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At least 793 records · Page 44Linked to original sources
PubMed2002

Pro-nociceptin/orphanin FQ and NOP receptor mRNA levels in the forebrain of food deprived rats.

Forebrain injections of nociceptin/orphanin FQ (N/OFQ), the endogenous ligand of the NOP opioid receptor, previously referred to as ORL1 or OP4 receptor, stimulate feeding in freely feeding rats, while the NOP receptor antagonist [Nphe(1)]N/OFQ(1-13)NH(2) inhibits food deprivation-induced feeding. To further evaluate whether the N/OFQ-NOP receptor system plays a physiological role in feeding control, the present study evaluated forebrain mRNA levels for the N/OFQ precursor (pro-N/OFQ), as well as for the NOP receptor in food deprived rats. The results obtained show that food deprived rats have lower mRNA levels for the NOP receptor in several forebrain regions; a significant reduction was found in the paraventricular and lateral hypothalamic nuclei and in the central nucleus of the amygdala. Food deprived rats also exhibited lower pro-N/OFQ mRNA levels in the central amygdala. These results suggest that the N/OFQ-NOP receptor system may have a physiological role in feeding control. The observation that food deprivation reduces gene expression of the N/OFQ-NOP receptor system is apparently not consistent with a direct hyperphagic action for N/OFQ. Taking into account that N/OFQ exerts inhibitory actions at cellular level, the present results may be in keeping with the hypothesis that N/OFQ stimulates feeding by inhibiting neurons inhibitory for food intake; under conditions of food deprivation, these neurons may be silent and the N/OFQ-NOP receptor system, which controls them, may also be regulated at a lower level. Consistently, in the present study N/OFQ stimulated food intake in freely feeding rats, but did not further increase feeding in food deprived rats.

Amygdala↗
PubMed1998

Postnatal leptin surge and regulation of circadian rhythm of leptin by feeding. Implications for energy homeostasis and neuroendocrine function.

Leptin is thought to regulate energy balance through effects on food intake and thermogenesis. In addition, leptin may serve as a mediator of the neuroendocrine response to starvation, and may modulate the stress response and the timing of puberty. A role for leptin in development is suggested by the presence of neuroendocrine and structural neuronal abnormalities in ob/ob mice with genetic leptin deficiency. Here, we sought to determine the ontogeny of leptin expression and its relationship to the developing neuroendocrine axis. Leptin increased 5-10-fold in female mice during the second postnatal week independent of fat mass, and declined after weaning. The rise in leptin preceded the establishment of adult levels of corticosterone, thyroxine, and estradiol. In contrast to adult mice, leptin was not acutely regulated by food deprivation during the early postnatal period. Circadian rhythms of leptin, corticosterone, and thyroxine were regulated by food intake in adult mice. When ad libitum feeding was restricted to the light cycle, peak corticosterone levels were shifted to the beginning of the light cycle and coincided with the nadir of leptin. The inverse relationship between leptin and corticosterone was maintained such that a rise in leptin after feeding was associated with a decline in corticosterone. To determine whether changes in corticosterone during food restriction are mediated by leptin, we compared the patterns of corticosterone levels among ob/ob, db/db, and lean mice. Despite their higher basal levels of corticosterone, leptin deficiency in ob/ ob mice did not prevent the nocturnal rise in corticosterone. In contrast, the nocturnal surge of corticosterone was blunted in db/db mice. Therefore, it is likely that factors in addition to leptin are involved in the regulation of the circadian rhythm of corticosterone. The temporal relationship between leptin and other hormones in neonatal and adult mice suggests that leptin is involved in the maturation and function of the neuroendocrine axis.

Animals↗
PubMed2006

The unfolding cannabinoid story on energy homeostasis: central or peripheral site of action?

Presentations in this symposium addressed effects and modes of action of endocannabinoids in various tissues in relation to metabolic disorders. Endocannabinoids are produced and exert their effect in various brain sites, including the mesolimbic reward circuitry and the hypothalamus. Both of these regions have direct ties to energy metabolism regulation, particularly food intake and energy expenditure. These data clearly suggest that the observed beneficial effects of CB1 (cannabinoid receptor 1) receptor antagonists on obesity may be related to the central endocannabinoid system. On the other hand, data presented on cannabinoid action in the liver and white adipose tissues clearly indicate that CB1-mediated events in affecting metabolic phenotype may occur in peripheral tissues as well. This together with the reported results from human trials on CB1 antagonists showing that the initial anorectic effect of rimonabant is diminished after the first weeks while longer lasting weight loss is achieved do indicate that peripheral action of cannabinoids are very important in body weight regulation. Should this hold true in the long run, antagonizing CB1 receptors with compound not crossing the blood-brain barrier could revolutionize pharmaceutical approaches to obesity by offering a tool that short cuts the central nervous system.

Adipose Tissue↗
PubMed2001

A role for dietary fat in leptin receptor, OB-Rb, function.

Leptin is a hormone believed to control appetite and regulate body weight via receptors in the hypothalamus. Much is known about the structure of the functional, or long, form of the leptin receptor, OB-Rb. However, the mechanism by which the receptor regulates leptin's biological action is unknown. Both the type and amount of dietary fat have been shown to affect factors involved in OB-Rb binding and signaling, as well as the morphology of hypothalamic cell membranes. Thus, the following review article examines possible mechanisms by which dietary fat may affect OB-Rb functioning at the hypothalamic level. Dietary fat can alter the fatty acid make-up of membranes, such as the polyunsaturated:saturated fat ratio, changing membrane fluidity and possibly leading to an enhancement or impairment of the structure and/or function of any membrane-associated receptor complexes. Dietary fat also interferes in biochemical pathways involving leptin, OB-Rb, and other neurons containing neuropeptides under OB-Rb's control, such as neuropeptide Y (NPY), proopiomelanocortin (POMC), and cocaine- and amphetamine-regulated transcript (CART). Increased monounsaturated fat increases cyclic adenosine monophosphate (cAMP) levels, possibly reducing mitogen-activated protein kinase (MAPK) activation and interrupting leptin signaling through Janus kinase/signal tranducers and activators of transcription (JAK/STAT) pathways. Dietary induced alterations in hypothalamic cell membranes, SNS activity, or other factors involved in OB-Rb function form a possible basis for the control of leptin's effects on body composition and appetite. Improving the biological activity of leptin by diet modification may exist as a practical strategy for the treatment of obesity and related disorders.

Animals↗
PubMed2006

Dietary therapy for obesity is a failure and pharmacotherapy is the future: a point of view.

1. We confront an escalating epidemic of obesity. The precipitating factors are undoubtedly environmental and include increasingly immobilizing occupations and technologies and an abundance of food in many societies. This understanding has led to the view that the obesity epidemic is entirely environmental and that obesity should be treated primarily by behavioural (particularly dietary) therapy. That is, a prominent view is that common human obesity is an environmental disease and is not, like hypertension and hypercholesterolaemia, a complex, multifactorial disease resulting from the interaction of genetic and environmental variance. 2. In the first part of the present article, I argue that this view has obscured a strong genetic-biological contribution to body mass and adiposity in humans. This is supported by studies of adopted children and twins and by rare Mendelian forms of human obesity. 3. In the second part of the present article, I argue that behavioural therapy for maintenance of weight loss is, overall, a failure. The overwhelming majority of people who lose weight by dieting regain it in several years. Many have blamed this on patients' lack of will-power and discipline, but there is mounting evidence that biological mechanisms contribute substantially to relapse from weight loss during dietary therapy. These include a compensatory decrease in energy expenditure during dieting and compensatory adaptations that would be expected to increase appetite. 4. We live in an era of evidence-based medicine; the evidence does not support the efficacy of diet therapy for maintenance of weight loss in obesity. This has been true for decades, despite efforts to improve behavioural therapy. Despite what we want to happen, this will not likely improve, because the failure of diet therapy for the maintenance of weight loss in obesity is probably primarily biological, not behavioural. 5. In the third part of the article, I argue that drugs will increasingly dominate the treatment of obesity. We are in the midst of a revolution in understanding the biological regulation of appetite and metabolism that began with the pioneering discovery of leptin. In my judgement, this will lead inevitably to the development of safe, effective therapy for obesity. 6. This transformation from behavioural to pharmacological therapy proved true with hypertension and hypercholesterolaemia. Pharmacological therapy for hypertension and hypercholesterolaemia followed the discovery of the pathways regulating arterial pressure and cholesterol biosynthesis, respectively, and behavioural therapy for these diseases is now secondary. Despite the skepticism, I predict that the same transformation will occur in the treatment of obesity. This is not to argue against the need for environmental modification to slow the escalating epidemic of obesity, but it is to suggest that future effective treatment of common human obesity should recognize the limitations of dietary therapy for maintenance of weight loss and the promise of pharmacological therapy.

Body Mass Index↗
PubMed2000

[Etiology of overweight and obesity].

Obesity results from a predominance of caloric intake over energy expenditure. Twin, adoption and family studies have demonstrated that, together with environmental conditions, various genetic factors play an important role in the pathogenesis of obesity. In recent years, it was possible to identify several defects in single genes responsible for obesity in rodents, some of which may also be involved in human obesity. Besides leptin as the most notable example, numerous other proteins and neuropeptides have been identified in recent years that participate in a complex network to regulate food intake and energy expenditure. The ongoing search for the important obesity genes should not only result in a better understanding of energy metabolism, but may also help in the development of new strategies for the treatment of obese patients.

Appetite Regulation↗
PubMed1976

[Physiological equilibration of water, electrolytes and nutrients].

An account is given of the fundamental mechanisms concerned with the regulation of hunger and thirst, and of the physiological processes involved in the uptake of nutrients, water and electrolytes. Several reflex chains ensure that the organism does not take up too much water and also protect it from excessive loss of water and salt.

Adult↗
PubMed1998

Appetite suppression and weight loss after the cannabinoid antagonist SR 141716.

The effect of the cannabinoid CB1 receptor antagonist, SR 141716, on food intake and body weight was assessed in adult, non-obese Wistar rats. The daily administration of SR 141716 (2.5 and 10 mg/kg; i.p.) reduced dose-dependently both food intake and body weight. Tolerance to the anorectic effect developed within 5 days; in contrast, body weight in SR 141716-treated rats remained markedly below that of vehicle-treated rats throughout the entire treatment period (14 days). The results suggest that brain cannabinoid receptors are involved in the regulation of appetite and body weight.

Animals↗
PubMed2000

Eating behavior: lessons from the real world of humans.

Food intake by normal humans has been investigated both in the laboratory and under free-living conditions in the natural environment. For measurement of real-world intake, the diet-diary technique is imperfect and tends to underestimate actual intakes but it appears to be sensitive, can detect subtle influences on eating behavior, and produces reliable and valid measures. Research studies in the real world show the multivariate richness of the natural environment, which allows investigation of the complexities of intake regulation, and even causation can be investigated. Real-world research can overcome some of the weaknesses of laboratory studies, where constraints on eating are often removed or missing, facilitatory influences on eating are often controlled or eliminated, the importance of variables can be overestimated, and important influences can be missed because of the short durations of the studies. Real-world studies have shown a wide array of physiologic, psychological, and social variables that can have potent and immediate effects on intake. Compensatory mechanisms, including some that operate with a 2- to 3-d delay, adjust for prior excesses. Heredity affects all aspect of food-intake regulation, from the determination of body size to the subtleties of the individual preferences and social proclivities and the extent to which environmental factors affect the individual. Hence, real-world research teaches valuable lessons, and much more is needed to complement laboratory studies.

Appetite Regulation↗
PubMed1993

Recent advances in breast feeding.

Increasingly, epidemiological studies are showing the benefits of exclusive breast-feeding to infants in industrialized countries, as they have previously for those in developing countries. In this review we have focused on several recent developments, in particular on the interplay between infant behaviour and maternal physiology in regulating breast milk supply. This will illustrate that many past and current clinical problems concerning breast-feeding are likely to be of iatrogenic origin, the products of imposing arbitrary rules for breast-feeding management. In order for the protective benefits to be fully realized it is necessary to ensure that breast-feeding is free from prescriptive practices. We will illustrate the key role played by the infants' control of appetite in the hope of encouraging clinicians to empower infants to exercise more control over the feeding process.

Appetite Regulation↗
PubMedDate not supplied

The endocrine function of the fat cell-regulation by the sympathetic nervous system.

The landmark discovery of leptin established beyond question the fact that adipose tissue is a crucial active regulator of body weight, an endocrine organ in its own right and part of a feedback circuit possessing both afferent and efferent loops. This is in addition to its more established roles as a receiver of incoming endocrine signals and modulator of circulating hormones such as sex steroids. Since this discovery, much has been learned about the role of leptin in the afferent loop of the hypothalamic regulation of body weight and indeed about some of the neuro-endocrine circuitry involved in the regulation of appetite and weight. Much less, however, is known about the efferent limb of the circuit, specifically relating to how the hypothalamus is able to influence adipocyte behaviour and how this link may itself be influenced by endocrine and paracrine signals, both acting on and emanating from adipocytes themselves, acting at multiple levels. This review will focus on the role of the sympathetic nervous system (SNS) and adreno-medullary system in relation to the regulation of adipose tissue physiology and endocrine function. The evidence in support of the hypothesis that the SNS is a crucial mediator of the efferent loop of this feedback circuit will be considered.

Adipocytes↗
PubMed2004

N-acetylation of hypothalamic alpha-melanocyte-stimulating hormone and regulation by leptin.

The central melanocortin system is critical in the regulation of appetite and body weight, and leptin exerts its anorexigenic actions partly by increasing hypothalamic proopiomelanocortin (POMC) expression. The POMC-derived peptide alpha-melanocyte-stimulating hormone (alphaMSH) is a melanocortin 4 receptor agonist, and its potency in reducing energy intake is strongly increased by N-acetylation. The reason for the higher biological activity of N-acetylated alphaMSH (Act-alphaMSH) compared with that of N-desacetylated alphaMSH (Des-alphaMSH) is unclear, and regulation of acetylation by leptin has not been investigated. We show here that total hypothalamic alphaMSH levels are decreased in leptin-deficient ob/ob mice and increased in leptin-treated ob/ob and C57BL/6J mice. The increase in total alphaMSH occurred as soon as 3 h after leptin injection and was entirely due to an increase in Act-alphaMSH. Consistent with this observation, leptin rapidly induced the enzymatic activity of a N-acetyltransferase in the hypothalamus of mice. In 293T cells expressing the melanocortin 4 receptor, Act-alphaMSH is far more potent than Des-alphaMSH in stimulating cAMP accumulation, an effect caused by a dramatically increased stability of Act-alphaMSH. Moreover, Des-alphaMSH is rapidly degraded in the hypothalamus after intracerebroventricular injection in rats and was less potent in inhibiting energy intake. The results suggest that leptin activates a N-acetyltransferase in POMC neurons, leading to increased hypothalamic levels of Act-alphaMSH. Due to its increased stability, this posttranslational modification of alphaMSH may play a critical role in leptin action via the central melanocortin pathway.

Acetylation↗
PubMed2002

The temporal organization of ingestive behaviour and its interaction with regulation of energy balance.

Body weight of man and animals is under homeostatic control mediated by the adjustment of food intake. It is discussed in this review that besides signals reporting energy deficits, optimized programs of body clocks take part in feeding behaviour as well. Circadian light- and food-entrainable clocks determine anticipatory adaptive behavioural and physiological mechanisms, promoting or inhibiting food intake. In fact these clocks form the constraints within which the homeostatic regulation of feeding behaviour is operating. Therefore, a strong interaction between circadian and homeostatic regulation must occur. In this homeostatic control, a wide variety of regulatory negative feedback mechanisms, or satiety signals, play a dominant role. In this respect several gut hormones and body temperature function as 'short-term' satiety factors and determine meal sizes and intermeal intervals. Leptin, secreted by fat cells in proportion to the size of adipose tissue mass, is probably an important determinant of the 'long-term' regulation of feeding behaviour by setting the motivational background level for feeding behaviour. Thus, initiation or termination of meals at any particular point in time, depends on the resultant of all satiety signals and on constraints imposed by circadian light- and food-entrainable oscillators.

Adipose Tissue↗
PubMed2004

[Pathogenesis of obesity].

During the last years various studies have been able to offer an insight into the regulation of appetite, satiety and energy balance, as well as adipocyte differentiation and the role of adipose tissue as an endocrine organ. These mechanisms add new aspects to the pathogenesis of obesity, but also to the development of weight-reducing medications. Life-style factors, including reduced physical exercise and a high calorie intake, are responsible for the increase in obesity in industrialized countries. As a result of twin and adoption studies, the genetic influence on the development of obesity is estimated to be 30-70%. As regards the common form of obesity, more than 70 gene loci have been described as possible candidate genes. These comprise genes involved in central nervous regulation systems, including leptin, the leptinreceptor, POMC, MCR-4, as well as energy expenditure and adipocyte differentiation such as beta-adrenergic receptors, UCPs, and the nuclear receptor PPARy. The common form of obesity seems to be mainly due to an interaction between genetic disposition and environmental factors.

Adoption↗
PubMed2006

Leptin and its receptors are present in the rat olfactory mucosa and modulated by the nutritional status.

Leptin is an adipocyte-derived cytokine that regulates body weight mainly via the long form of the leptin receptor (Ob-Rb). Leptin and its receptors are expressed in several tissues, suggesting that leptin might also be effective peripherally. We hypothesized that, as shown in taste cells, leptin and its receptors isoforms (Ob-Rs) could be present in the rat olfactory mucosa (OM). Using RT-PCR, light and electron microscopy immunohistochemistry (ICC), we found that different isoforms of the receptor were expressed in OM and localized in sustentacular cells and in a subpopulation of maturating neurons; in addition, immunoreactivity was also present in differentiated neurons and enriched at the cilia membranes, where the odorants bind to their receptors. Moreover, using RT-PCR, ICC and RIA measurements, we showed that leptin is synthesized locally in the olfactory mucosa. In addition, we demonstrate that fasting causes a significant enhanced transcription of both leptin and Ob-Rs in rat OM by quantitative RT-PCR data. Altogether, these results strongly suggested that leptin, acting as an endocrine or a paracrine factor, could be an important regulator of olfactory function, as a neuromodulator of the olfactory message in cilia of mature olfactory receptors neurons (ORN), but also for the homeostasis of this complex tissue, acting on differentiating neurons and on sustentacular cells.

Animals↗
PubMed2003

Precursor-protein convertase 1 gene expression in the mouse hypothalamus: differential regulation by ob gene mutation, energy deficit and administration of leptin, and coexpression with prepro-orexin.

The expression of precursor-protein convertase (PC)1, PC2 and paired basic amino acid cleaving enzyme four mRNA was studied by in situ hybridisation in regions of the hypothalamus involved in energy regulation in relation to obese (ob) gene mutation and energy deficit. PC1 gene was differentially expressed in hypothalamic nuclei of mice from different genetic backgrounds or energetic status, whereas no differences in expression were observed for either the PC2 or paired basic amino acid cleaving enzyme four genes. In obese ob/ob mice, PC1 mRNA levels were increased in the paraventricular nucleus, decreased in the lateral hypothalamus and unchanged in the ventromedial nucleus and arcuate nucleus relative to lean controls. In response to intraperitoneal injection of murine leptin, PC1 mRNA levels in obese ob/ob mice decreased in the arcuate nucleus, increased in the lateral hypothalamus and were unchanged in both the paraventricular nucleus and ventromedial nucleus. In mice deprived of food for 24 h, PC1 mRNA levels were reduced in the ventromedial nucleus, increased in the lateral hypothalamus and unchanged in the paraventricular nucleus and arcuate nucleus relative to ad libitum-fed controls. Overall, whilst the data show effects related to leptin and energetic status, they do not support a strong and consistent link between PC1 gene expression and energy balance. This suggests that if PC1 is important to the control of energy balance then protein expression and activity, rather than gene expression may be the more critical parameters of regulation. The relationship between PC1 and candidate energy balance-related genes in the lateral hypothalamus was investigated by dual in situ hybridisation. PC1 mRNA was localised in prepro-orexin mRNA expressing neurons in the lateral hypothalamus, which suggests a functional relationship.

Animals↗
PubMed1999

The role of apolipoprotein A-IV in food intake regulation.

Apolipoprotein (apo) A-IV is a glycoprotein synthesized by the human intestine. In rodents, both the small intestine and the liver secrete apo A-IV; the small intestine, however, is by far the major organ responsible for the circulating apo A-IV. Intestinal apo A-IV synthesis is markedly stimulated by fat absorption and appears not to be mediated by the uptake or reesterification of fatty acids to form triglycerides. Rather, it is the formation of chylomicrons that acts as a signal for the induction of intestinal apo A-IV synthesis. Intestinal apo A-IV synthesis is also enhanced by a factor from the ileum and that factor is probably peptide tyrosine-tyrosine (PYY). The inhibition of food intake by apo A-IV is probably mediated centrally. The stimulation of intestinal synthesis and secretion of apo A-IV by lipid absorption are rapid; thus, apo A-IV likely plays a role in the short-term regulation of food intake. Other evidence suggests that apo A-IV may also be involved in the long-term regulation of food intake and body weight. Chronic ingestion of a high fat diet blunts the intestinal apo A-IV response to lipid feeding and may explain why the chronic ingestion of a high fat diet predisposes both animals and humans to obesity.

Animals↗
PubMed2003

[Role of apolipoprotein A-IV in the regulation of food intake].

Although many exciting functions of Apolipoprotein A-IV(apo-A IV) have been proposed, this review focuses on its unique role in regulating food intake. Apo-A IV is a glycoprotein produced by human intestine and rodent intestine and liver, but the small intestine is the major organ responsible for the circulating apo-A-IV. Our Laboratory recently demonstrated that apo-A IV protein and apo-A IV mRNA were present in rat hypothalamus. Intestinal apo-A IV synthesis is markedly stimulated by fat absorption and the formation of chylomicrons. Intestinal apo-A IV synthesis is also enhanced by the peptide tyrosine-tyrosine. The inhibition of food intake by apo-A IV is mediated centrally. Apo-A IV likely plays a role in the short-term regulation of food intake. Other evidence suggests that apo-A IV may also be involved in the long-term regulation of food intake and body weight. Reduction of apo-A IV in response to lipid feeding in both animal and humans that chronically consume a high-fat diet may explain in part why the chronic ingestion of a high-fat diet predisposes to obesity.

Animals↗