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PubMed2005

[Peptides regulating food intake and body weight].

Regulation of food intake and body weight depends on direct and feedback signals from adipose tissue, alimentary canal and pancreas to the hypothalamus nuclei, where hunger and satiety centers are. During the last decade a few signaling molecules of peptide origin were discovered, which play an important role in the regulation of energy intake and energy expenditure as well as in obesity. So, adipocytes synthesize and express leptin, the product of Ob gene, a regulator of long-term food intake, in amounts proportional to the fat amount, while alimentary canal hormones are regulators of short-term food intake (from meal to meal). Some peptides decrease food intake as they promote satiety (anorexigenic signals), other peptides, contrary, increase food intake as they induce appetite (orexigenic signals). Disturbed equilibrium between the anorexigenic and orexigenic factors manifests as food intake disorders, increase in body weight and obesity or decrease in body weight, i.e. cachexia.

Adipocytes↗
PubMed2003

Co-existence of leptin- and orexin-receptors in feeding-regulating neurons in the hypothalamic arcuate nucleus-a triple labeling study.

The arcuate nucleus (ARC) of the hypothalamus has been identified as a prime feeding regulating center in the brain. Several feeding regulating peptides, such as neuropeptide Y (NPY) and proopiomelanocortin (POMC), are present in neurons of the ARC, which also serves as a primary targeting site for leptin, a feeding inhibiting hormone secreted predominantly by adipose tissues, and for orexin (OX)-containing neurons. OX is expressed exclusively around the lateral hypothalamus, an area also established as a feeding regulating center. Some recent physiological analyses have shown that NPY- and POMC-containing neurons are activated or inactivated by leptin and OX. Moreover, we have already shown, using double immunohistochemical staining techniques, that NPY- and POMC-containing neurons express leptin receptors (LR) and orexin type 1 receptors (OX-1R). However, no morphological study has yet described the possibility of whether or not these arcuate neurons are influenced by both leptin and OX simultaneously. In order to address this issue, we performed histochemistry on ARC neurons using a triple immunofluorescence method. We found that 77 out of 213 NPY- and 99 out of 165 POMC-immunoreactive neurons co-localized with both LR- and OX-1R-immunoreactivities. These findings strongly suggest that both NPY- and POMC-containing neurons are regulated simultaneously by both leptin and OX.

Animals↗
PubMed2002

Control of energy homeostasis and insulin action by adipocyte hormones: leptin, acylation stimulating protein, and adiponectin.

Adipose tissue performs complex metabolic and endocrine functions. This review will focus on the recent literature on the biology and actions of three adipocyte hormones involved in the control of energy homeostasis and insulin action, leptin, acylation-stimulating protein, and adiponectin, and mechanisms regulating their production. Results from studies of individuals with absolute leptin deficiency (or receptor defects), and more recently partial leptin deficiency, reveal leptin's critical role in the normal regulation of appetite and body adiposity in humans. The primary biological role of leptin appears to be adaptation to low energy intake rather than a brake on overconsumption and obesity. Leptin production is mainly regulated by insulin-induced changes of adipocyte metabolism. Consumption of fat and fructose, which do not initiate insulin secretion, results in lower circulating leptin levels, a consequence which may lead to overeating and weight gain in individuals or populations consuming diets high in energy derived from these macronutrients. Acylation-stimulating protein acts as a paracrine signal to increase the efficiency of triacylglycerol synthesis in adipocytes, an action that results in more rapid postprandial lipid clearance. Genetic knockout of acylation-stimulating protein leads to reduced body fat, obesity resistance and improved insulin sensitivity in mice. The primary regulator of acylation-stimulating protein production appears to be circulating dietary lipid packaged as chylomicrons. Adiponectin increases insulin sensitivity, perhaps by increasing tissue fat oxidation resulting in reduced circulating fatty acid levels and reduced intramyocellular or liver triglyceride content. Adiponectin and leptin together normalize insulin action in severely insulin-resistant animals that have very low levels of adiponectin and leptin due to lipoatrophy. Leptin also improves insulin resistance and reduces hyperlipidemia in lipoatrophic humans. Adiponectin production is stimulated by agonists of peroxisome proliferator-activated receptor-gamma; an action may contribute to the insulin-sensitizing effects of this class of compounds. The production of all three hormones is influenced by nutritional status. These adipocyte hormones, the pathways controlling their production, and their receptors represent promising targets for managing obesity, hyperlipidemia, and insulin resistance.

Adipocytes↗
PubMed2005

Metabolic and endocrine effects of sleep deprivation.

Sleep deprivation has multiple effects on endocrine and metabolic function. In particular, sleep restriction is accompanied by increased cortisol levels in the afternoon and early evening and a shorter quiescent period compared with extended sleep periods. Those alterations could facilitate central and peripheral disturbances that are associated with glucocorticoid excess, such as memory deficits, and are similar to those observed in aging. Thus, chronic sleep loss could contribute to acceleration of the aging process. Sleep restriction is also associated with an impairment of carbohydrate tolerance, similar to that observed in individuals with clinically significant impaired glucose tolerance. Thus, chronic sleep deprivation may increase the risk for diabetes. Finally, sleep plays an important role in energy balance. Partial sleep deprivation was found to be associated with a decrease in plasma levels of leptin and a concomitant increase in plasma levels of ghrelin; subjective ratings of hunger and appetite also increased (the appetite for protein-rich foods was not significantly affected). Moreover, a remarkable correlation was found between the increase in hunger and the increase in the ghrelin:leptin ratio. Thus, the neuroendocrine regulation of appetite and food intake appears to be influenced by sleep duration, and sleep restriction may favor the development of obesity.

Appetite↗
PubMed2004

Synergistic effects of cannabinoid inverse agonist AM251 and opioid antagonist nalmefene on food intake in mice.

Oral administration of the opioid antagonist nalmefene alone (up to 20 mg/kg) failed to show a significant effect on acute food intake in mice. However, combined oral dosing of nalmefene and subthreshold doses of AM251, a cannabinoid CB1 receptor inverse agonist, led to a significant reduction in food intake in both lean and diet-induced obese (DIO) mice. Furthermore, the anorectic effect of a high dose of AM251 was further enhanced when co-administered with nalmefene. The results support a synergistic interaction between opioid and cannabinoid systems in regulating feeding behavior.

Animals↗
PubMed2004

Formation of projection pathways from the arcuate nucleus of the hypothalamus to hypothalamic regions implicated in the neural control of feeding behavior in mice.

The arcuate nucleus of the hypothalamus (ARH) is a critical component of forebrain pathways that regulate a variety of neuroendocrine functions, including an important role in relaying leptin signals to other parts of the hypothalamus. However, neonatal rodents do not lose weight in response to leptin treatment in the same way as do adults, suggesting that certain aspects of leptin signaling pathways in the hypothalamus may not be mature. We tested this possibility by using DiI axonal labeling to examine the development of projections from the ARH to other parts of the hypothalamus in neonatal mice, paying particular attention to the innervation of the paraventricular nucleus (PVH), the dorsomedial nucleus (DMH), and the lateral hypothalamic area (LHA), each of which have been implicated in the regulation of feeding. The results indicate that ARH projections are quite immature at birth and appear to innervate the DMH, PVH, and LHA in succession, within distinct temporal domains. The projections from the ARH to the DMH develop rapidly and are established by the sixth postnatal day (P6), whereas those to the PVH develop significantly later, with the mature pattern of innervation first apparent between postnatal day 8 (P8)-P10. Furthermore, the ability of leptin to activate Fos in the PVH, DMH, and LHA appears to be age-dependent and correlates with the arrival of ARH projections to each nucleus. Taken together, these findings provide new insight into development of hypothalamic circuits and suggest an anatomical basis for the delayed postnatal regulation of food intake and body weight by leptin.

Aging↗
PubMed1999

Low protein diets administered to lactating rats affect in a time-dependent manner the development of young.

The effects of diets with different protein levels were evaluated when given at different intervals to lactating rats. Food intake by the litter and weight gain by the young are investigated. From the time of birth, groups of five litters were fed with commercial diet (23% protein) or with semi-synthetic diets (4,8,12 and 16% protein) during the 1st, 1st and 2nd, or 1st, 2nd and 3rd weeks of lactation. After weaning, the young of dams, which were fed hypoprotein diets (4 and 8%), showed less food intake capacity, reduced growth capacity and, in adult life, low body weight in comparison to animals raised on commercial ration with higher protein contents. 12 and 16% protein diets did not cause any change in feeding behavior or in weight development as opposed to the 4 and 8% protein diets. Results suggest that the effects of early undernourishment are time-dependent and may cause irreversible changes in the regulation of metabolism and pathogenesis.

Animals↗
PubMed1989

Effect of intraperitoneal administration of amino acids on the food intake of piglets on a liquid diet during the first month after birth.

The effect of single intraperitoneal 1 g.kg-1 doses of a solution of 20 amino acids (AA) on food intake was investigated in 20 piglets examined repeatedly between 2 and 26 days of age. The animals were reared individually from day 1 after birth in cages and bottle-fed a liquid diet nine times per day at two-hour intervals from 6 to 22 h. Although amino acid administration did not significantly affect plasma concentrations of total free AA throughout the experiment (as measured just before and 2 and 5 h after AA administration in blood withdrawn from the external jugular vein) it did produce a downward trend in food intake of piglets at 9-10 d of age. In older animals, the depressive effect on food intake was significantly greater and lasted longer. It is suggested that the aminostatic component of food intake regulation in piglets does not begin to operate until the weaning period.

Aging↗
PubMed1994

Sodium appetite, thirst, and body fluid regulation in humans during rehydration without sodium replacement.

After a 7-h H2O and Na+ depletion period (DP), produced by intermittent light exercise (8 bouts) at 35 degrees C, we examined thirst and taste palatability responses to 10 different NaCl solutions during 23 h of rehydration (RH) at 25 degrees C. During DP, net H2O and Na+ loss were 27.2 +/- 2.9 ml/kg and 3.29 +/- 0.45 meq/kg, respectively. Plasma osmolality (POsm) and plasma Na+ concentration ([Na+]p) increased significantly during DP by 3.4 +/- 1.2 mosmol/kgH2O and 3.0 +/- 1.0 meq/kgH2O, respectively. Plasma volume (PV) decreased by 6.5 +/- 1.9%. Thirst rating, renal fractional reabsorption of H2O, and plasma arginine vasopressin concentration (PAVP) increased as POsm increased. This increased thirst was accompanied by increased palatability ratings to H2O. During RH, subjects drank deionized H2O ad libitum and ate a Na(+)-free diet for 23 h. POsm and [Na+]p returned to control levels within 1 h RH and remained at or below the control thereafter. PV remained reduced by approximately 5% throughout RH. The increased thirst and PAVP returned to their respective control levels within 1 h of RH as POsm decreased, but thirst rating increased against between 17 and 23 h of RH without increase in POsm or PAVP. Palatability ratings to a 1 M NaCl solution at and after 3 h RH and palatability ratings to 0.3 M at 17 and 23 h RH were significantly higher than control. Plasma aldosterone concentration (PAldo) increased after DP, decreased with drinking, and increased again between 6 and 23 h of RH, accompanied by a marked decrease in fractional Na+ excretion to < 0.07%. Thus both Na+ preference and thirst in humans are influenced by body fluid and electrolyte status. The increased Na+ palatability (Na+ appetite) was preceded by osmotically induced thirst, and accompanied by nonosmotically driven thirst [extracellular fluid (ECF) thirst] and increased PAldo. The "Na+ appetite" and "ECF thirst" along with increased renal Na+ retention could contribute to ECF volume regulation after thermally induced H2O and Na+ depletion.

Adult↗
PubMed2004

Water and salt consumption and suppression of Angiotensin-induced thirst in rats after carotid glomectomy.

Carotid glomectomy in rats reduced daily water consumption and increased daily consumption of NaCl solution. Sham operation did not modify water and salt consumption. Intraperitoneal injection of angiotensin-II did not stimulate drinking motivation in the majority of rats subjected to carotid glomectomy. Injection of angiotensin-II to sham-operated and intact animals induced active consumption of both fluids during one hour. These results attest to the involvement of the carotid body in the regulation of consumption of water and sodium ions (the main elements of osmotic blood pressure) and the involvement of angiotensin-sensitive receptors of carotid body cells in the formation of thirst and salt appetite motivation, regulated by the renin-angiotensin system.

Angiotensin II↗
PubMed2005

Body weight is regulated by the brain: a link between feeding and emotion.

Regulated energy homeostasis is fundamental for maintaining life. Unfortunately, this critical process is affected in a high number of mentally ill patients. Eating disorders such as anorexia nervosa are prevalent in modern societies. Impaired appetite and weight loss are common in patients with depression. In addition, the use of neuroleptics frequently produces obesity and diabetes mellitus. However, the neural mechanisms underlying the pathophysiology of these behavioral and metabolic conditions are largely unknown. In this review, we first concentrate on the established brain machinery of food intake and body weight, especially on the melanocortin and neuropeptide Y (NPY) systems as illustration. These systems play a critical role in receiving and processing critical peripheral metabolic cues such as leptin and ghrelin. It is also notable that both systems modulate emotion and motivated behavior as well. Secondly, we discuss the significance and potential promise of multidisciplinary molecular and neuroanatomic techniques that will likely increase the understanding of brain circuitries coordinating energy homeostasis and emotion. Finally, we introduce several lines of evidence suggesting a link between the melanocortin/NPY systems and several neurotransmitter systems on which many of the psychotropic agents exert their influence.

Animals↗
PubMed2000

Obesity: a disease or a biological adaptation?

The increase in obesity prevalence is problematic as this condition is associated with health complications such as diabetes and cardiovascular diseases, more particularly when the excess body fat is stored in the deep abdominal region. On the other hand, obesity facilitates the maintenance of body homeostasis probably because of an increased hormonal gradient which favours the regulation of energy balance, to give but one example. The regulation potential of excess body fat is particularly apparent in the reduced-obese state where a reduction of energy expenditure, fat oxidation and some immune system markers, as well as an increase in appetite, stress vulnerability and circulating and adipose tissue organochlorines have been observed. These constitute another category of risk factors which can certainly favour the accumulation of body fat to reestablish body homeostasis on other fronts. Under such conditions, obesity is perceived by the physiologist as a necessary biological adaptation rather than a disease. For health professionals, this emphasizes the importance to seek a reasonable compromise between the favourable reduction of risk to develop metabolic complications by body weight loss and the physiological vulnerability which is also generated by such an intervention.

Adaptation, Physiological↗
PubMed2006

Overexpression of glucose transporter 2 in GT1-7 cells inhibits AMP-activated protein kinase and agouti-related peptide expression.

Glucose transporter 2 (GLUT2) has been proposed as a glucose sensor in pancreatic beta cells. GLUT2 has been found widely expressed in the brain and GLUT2 in the hypothalamus and hindbrain has been suggested to be involved in the central glucose sensing and regulation of glucose homeostasis and food intake. In this study, we overexpressed GLUT2 in GT1-7 neuroblastoma cells and investigated the effect of GLUT2 overexpression on cellular energy status in these cells. Compared with control cells, GLUT2 overexpression resulted in significantly increased cellular ATP levels at 5 and 25 mM glucose concentrations, more inhibition of agouti-related peptide (AgRP) mRNA and AMP-activated protein kinase (AMPK) phosphorylation by glucose, and attenuated stimulation of AgRP mRNA and AMPK by 2-deoxy-d-glucose (2DG), implicating that brain GLUT2 may be important in the regulation of food intake.

AMP-Activated Protein Kinases↗
PubMed1999

Peripheral and central mechanisms regulating food intake and macronutrient selection.

Food intake is regulated by a complex interaction of central and peripheral pathways. A range of neuropeptides affects feeding either through actions at the gastrointestinal/hepatic level or in the central nervous system. Circulating signals such as leptin and insulin modulate and interact with these neuropeptide systems to control energy balance. The roles of the melanocortin MC4 receptor pathway, agouti-related protein, melanocyte concentrating hormone, cocaine-amphetamine-regulated transport, neuropeptide Y, and enterostatin in the control of food intake and macronutrient selection are described.

Adrenal Glands↗
PubMed1992

Tissue-specific expression of the human neuropeptide Y gene in transgenic mice.

Neuropeptide Y (NPY) is the most abundant neuropeptide detected in the mammalian brain, and is found throughout the central and peripheral nervous system. This peptide is a proposed regulator of appetite, blood pressure, and pituitary hormone release. Previous experiments have demonstrated the ability of 5' sequences within the human NPY gene to promote transcription in cultured neuronal cells. To identify sequences in this gene that regulate tissue-specific expression, a NPY/CAT fusion gene, containing approximately 850 bp of NPY sequences, was microinjected into fertilized mouse ova. Five lines of transgenic mice were derived from these ova and several tissues from mice of each line were tested for transgene expression using the CAT assay. One line demonstrated X-chromosome-linked transmission of the transgene while the other lines demonstrated autosomally-linked transmission. Three lines demonstrated transgene expression with significant levels of CAT activity detectable only in tissues which have been shown to express endogenous NPY. One autosomally-linked line did not demonstrate significant levels of transgene activity because the transgene appeared to have undergone structural alteration during genomic integration. No transgene activity was detected in either male of female mice from the X-linked line, suggesting a positional regulation of the transgene locus other than X-inactivation in this line. The present research demonstrated the NPY regulatory sequences included in pCATNPY delta 796 sufficiently directed tissue-appropriate gene expression in transgenic mice.

Animals↗
PubMed2005

Therapeutic perspectives of adipocytokines.

Various adipocyte-secreted factors have been described which profoundly affect insulin sensitivity and might potentially link obesity, insulin resistance and cardiovascular disease. Among those, adiponectin, visfatin and omentin appear as insulin-sensitising adipocytokines, whereas TNF-alpha, IL-6 and resistin induce insulin resistance. Moreover, leptin is a fat-derived key regulator of appetite and energy expenditure. Due to their profound effect on whole-body glucose and energy metabolism, adipocytokines have attracted interest as potential new therapeutics for diabetes mellitus and obesity. The current knowledge on function, regulation and therapeutic potential of various adipocytokines, as well as their clinical implications, are discussed in this review.

Adipocytes↗