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PubMed2003

The differential effects of food restriction on 5-HT1A and 5-HT1B receptor mediated control of serotonergic transmission in the hippocampus and hypothalamus of rats.

Serotonergic pathways are considered important in the regulation of appetite. We have determined, in female rats, the effects of 4 weeks food restriction (FR) on serotonin function, using in vivo microdialysis. We recorded basal 5-HT release in the hypothalamus and hippocampus, and the sensitivity of the somatodendritic 5-HT1A autoreceptors in the raphe nuclei, and the nerve terminal 5-HT1B autoreceptors which together regulate the synthesis and release of 5-HT in these regions. Sensitivity of the somatodendritic 5-HT1A autoreceptors was assessed by measuring the reduction in extracellular 5-HT induced by systemic administration of the 5-HT1A receptor agonist 8-hydroxy-2-di-n-(propylamino)-tetralin (8-OH-DPAT), while sensitivity of nerve terminal 5-HT1B autoreceptors was measured by observing the increase in 5-HT release after systemic injection of the 5-HT1B receptor antagonist GR 127935. Basal release of 5-HT was not affected by FR. 8-OH-DPAT decreased 5-HT release in the hippocampus and hypothalamus in both groups, while GR 127935 increased 5-HT release in both areas in the control animals but not in the hypothalamus of the FR animals. Since 5-HT1B receptors regulate 5-HT release by a negative feedback mechanism, the decrease in sensitivity of 5-HT1B receptors in the hypothalamus of FR rats indicates increased serotonergic transmission in these rats. The fact that such differential effects on 5-HT release appeared only in the hypothalamus, the center of regulation of energy balance, suggests a compensatory role in FR by increasing 5-HT secretion, thereby reducing feeding behavior.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed2006

Relationship between portion size and energy intake among infants and toddlers: evidence of self-regulation.

OBJECTIVES: To assess whether dietary intakes of infants and young toddlers show evidence of energy self-regulation. DESIGN: Data from 24-hour recalls collected in the 2002 Feeding Infants and Toddlers Study were analyzed. Multivariate regressions were used to explore the relationship between portion size and usual energy intake as well as the relationship between portion size, number of eating occasions, number of unique foods, and energy density. SUBJECTS/SETTING: A national random sample of 3,022 US infants and toddlers 4 to 24 months of age. STATISTICAL ANALYSES PERFORMED: To measure variability in portion size, an average portion size z score was computed for each child in the sample, across 45 different food groups. The number of eating occasions was defined as the total number of times a child had anything to eat or drink during the day, excluding eating occasions that included only water and/or supplements. The total number of unique foods in a day was defined as the number of unique food codes included in the 24-hour recall, and energy density was computed as kilocalories/gram, including all foods, beverages, and water. Linear regression models were used to assess the effect of portion size and other self-regulation mechanisms on energy intake and to assess the effect of these self-regulation mechanisms on portion size. Separate analyses were performed for three age groups: 4 to 5 months, 6 to 11 months, and 12 to 24 months. RESULTS: A significant negative association was found for all age groups between the number of eating occasions and average portion size z scores, indicating that children who eat less often during the day consume larger-than-average-portion sizes and children who eat more often during the day consume smaller-than-average portions. For infants (11 months and younger), a significant negative association was noted between energy density and average portion size z scores, indicating that, as the energy density of the diet goes down, infants consume larger-than-average portions and, as the energy density of the diet goes up, they consume smaller-than-average portions. Among infants 6 to 11 months, there was a significant positive relationship between portion size and the number of unique foods consumed. For toddlers, there was no association between average portion size z scores and energy density, suggesting that energy self-regulation mechanisms are diminished in this age group. CONCLUSIONS: Our findings confirm the presence of energy self-regulation among infants and young toddlers. These findings can be used to assure parents and caregivers that infants have an innate ability to regulate energy intake. At the same time, it is important to educate parents and caregivers about the potential for environmental cues to diminish natural hunger-driven eating behaviors, even among young toddlers. Dietetics professionals should emphasize the potential adverse effects that coercive feeding behaviors can have on children's innate ability to regulate energy intake. This includes not only admonitions to "clean your plate," but overrestriction of intake that may be motivated by concerns that children are overeating.

Appetite Regulation↗
PubMed2004

Effect of central administration of prolactin-releasing peptide on feeding in chicks.

Prolactin-releasing peptide (PrRP) is one of the inhibitory factors in feeding regulation of mammals. However, no information is available for avian species. The present study was done to clarify the effect of intracerebroventricular (ICV) injection of PrRP on feeding in chicks. Firstly, we found that ICV injection of PrRP (94-1500 pmol) significantly increased food intake in chicks. The result was completely different from those obtained in mammals. The orexigenic effect of PrRP was significantly weaker than that of neuropeptide Y (NPY), a potent orexigenic peptide, on an equimolar basis. The orexigenic effect of NPY was further enhanced with coinjection of PrRP. These results suggest the existence of a novel orexigenic mechanism in the chick brain, which might differ from NPY-involved feeding regulatory pathway. In addition, ICV injection of PrRP significantly decreased the rectal temperature, but the effect was weaker than that of NPY, suggesting that PrRP may inhibit energy expenditure in chicks. Taken together, we showed here that PrRP may be involved in the regulation of both feeding behavior and energy metabolism in the chick brain.

Animals↗
PubMed2000

Regulation of energy intake in older adults: recent findings and implications.

Inadequate energy intake is common in older individuals and is probably the major cause of unexplained weight loss. This summary highlights recent studies on possible causes of negative energy balance in older individuals suggesting that aging is associated with a significant impairment in the regulation of food intake that inhibits appropriate short-term and long-term compensation for normal fluctuations in energy intake. The combination of a reduced ability to regulate energy intake, decreased dietary variety, and disadvantageous social factors such as functional limitations, social isolation and depression, increases the risk of negative energy balance leading to weight loss in older individuals.

Aged↗
PubMed2001

Gastric leptin.

The recent discovery of gastric leptin has initiated several investigations on the possible role of leptin in digestive physiology. The following clues are currently suggested: leptin might control meal size in cooperation with Cholecystokinin, help cytoprotection of the gastric mucosa, play a role in gut inflammatory processes, regulate secretion of gastric hormones such as gastrin and somatostatin, and modulate intestinal transport of small peptides. The present review is a brief survey of the most significant advances in these issues.

Animals↗
PubMed2006

The melanocortin system and energy balance.

The melanocortins, a family of peptides produced from the post-translational processing of pro-opiomelanocortin (POMC), regulate ingestive behavior and energy expenditure. Loss of function mutations of genes encoding POMC, or of either of two melanocortin receptors expressed in the central nervous system (MC3R, MC4R), are associated with obesity. The analyses of MC4R knockout mice indicate that activation of this receptor is involved in the regulation of appetite, the adaptive metabolic response to excess caloric consumption, and negative energy balance associated with cachexia induced by cytokines. In contrast, MC3R knockout mice exhibit a normal, or even exaggerated, response to signals that induce a state of negative energy balance. However, loss of the MC3R also results in an increase in adiposity. This article discusses the regulation of energy balance by the melanocortins. Published and newly presented data from studies analyzing of energy balance of MC3R and MC4R knockout mice indicate that increased adiposity observed in both models involves an imbalance in fat intake and oxidation.

Animals↗
PubMed2002

Total gastrectomy severely alters the central regulation of food intake in rats.

OBJECTIVE: To investigate the central regulation of food intake by quantifying neuron activation of the nucleus of the solitary tract (NTS) after injection of cholecystokinin (CCK) or food intake in gastrectomized rats. SUMMARY BACKGROUND DATA: Total gastrectomy is followed by early satiety, low calorie intake, and weight loss in the majority of patients. The etiology of these effects is unknown. Sixty percent to 70% of patients remain underweight after total gastrectomy, the weight loss averaging 25% of preoperative body weight. About two thirds of gastrectomized patients report early satiety, and about 60% do not reach the recommended daily calorie intake. The NTS is a brain stem center involved in the regulation of food intake; thus, the extent and pattern of neuronal activation provide information on the process involved in the initiation of satiation and the regulation of food intake. METHODS: The authors investigated neuronal activation in the NTS using c-fos immunohistochemistry following CCK injection or food intake in healthy control rats, sham-operated control rats, age-matched control rats, weight-matched control rats, and vagotomized or gastrectomized rats. RESULTS: Neuronal activation in the NTS after CCK injection was significantly decreased 21 days after total gastrectomy, but increased by up to 51% 3 months and by up to 102% 12 months after surgery compared to age-matched unoperated control rats. Neuronal activation in the NTS in response to feeding was markedly increased up to fivefold in gastrectomized rats. This increase was early in onset and sustained, and occurred despite significantly reduced food intake. Administration of MK329, a CCK-A receptor antagonist, significantly reduced the number of postprandially activated neurons in both gastrectomized and control rats. CONCLUSIONS: The early postprandial activation of NTS neurons after total gastrectomy in rats may correspond to early satiety reported by patients, while the sustained activation of NTS neurons after a meal could contribute to a reduced daily calorie intake. These data suggest that a disturbed central regulation of food intake might contribute to early satiety, reduced food intake, and weight loss after total gastrectomy.

Animals↗
PubMed1998

Cystic fibrosis transmembrane conductance regulator expression in human hypothalamus.

We have previously characterized the expression of the cystic fibrosis transmembrane conductance regulator protein (CFTR) gene, mRNA and protein in rat brain with reverse transcriptase (RT)-PCR amplification, in situ hybridization and immunocytochemistry. We now report that the CFTR mRNA is expressed in the human anterior hypothalamus, an area involved in regulation of appetite, resting energy expenditure and sexual differentiation. Expression of CFTR in neurons localized to this region may elucidate the pathogenesis of other non-pulmonary manifestations of cystic fibrosis which commonly are observed in children with CF, including congenital absence of the vas deferens. Neuron-specific expression of CFTR in brain may be involved in the regulation of homeostatic functions including reproductive function and fertility through effects on neurosecretion, i.e. GnRH release. Dysregulation of normal neuropeptide vesicle trafficking by mutant CFTR in brain my lead to alteration in physiological function.

Cystic Fibrosis Transmembrane Conductance Regulato↗
PubMed2006

Effect of zinc on biochemical parameters and changes in related gene expression assessed by cDNA microarrays in pituitary of growing rats.

OBJECTIVE: The present study simultaneously investigated the effects of different zinc (Zn) levels on the growth performance and relative biochemical parameters in growing rats and analyzed the molecular mechanism of zinc influencing food intake. METHODS: Three diets with different Zn levels--Zn adequate (ZA; 35.94 mg/kg, control), Zn deficient (ZD; 3.15 mg/kg), and Zn overdose (ZO; 347.50 mg/kg)--were fed to rats for 6 wk. Dietary Zn was supplemented with ZnSO4. The relation between zinc and food intake was studied by pituitary cDNA microarrays. RESULTS: Compared with ZA group, rats fed the ZD diet showed decreases in body weight (P < 0.01), food intake (P < 0.05), tissue zinc concentrations (P < 0.01), and specific activities of alkaline phosphatase (P < 0.01) and copper/Zn superoxide dismutase (P < 0.05), whereas the ZO diet had positive effects on body weight (P < 0.05), zinc concentrations (P < 0.01), and alkaline phosphatase activity (P < 0.05). The villi of the jejunum became shorter (P < 0.01), shriveled, and flattened. This change in morphology decreased absorption surface area, and there was a substantial decrease (P < 0.01) in villi number per unit area in ZD rats. Metallothionein concentration was increased in livers of rats fed ZD (P < 0.01) and ZO (P < 0.05) diets. Moreover, ZD and ZO influenced normal growth and development of organs. The results from pituitary cDNA arrays indicated that different Zn levels affect gene expression of appetite-related peptides, including neuropeptide-Y, melanin-concentrating hormone, ghrelin, calcitonin gene-related product, and serotonin. CONCLUSION: The present results showed that zinc deficiency has a negative effect on the growth performance and biochemical parameters of rats. The ZO diet increased body weight (P < 0.05) but had no effect (P > 0.05) on food intake, copper/Zn superoxide dismutase activity, and intestinal morphology. The ZD diet decreased rat food intake by regulating appetite-related gene expression in the pituitary gland.

Alkaline Phosphatase↗
PubMed2000

Regulation of energy intake in relation to metabolic state and nutritional status.

Inadequate energy intake can be an important contributor to weight loss in older individuals. This review highlights recent studies on possible causes of negative energy balance in older individuals. Studies of the regulation of food intake suggest that aging is associated with a significant impairment in the regulation of food intake that inhibits appropriate short-term and long-term compensation for imposed alterations in energy intake. The combination of a reduced ability to regulate energy intake, decreased sensory-specific satiety, and disadvantageous social factors such as functional limitations, social isolation and depression, increases the risk of negative energy balance leading to weight loss in older individuals.

Aged↗
PubMed2006

Endocrine receptors as targets for new drugs.

Increasingly detailed knowledge of cellular signalling pathways is providing a sound basis for the development of specific drugs aimed at selected components of the pathways. Many of these targets are receptors and the multitude of hormone receptors makes endocrine functions a rich proving ground for this research. This article reviews a recent meeting (Insights into Receptor Function and New Drug Development Targets; 5th Endocrinology Colloquium of the Fondation Ipsen, Paris, December 5, 2005) where progress in defining suitable targets for drug therapies in the endocrine system and in designing drugs for some of these targets was discussed. Although the family of G-protein-coupled receptors, ubiquitous in the endocrine system, was the central focus, comparisons with other receptor families were made. Many mutations affecting genes coding for receptors or other components of signalling pathways have been found in a wide range of endocrine disorders including obesity, parathyroid malfunction, disorders involving thyroid-stimulating hormone and follicle-stimulating hormone, and tumours in the anterior pituitary, as well as in many types of cancer. These are being used to dissect the normal control mechanisms as well as to provide information for the development of selective drugs. Recently identified mutations that affect the intracellular traffic in newly synthesised receptors open up possibilities of another dimension of cellular regulation of signalling. Both the discovery of hormones such as apelin and its pairing with an 'orphan' receptor, and the unexpected action of a drug against cannabinoid receptors point to further levels of complexity in cardiovascular regulation. Deeper understanding of the evolution of receptor families and of the molecular mechanisms of signal transduction is enabling the design of highly specific agonists and antagonists. Pharmacological intervention is not limited to the ligand-receptor interaction but can extend to inhibition of selected steps in the intracellular pathway, such as the regulation of G protein deactivation. The progress in this area is both leading to improved treatment for a range of endocrine disorders and serving as a model for the study of signalling in other physiological systems.

Animals↗
PubMed2000

The regulation of leptin gene expression in the C6 glioblastoma cell line.

The hormone leptin is implicated in the regulation of appetite and body weight in rodents, primates and humans. We reported that the leptin gene (ob) is expressed in the brain, but the factors which control ob expression in the central nervous system are not known. We previously showed that brain-derived rat C6 glioblastoma cells express ob mRNA and protein. In the present study we examined the regulation of ob expression in C6 cells. Leptin and leptin receptor immunoreactivity was detected in C6 cells, suggesting a possible autocrine role for leptin. The identity of the leptin immunoreactivity (OB-ir) in C6 cells was confirmed by immunoprecipitation and Western blotting using two leptin specific polyclonal antibodies. Using RT-PCR analysis a product of the expected size for the short, but not the long, leptin receptor isoform was detected in C6 cells. Cells were maintained in serum-free (SF) media for 0-24 h in the presence of various regulators of leptin expression. Leptin mRNA levels were significantly higher in cells treated with dbcAMP (1 mM), IGF 1 (100 ng/ml) or insulin (5 microg/ml) compared to SF controls. In contrast, corticosterone (10(-7)M) reduced leptin mRNA. In the presence of dbcAMP, C6 cells undergo a dramatic alteration in morphology which is coincident with an apparent increase in the number of leptin-ir nuclei and an increase in leptin immunoreactivity. In contrast to C6 cells, glucocorticoids are reported to increase leptin levels in adipocytes/adipose tissue, while increases in intracellular cAMP levels are reported to reduce leptin levels. Overall, our in vitro data suggest that the regulation of leptin gene expression in C6 glioblastoma cells is different from that in adipocytes.

Animals↗
PubMed2006

Thinking globally and acting locally with TOR.

The target of rapamycin (TOR) pathway regulates ribosome biogenesis, protein synthesis, nutrient import, autophagy and cell cycle progression. After 30 years of concentrated attention, how TOR controls these processes is only now beginning to be understood. Recent advances have identified a wide array of TOR inputs, including amino acids, oxygen, ATP and growth factors, as well the regulatory proteins that facilitate their effects on TOR. Such proteins include AMPK, Rheb and the tumor suppressors LKB1, p53, and Tsc1/2. It has only recently been appreciated that TOR resides in two distinct signaling complexes with differing regulatory roles, only one of which is rapamycin-sensitive, thus opening a new avenue of inquiry into TOR function. Finally, TOR appears to regulate feeding behavior by facilitating communication between organ systems, and is thus implicated in the regulation of glucose and fat homeostasis, and possibly diabetes and obesity. TOR thus functions to coordinate growth-permitting inputs with growth-promoting outputs on both a cellular and an organismal level.

Animals↗
PubMed2005

Ghrelin and immunity: a young player in an old field.

There is increasing evidence of the coupling of immune status to the metabolic system. The communication between the state of systemic and cellular energy balance to immune compartment is mediated via a complex array of cytokines, hormones and neuropeptides. Ghrelin, a recently described orexigenic peptide hormone, is predominantly produced by the stomach and functions as a positive regulator of the somatotropic axis and a peripheral signal of negative energy balance. Apart from its well-studied metabolic effects, ghrelin also exerts multiple regulatory effects on several other organ systems including the cardiovascular, central nervous and immune systems. Here, we summarize the growing evidence of ghrelin as a significant player in the regulation of inflammation and the immune function and the potential therapeutic targeting of ghrelin or its receptor, the growth hormone secretagogue receptor (GHS-R), in various inflammatory and cachexic disease states.

Aging↗
PubMed2001

[Glucagon-like peptide 2, a neurotransmitter with a newly discovered role in the regulation of food ingestion].

We report here that glucagon-like peptide 2(GLP-2) and its receptor constitute a distinct projection system connecting the nucleus of the solitary tract with the dorsomedial hypothalamic nucleus (DMH). The DMH contains a dense plexus of GLP-2 immunoreactive fibres and is the only hypothalamic nucleus expressing GLP-2 receptor mRNA. Consistent with this, central application of GLP-2 activates the expression of neurones solely in the DMH. Furthermore, central administration of GLP-2 causes a dose-related, a pharmacologically and behaviourally specific inhibition of food intake in rats. Surprisingly, the alleged GLP-1 receptor antagonist, Exending (9-39), proved a functional antagonist of centrally applied GLP-2. These data implicate GLP-2 as an important neurotransmitter in the regulation of food intake and likely bodyweight. Our data therefore point to the DMH as a crossroad for endocrine and visceral information affecting feeding behaviour.

Animals↗
PubMed2002

Effects of continuous lumbar intrathecal infusion of leptin in rats on weight regulation.

Intracranial leptin alters food consumption and body weight. To systematically characterize the effects of extended continuous spinal intrathecal delivery on such regulation, female rats received continuous lumbar spinal infusion (14 days) through catheters connected to osmotic minipumps of a vehicle or one of several doses of recombinant murine leptin (0.03-10 microg/day). The following observations were made. (1) Leptin resulted in a dose-dependent suppression in body weight and food consumption at doses above 0.3 microg/day. (2) Food consumption was initially reduced. Weight fell for 7 days and then plateaued at a level proportional to dose. (3) The ratio of food consumed to body weight was constant for control animals across the study. Leptin-infused rats slowed the initial fall in weight by increasing food consumption, such that the food to body weight ratio returned to that of control values. Rats were thus regulating food consumption to sustain body weight as defined by leptin dose. (4) On day 14, cisternal cerebrospinal fluid was obtained and leptin measured. Concentrations covaried in a log linear fashion with infusion dose. Body weight and food consumption covaried similarly with cisternal leptin concentrations across dose groups. Our data suggest that steady state infusions of leptin induce a degree of appetite suppression that leads to a steady state level of body weight loss and not simply to a simple block of consumatory behavior. The unexpected potency of the observed effects of intrathecal leptin relative to doses that are required after i.c.v. delivery suggests that at least a portion of the effects of intrathecal leptin may reflect a medullary action. The observed correlation of cisternal leptin levels with the behavioral effects is also consistent with a reliable distribution of the infused leptin to target supraspinal sites.

Animals↗
PubMed2003

Gastric leptin: a putative role in the short-term regulation of food intake.

The discovery of the production of leptin by the stomach, in addition to its production by adipose tissue, has initiated new investigation into the possible role of this protein in the digestive physiology, in particular in the short-term control of energy balance. Leptin has been identified in the lower half of the stomach glands both in the pepsinogen granules of chief cells and in the granules of a specific endocrine cell type, suggesting that leptin action is exerted by both exocrine and endocrine pathways. Gastric leptin is sensitive to the nutritional state, being rapidly mobilized in response to food intake following fasting, or after the administration of satiety factors; this suggests a role for this protein in the short-term regulation of feeding, acting in collaboration with satiety peptides such as cholecystokinin. Leptin, produced by gastric cells and by adipocytes, could act on both acute and chronic regulation of feeding behaviour respectively, giving information to the brain on the availability of external (food) and internal (fat depots) energy resources, thus participating in short- and long-term satiation.

Adipose Tissue↗
PubMed2004

Plasma and hypothalamic peptide-hormone levels regulating somatotroph function and energy balance in fed and fasted states: a comparative study in four strains of rats.

Both growth hormone (GH)/insulin growth factor (IGF)-1 axis and energy balance have been implicated in longevity independently. The aim of the present study was to characterize the effect of a 72-h fasting period at 3 months of age in four different rat strains: (i) Wistar and (ii) Fischer 344 rats, which develop obesity with age, and (iii) Brown Norway and (iv) Lou C rats, which do not. Wistar rats ate more, were significantly bigger, and presented with higher plasma leptin and lower ghrelin levels and hypothalamic growth hormone-releasing hormone (GHRH) content than rats from the three other strains. Plasma insulin and IGF-1 levels were lower in Brown Norway and Lou C rats, and somatostatin content was lower in Brown Norway rats only. Glycaemia was lower in Lou C rats that displayed a lower relative food intake compared to Fischer and Wistar rats. Brown Norway rats showed a greater caloric efficiency than the three other strains. Concerning major hypothalamic neuropeptides implicated in feeding, similar amounts were detected in the four strains for neuropeptide Y, agouti-related peptide, galanin, melanin-concentrating hormone, alpha-melanocortin-stimulating hormone (alpha-MSH) and corticotropin-releasing hormone. Orexin A appeared to be slightly elevated in Fischer rats and cocaine amphetamine-regulated transcript (CART)(55-102) diminished in Brown Norway. At the mRNA level, orexin A, GHSR1, alpha-MSH and CART expression were higher in Wistar and Lou C rats. Principal component analysis confirmed the presence of two main factors in the ad libitum rat population; the first being associated with growth-related parameters and the second being associated with food intake regulation. Hypothalamic GHRH and somatostatin content were positively correlated with feeding-related neuropeptides such as alpha-MSH for GHRH, and orexin A and CART for both peptides. Plasma ghrelin levels were negatively correlated with leptin and IGF-1 levels. Finally, a 72-h fasting period affected minimally body weight, plasma IGF-1 and leptin levels in Lou C rats compared to the three other strains, and plasma insulin levels were less affected in Brown Norway rats. In conclusion, Wistar shorter life span is consistent with its already fatter phenotype at 3 months of age. In terms of IGF-1, glycaemia and leptin responses to fasting, the Lou strain, which presents with a low food intake/body weight and caloric efficiency, is the least affected. The link between food intake regulation, GH axis and ageing is further demonstrated by principal component analysis, where GHRH and somatostatin were found to be strongly associated with energy homeostasis parameters.

Aging↗