suppressants, lithium, or any other usual approach, the use of the oral narcotic antagonist, Naltrexone, was given to three such patients. Naltrexone binds multiple opiate receptor sites in the hypothalamus, including the kappa receptors which have been implicated in appetite regulation, the use of this narcotic antagonist in hypothalamic hyperphagia appears to be a rational approach to this intractable problem. In this open trial, lasting from 4 1/2 to 9 months, the minimal effective dose appeared to be in the range of 100 mg per day. No side-effects (for example elevations in liver enzymes) were noted. All of the patients had an improved sense of well-being and their behaviours were less difficult to manage when on the Naltrexone. The significance of this preliminary trial is that narcotic antagonists may have a role in the treatment of brain-injured patients with bulimia. Also, Naltrexone may be useful in treating other maladaptive behavioural consequences of head trauma such as stealing, manipulation, demandingness, and depression. Likewise, the effects on the deranged endocrine system, such as the hypogonadism, are significant and deserve further exploration.

Adolescent↗
PubMed2004

Clarifying concepts about macronutrients' effects on satiation and satiety.

It seems that many people, including dietetics professionals and other nutrition experts, are unclear about some of the fundamental yet complex concepts behind the influence of dietary macronutrients (ie, protein, carbohydrate, and fat) on appetite regulation. Recent research has begun to unravel some of the more complicated physiological processes of appetite control and regulation generated by hormones such as leptin, ghrelin, and the gut hormone peptide YY3-35. Although the processes by which the macronutrients in our foods influence appetite regulation have been a topic of study for decades, they remain confusing and are often misunderstood. The objective of this article is to define the terminology commonly used to discuss the macronutrients' roles in appetite regulation and to discuss the interrelated concepts and roles of taste, palatability, and energy density.

Appetite↗
PubMed2003

Effect of sensory perception of foods on appetite and food intake: a review of studies on humans.

OBJECTIVE: How much do the sensory properties of food influence the way people select their food and how much they eat? The objective of this paper is to review results from studies investigating the link between the sensory perception of food and human appetite regulation. CONTENT OF THE REVIEW: The influence of palatability on appetite and food intake in humans has been investigated in several studies. All reviewed studies have shown increased intake as palatability increased, whereas assessments of the effect of palatability using measures of subjective appetite sensations have shown diverging results, for example, subjects either feel more hungry and less full after a palatable meal compared to a less palatable meal, or they feel the opposite, or there is no difference. Whether palatability has an effect on appetite in the period following consumption of a test meal is unclear. Several studies have investigated which sensory properties of food are involved in sensory-specific satiety. Taste, smell, texture and appearance-specific satieties have been identified, whereas studies on the role of macronutrients and the energy content of the food in sensory-specific satiety have given equivocal results. Different studies have shown that macronutrients and energy content play a role in sensory-specific satiety or that macronutrients and energy content are not a factor in sensory-specific satiety. Sensory-specific satiety may have an important influence on the amount of food eaten. Studies have shown that increasing the food variety can increase food and energy intake and in the short to medium term alter energy balance. Further knowledge about the importance of flavour in appetite regulation is needed, for example, which flavour combinations improve satiety most, the possible connection between flavour intensity and satiety, the effect of persistence of chemesthetic sensation on palatability and satiety, and to what extent genetic variation in taste sensitivity and perception influences dietary habits and weight control.

Appetite↗
PubMedDate not supplied

A review of endocrine changes in anorexia nervosa.

Anorexia nervosa is a syndrome of unknown etiology. It is associated with multiple endocrine abnormalities. Hypothalamic monoamines (especially serotonin), neuropeptides (especially neuropeptide Y and cholecystokinin) and leptin are involved in the regulation of human appetite, and in several ways they are changed in anorexia nervosa. However, it remains to be clarified whether the altered appetite regulation is secondary or etiologic. Increased secretion of corticotropin-releasing hormone and proopiomelanocortin seems to be secondary to starvation, however, there is evidence that it may maintain and intensify anorexia, excessive physical activity and amenorrhea. Hypothalamic amenorrhea, which is a diagnostic criterion in anorexia nervosa, is not solely related to the low body weight and exercise. Growth hormone resistance with low production of insulin-like growth factor I and high growth hormone secretion reflect the nutritional deprivation. The nutritional therapy of patients with anorexia nervosa might be improved by administering an anabolic agent such as growth hormone or insulin-like growth factor I. So far none of the endocrine abnormalities have proved to be primary, however, there is increasing evidence that some of these might participate in a vicious circle.

Anorexia Nervosa↗
PubMed2000

Dual regulation of leptin secretion: intracellular energy and calcium dependence of regulated pathway.

Rodent leptin is secreted by adipocytes and acutely regulates appetite and chronically regulates body weight. Mechanisms for leptin secretion in cultured adipocytes were investigated. Acutely, energy-producing substrates stimulated leptin secretion about twofold. Biologically inert carbohydrates failed to stimulate leptin secretion, and depletion of intracellular energy inhibited leptin release. There appears to be a correlation between intracellular ATP concentration and the rate of leptin secretion. Insulin increased leptin secretion by an additional 25%. Acute leptin secretion is calcium dependent. When incubated in the absence of calcium or in the presence of intracellular calcium chelators, glucose plus insulin failed to stimulate leptin secretion. In contrast, basal leptin secretion is secreted spontaneously and is calcium independent. Adipocytes from fatter animals secrete more leptin, even in the absence of calcium, compared with cells from thinner animals. Acute stimulus-secretion coupling mechanisms were then investigated. The potassium channel activator diazoxide and the nonspecific calcium channel blockers nickel and cadmium inhibited acute leptin secretion. These studies demonstrate that intracellular energy production is important for acute leptin secretion and that potassium and calcium flux may play roles in coupling intracellular energy production to leptin secretion.

Adenosine Triphosphate↗
PubMed2001

[Endocrine and reproductive disturbances in anorexia nervosa and bulimia nervosa].

Numerous endocrine abnormalities are associated with anorexia nervosa and bulimia nervosa. The principal complication is amenorrhoea. Hypothyroidism and hypercortisolism have been described as a protective mechanism to conserve energy. Growth hormone concentrations are often increased as a result of starvation. Insulin and blood sugar concentrations are decreased, but prolactin concentrations are remain normal. Considerable evidence exists of hypothalamic dysfunction in patients with eating disorders. This dysfunction is reflected in disturbances of endocrine function. Endocrine disturbances may be not solely related to the low body weight. Hypothalamic monoamines, neuropeptides and leptin are involved in the regulation of human appetite, and in several ways they are changed in eating disorders. However, it remains to be clarified whether the altered appetite regulation is secondary or etiologic.

Amenorrhea↗
PubMed1981

Regulation of calcium appetite in broiler chickens.

The regulation of the appetite for calcium was studied in broiler chickens which had been trained to meet their calcium requirement by consuming a calcium supplement (10% Ca) provided separately from a calcium-deficient feed (0.12% Ca). Calcium supplement intake was reduced within 150 minutes after intravenous injection of 60 U/kg parathyroid hormone or continuous infusion of 0.077 mg/minute calcium into one common carotid artery. Supplement consumption was also depressed during the first 8 days of continuous infusion of 1 U/kg/hour parathyroid hormone; after 8 days the birds became refractory. Continuous infusion of 0.2 Medical Research Council (MRC) units/kg salmon calcitonin for 10 days or daily intramuscular injections of 1 mg/kg testosterone propionate and 2 mg/kg estradiol dipropionate for 12 days, either alone or in combination, had no effect on calcium appetite. It is concluded that the calcium appetite may be inhibited by increased concentrations of ionic calcium in blood and that the change in behavior is sufficiently rapid to play a role in the calcium homeostasis of birds.

Animals↗
PubMed1979

[Substrate and parasubstrate regulation of physiological processes at various levels of the organization of living systems as illustrated by examples of the regulation of appetite, of the specific dynamic action of food and of the inhibition of processes of absorption].

It was demonstrated that in the organism of higher animals the adaptation regulation of food uptake and nutrient absorption and transport comprises, in addition to the classic mechanisms of substrate regulation, specialized non-substrate and parasubstrate mechanisms which control the uptake of food and other substrates at all three levels (organosystemic, organic and cellular). As to the organosystemic level, it was observed in duodenectomized rats that appetite inhibition is produced not only by a stimulation of the receptors and by an increase in the concentration of the food substrates and of the metabolites in the blood, but also by one of the intestinal appetite-inhibiting hormones, arenterin. As to the organic level, it was evidenced that the enzymatic and transport functions of the small intestine and the numerical composition of the enterocyte population in the different segments are determined by the substrate load on the respective areas of the small intestine as well as by the blood and chyme-mediated intersegmental reactions in the small intestine. As to the tissular and cellular levels, the possibility of a regulation of the enzymatic and transport systems of the microvilli by means of substrates contained in the mucous membrane of the small intestine and endogenous substances (permein and antipermein) was evinced.

Adaptation, Physiological↗