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PubMed2006

Active immunization against ghrelin decreases weight gain and alters plasma concentrations of growth hormone in growing pigs.

Ghrelin has been implicated in the control of food intake and in the long-term regulation of body weight. We theorize that preventing the ability of ghrelin to interact with its receptors, would eventually lead to decreased appetite and thereby decrease body weight gain. To test our hypothesis, pigs were actively immunized against ghrelin. Ghrelin((1-10)) was conjugated to BSA and emulsified in Freund's incomplete adjuvant and diethylaminoethyl-dextran. Primary immunization was given at 19 weeks of age (WOA), with booster immunizations given 20 and 40 days after primary immunization. Body weight (BW) and plasma samples were collected weekly beginning at 19 WOA, and feed intake was measured daily. Fourteen days after primary immunization, the percentage of bound (125)I-ghrelin in plasma from immunized pigs was increased compared with control animals (P<0.001). Voluntary feed intake was decreased more than 15% in animals that were actively immunized against ghrelin compared with controls. By the end of the experiment, immunized pigs weighed 10% less than control animals (P<0.1). Concentrations of GH were increased (P<0.05) in immunized pigs. Apoptosis was not observed in post-mortem samples obtained from the fundic region of the stomach. Our observations suggest that immunization against ghrelin induces mild anorexia. This procedure could potentially be used as a treatment to control caloric intake and obesity.

Animals↗
PubMed2006

Central regulation of food intake in ageing.

Energy homeostasis and fuel metabolism undergo significant modifications in the course of ageing. During the second half of life many humans increase their body mass and develop glucose intolerance that may lead to obesity and type 2 diabetes. However, many old people suffer from being underweight, and this "anorexia of elderly" may seriously compromise their health under certain circumstances. Experimental studies into the causes of ageing-related impairments of food intake regulation were performed mainly on rat, and to some extent, on non-human primates. It was found that the expression of NPY, the most potent orexigenic peptide, and of NPY receptors, is highly suppressed in the hypothalamus of old rats. Moreover, the increase of NPY mRNA after fasting was severely blunted in old as compared to young rats. Similar reductions, although of lower magnitude, were reported for other hypothalamic orexigenic compounds such as, AgRP and orexins. Interestingly, ageing does not significantly alter hypothalamic mRNA levels of important anorexigens such as CART and aMSH. The presented findings suggest that, at least in rodents, ageing is associated with the general down-regulation of hypothalamic peptides that stimulate food intake and unchanged expression of anorexigenic peptides. This situation may be responsible for the decreased appetite drive in senescent animals and loss of weight at the end-of-life period. If similar changes of the central control of food intake underly "anorexia of ageing" observed in some elderly, it is possible that therapeutic intervention at this regulatory level may be possible in the future.

Aging↗
PubMed1993

Evidence for brain serotonin-mediated control of carbohydrate consumption in normal weight and obese humans.

A plasma insulin and amino acid-mediated mechanism is thought to modulate brain serotonin concentration, thereby regulating carbohydrate consumption on a meal to meal basis. It has been suggested that obesity is associated with a defect in the appetite control system. Furthermore, post-absorptive plasma levels of several amino acids are increased in obese subjects, which is ascribed to obesity-associated insulin resistance and/or hyperinsulinemia. We studied breakfast-induced changes in plasma ratios of tryptophan to other large neutral amino acids and associated differences in macro-nutrient composition of lunch food in normal weight and obese human subjects. The study was randomized, double blind and cross-over with a 2 x 2 factorial design with drug/placebo and type of breakfast as factors. Nineteen healthy, non-obese (body mass index (BMI) 22.5 +/- 1.9 kg/m2, mean +/- s.d.) and 19 obese (BMI 34.7 +/- 6.2 kg/m2) female volunteers were treated with either 60 mg fluoxetine (FXT), a serotonin re-uptake blocker specifically acting in the brain, or placebo for four days with a wash-out period between treatments of four weeks. The subjects received either a carbohydrate (CHO) breakfast (80 g maltodextrin, 300 kcal) or a protein-rich (PROT) breakfast (60% milk protein and 40% CHO, 300 kcal) on two consecutive days (days 4 and 5 of each treatment period). Plasma glucose, insulin and amino acids were measured at several time points after breakfast. Three hours after breakfast, subjects were able to choose from 29 different food items. Total energy content and weight of lunch food and energy percentage of each macronutrient were calculated.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

From dietary restraint to binge eating: some theoretical considerations.

A correlation between dietary restraint and the occurrence of binge eating has been convincingly shown in several investigations. However, the mediating mechanisms have not yet been elaborated in detail nor linked to empirical evidence. This theoretical gap is addressed in the following. After a short review of behavioral and metabolic correlates of dietary restraint, potential effects of restrained eating on the psychophysiological regulation of food intake are described. These effects may lead to the disruption of intake regulation and therefore can be regarded as direct causes of binge eating.

Appetite Regulation↗
PubMed1976

Glycogen levels and peripheral mechanisms of glucose-induced spppression of feeding.

Rabbits deprived of food for 0, 2, 4, 6, 8, 16, and 24 h were assessed for glucose-induced feeding suppression, refeeding after deprivation, and liver glycogen. In previous research, we hypothesized a relationship between liver glycogen and the transition from duodenal to hepatic glucose suppression. In duodenally cannulated rabbits, the infusion of 10 ml of isotonic glucose in awake, free-feeding animals significantly suppressed food intake but did not do so in those food deprived for 2, 4, 6, 8, or 24 h. In hepatic-cannulated rabbits, similar amounts of glucose significantly suppressed food intake in 4-, 6-, 16-, and 24-h-deprived animals. Also, refeeding after deprivation increased as a function of continued deprivation until 6 or 8 h, when refeeding reached asymptote, or decreased through 24-h deprivations. In agreement with these observations, liver glycogen showed a sharp decline between 4, 6, and 8 h of deprivation (depending on circadian cycle). It is proposed that liver glycogen depletion, or some correlate, alters liver glucostatic regulation and determines refeeding after deprivation.

Animals↗
PubMed2006

Identification of nesfatin-1 as a satiety molecule in the hypothalamus.

The brain hypothalamus contains certain secreted molecules that are important in regulating feeding behaviour. Here we show that nesfatin, corresponding to NEFA/nucleobindin2 (NUCB2), a secreted protein of unknown function, is expressed in the appetite-control hypothalamic nuclei in rats. Intracerebroventricular (i.c.v.) injection of NUCB2 reduces feeding. Rat cerebrospinal fluid contains nesfatin-1, an amino-terminal fragment derived from NUCB2, and its expression is decreased in the hypothalamic paraventricular nucleus under starved conditions. I.c.v. injection of nesfatin-1 decreases food intake in a dose-dependent manner, whereas injection of an antibody neutralizing nesfatin-1 stimulates appetite. In contrast, i.c.v. injection of other possible fragments processed from NUCB2 does not promote satiety, and conversion of NUCB2 to nesfatin-1 is necessary to induce feeding suppression. Chronic i.c.v. injection of nesfatin-1 reduces body weight, whereas rats gain body weight after chronic i.c.v. injection of antisense morpholino oligonucleotide against the gene encoding NUCB2. Nesfatin-1-induced anorexia occurs in Zucker rats with a leptin receptor mutation, and an anti-nesfatin-1 antibody does not block leptin-induced anorexia. In contrast, central injection of alpha-melanocyte-stimulating hormone elevates NUCB2 gene expression in the paraventricular nucleus, and satiety by nesfatin-1 is abolished by an antagonist of the melanocortin-3/4 receptor. We identify nesfatin-1 as a satiety molecule that is associated with melanocortin signalling in the hypothalamus.

Animals↗
PubMed2004

Organic cation transporter 3 (Slc22a3) is implicated in salt-intake regulation.

Organic cation transporters (OCTs) are carrier-type permeases known to participate in general detoxification functions in peripheral tissues. Previous in vitro studies have suggested that OCTs ensure Uptake2, a low-affinity, corticosteroid-sensitive catecholamine removal system, which was characterized initially in sympathetically innervated tissues. Although the presence of both Uptake(2)-like transport and most OCT subtypes has also been demonstrated in the brain, the physiological role of this family of transporters in CNS remained totally unknown. In the present work, we show that the OCT3 transporter is found throughout the brain and highly expressed in regions regulating fluid exchange, including circumventricular organs such as area postrema and subfornical organ (SFO), and in other structures implicated in the sensing of changes in blood osmolarity and regulation of salt and water ingestion. OCT3/Slc22a3-deficient mice show an increase in the level of ingestion of hypertonic saline under thirst and salt appetite conditions, as well as alterations of the neural response in the SFO after sodium deprivation, as monitored by Fos immunoreactivity. This work demonstrates that the presence of OCT3 is critical for the balanced neural and behavioral responses to environmentally induced variations in osmolarity and provides for the first time physiological evidence of the importance of OCTs for CNS function.

Animals↗
PubMed2005

A new anti-obesity drug treatment: first clinical evidence that, antagonising glutamate-gated Ca2+ ion channels with memantine normalises binge-eating disorders.

The regulation of appetite relies on complex hypothalamic neurocircuitry of which the arcuate nucleus, and the hormone leptin play important roles. Arcuate nucleus neurones are essential for the regulation of eating behaviour, but they can be intoxicated by elevated serum levels of the amino acid glutamate (GLU). Neurotoxic effects of GLU are mediated by the N-methyl-D-aspartate receptor (NMDA-R). But the neurotoxic effects of GLU can be prevented. Concurrent administration of dizocilpine maleate (MK-801), a selective and highly potent non-competitive NMDA-R antagonist, antagonises GLU-gated Ca2+ ion channels and completely prevents the adverse effects of GLU. Also the non-competitive NMDA-R antagonist memantine displays neuroprotective properties. In view of a previously published hypothesis that human obesity results from chronic over-consumption of GLU, we performed a therapeutic trial in five obese, but otherwise healthy women. Memantine treatment markedly decreased appetite within few hours and complete suppressed the binge-eating disorder within 24 h. Body weight decreased markedly within a few days. The findings strongly support the hypothesis that elevated levels of nutritional GLU play an important role in the pathomechanism of human obesity. We suggest to treat human obesity by protecting the hypothalamic signalling cascade of leptin action with low to moderate affinity, non-competitive NMDA-R antagonists that selectively block the GLU-gated Ca2+ ion channels.

Adult↗
PubMed1998

What do we most need to learn about food intake regulation?

Many mechanisms are known to contribute to the regulation of food intake. This notwithstanding, variations in food intake from day to day and deviations from daily energy balance are substantial and very readily tolerated. Yet, despite this very loose short-term adjustment of food intake to energy expenditure, most adults maintain stable body compositions during long periods of their lives. This is particularly puzzling when it occurs in the face of an ubiquitous supply of appealing foods and under circumstances that, in many ways, promote food consumption. Thus, the question arises as to why people in affluent societies eat substantially less on most days, than the amounts that they can so readily consume on high-intake days? In addition to conscious decisions, physiological phenomena restraining food consumption must be presumed to play an important role in limiting weight. But what are the phenomena that cause spontaneous reduction in food intake after a few days of overeating? Our ignorance about the nature and impact of these effects stands in the way of a better understanding of body weight regulation and of the factors responsible for the induction and maintenance of obesity.

Appetite↗
PubMed2002

DNA demethylation modulates mouse leptin promoter activity during the differentiation of 3T3-L1 cells.

AIMS/HYPOTHESIS: The mouse leptin gene, a major hormonal regulator of appetite and fat cell mass, expresses during the differentiation of 3T3-L1 preadipocytes to adipocytes. To determine if DNA methylation is involved in regulating the expression of the leptin gene, we examined the methylation status and methylation-sensitive transcription factors during 3T3-L1 differentiation. METHODS: DNase I footprinting, electrophoretic mobility-shift assays, and a Southwestern analysis were carried out using nuclear extracts from preadipocytes and adipocytes. Promoter activity was measured by luciferase assays. The CpG methylation pattern was determined. RESULTS: Transient transfection of reporter constructs with the leptin promoter showed that preadipocytes that do not transcribe the leptin gene show enough transactivation, suggesting the presence of an additional regulatory mechanism. We identified eight CpG sites in the promoter up to nt -161, all of which were highly methylated ( > 92 %) in preadipocytes. Seven of these sites showed a varying degree of demethylation during differentiation, while the site at nt -54 remained methylated. In electrophoretic mobility-shift assays, DNA fragments from nt -115 to nt -70 generated a methylation-sensitive band with nuclear extracts from preadipocytes when the CpG sites were methylated. Southwestern analysis identified a 52 kMr protein that binds strongly to the methylated probes. Promoter activity was reduced by methylation of the CpG sites up to nt -115, but not up to nt -70. CONCLUSION/INTERPRETATION: These results suggest that methylation of specific CpG sites between nt -115 and nt -70 and a methylation-sensitive protein could contribute to leptin gene expression during adipocyte differentiation in 3T3-L1 cells.

3T3 Cells↗
PubMed2005

Inhibitory effects of pituitary adenylate cyclase-activating polypeptide (PACAP) and vasoactive intestinal peptide (VIP) on food intake in the goldfish, Carassius auratus.

Pituitary adenylate cyclase-activating polypeptide (PACAP) has a similar structure to that of vasoactive intestinal peptide (VIP) and both the polypeptides belong to the same molecular group, the secretin-glucagon superfamily. PACAP and VIP have possible potency as hypothalamic factors mediating the release of pituitary hormones in the fish pituitary. However, the roles of PACAP and VIP in the central nervous systems of fish have not yet been made clear. Recently, it was reported that PACAP and/or VIP are involved in the feeding behavior of the mouse and chick. Therefore, we investigated the effects of intracerebroventricular (ICV) and intraperitoneal (IP) administration of synthetic PACAP and VIP on food intake in the goldfish, Carassius auratus. Cumulative food intake was significantly decreased by ICV injection of PACAP (11 or 22 pmol/g body weight) or VIP (11 or 22 pmol/g) during a 60-min observation period after treatment. IP administration of PACAP (44 or 88 pmol/g) or VIP (22 or 44 pmol/g) induced a significant decrease in food intake during a 60-min observation period after treatment. These results suggest that PACAP and VIP may be involved as feeding regulators in goldfish.

Animals↗
PubMed1999

What are the major correlates of macronutrient selection in Western populations?

In order to better understand the factors that may influence and regulate the intake of the macronutrients carbohydrate, fat and protein a 7 d diet diary technique was employed to study eating behaviour in the natural environment of free-living human subjects. In general, factors that promote energy intake tend to promote fat and protein intake to a greater extent than carbohydrate intake. This increased intake occurs as the result of: environmental factors such as social facilitation and the time of day, week or lunar phase; subjective factors such as hunger and elation; individual difference factors such as obesity, restraint and ageing. There are indications that the intake of macronutrients is regulated by negative feedback systems. In the short term, the amount of protein remaining in the stomach at the onset of a meal appears to have a restraining effect on intake, especially protein intake. Over several days, macronutrient intake appears to be affected by a nutrient-specific delayed negative feedback. Protein intake during 1 d is negatively associated with protein intake 2 and 3 d later, while carbohydrate intake is negatively related to later carbohydrate intake, and fat intake to later fat intake; both peaking after a 2 d delay. Studies of the intakes of twins suggested that many aspects of the control of macronutrient intake are influenced by inheritance; these factors include the overall amounts ingested, the before-meal stomach contents and the responsiveness of the subject to the negative impact of the stomach contents. The results indicate that macronutrient intakes are regulated by multiple persistent processes that are to a large extent inherited.

Appetite Regulation↗
PubMed1997

Sodium mercaptoacetate is not a useful probe to study the role of fat in regulation of feed intake in dairy cattle.

Inhibition of fatty acid oxidation by mercaptoacetate stimulates food intake of rats fed dietary fat. To study regulation of feed intake of ruminants fed fat, dry matter intake and plasma concentrations of insulin and metabolites were determined in eight nonpregnant Holstein heifers in a cross-over design with two 14-d feeding periods by using a 2 x 2 factorial arrangement of treatments. Treatments were combinations of diet (27 or 103 g fatty acids/kg food dry matter) and injection (mercaptoacetate or saline). Half the heifers were fed each diet in Period 1, and diets were reversed in Period 2. On d 10 of each period, two animals per treatment were injected intravenously with either mercaptoacetate (300 mumol/kg body weight 0.75) or saline at 2 h postfeeding. Injections were reversed on d 12. Dry matter intake was suppressed by the high fat diet. Intravenous injection of mercaptoacetate decreased dry matter intake to 25% that of the control during 4 h postinjection. Both the high fat diet and mercaptoacetate injection increased plasma non-esterified fatty acid concentration, whereas plasma beta-hydroxybutyrate concentration was lowered by the high fat diet and by mercaptoacetate injection. Plasma triglyceride concentration was increased by the high fat diet, but was decreased by mercaptoacetate injection. Mercaptoacetate elevated plasma glucose concentrations at 2 and 3 h postinjection, possibly because plasma insulin concentration was lower. Effects of mercaptoacetate on plasma insulin and metabolite concentrations may have been confounded by the effects of decreased feed intake. Therefore, direct effects of mercaptoacetate injection were not separated from effects of feed intake on plasma insulin and metabolite concentration. Because mercaptoacetate injection decreased dry matter intake it was not a useful probe to study mechanisms of feed intake regulation in dairy cattle fed fat.

Animals↗
PubMed2005

Fast food, central nervous system insulin resistance, and obesity.

Rates of obesity and insulin resistance have climbed sharply over the past 30 years. These epidemics are temporally related to a dramatic rise in consumption of fast food; until recently, it was not known whether the fast food was driving the obesity, or vice versa. We review the unique properties of fast food that make it the ideal obesigenic foodstuff, and elucidate the mechanisms by which fast food intake contributes to obesity, emphasizing its effects on energy metabolism and on the central regulation of appetite. After examining the epidemiology of fast food consumption, obesity, and insulin resistance, we review insulin's role in the central nervous system's (CNS) regulation of energy balance, and demonstrate the role of CNS insulin resistance as a cause of leptin resistance and in the promotion of the pleasurable or "hedonic" responses to food. Finally, we analyze the characteristics of fast food, including high-energy density, high fat, high fructose, low fiber, and low dairy intake, which favor the development of CNS insulin resistance and obesity.

Animals↗
PubMed2005

Multi-transcriptional profiling of melanin-concentrating hormone and orexin-containing neurons.

1.Melanin-concentrating hormone (MCH) and orexin-containing neurons participate in hypothalamic circuits that control energy homeostasis. While these two systems have projections to widespread target areas within the central nervous system, little is known about intrinsic characteristics and the molecular composition of both the MCH and orexin neurons themselves. 2. By a combinatory approach of quantitative immunocytochemical identification and analysis with laser microdissection and semi-quantitative Real-time RT-PCR, here we present multi-transcriptional profiling of MCH and orexin neurons in the rat lateral hypothalamus. 3. Immunocytochemical analysis showed that orexin peptide expression was increased after fasting both during the activity and resting period of rats, whereas MCH peptide content was only clearly upregulated at resting phase. Subsequent transcriptional profiling showed distinct expression patterns of MCH, orexin and cocaine-amphetamine regulated transcript (CART) between MCH and orexin neurons. A low expression level of dynorphin was found both in MCH and orexin neurons. Receptor expression profiles, reflecting interaction with neuropeptide Y, melanocortins, leptin, glucocorticoids and GABA, showed approximately similar expression patterns among the MCH and orexin neuronal systems. Expression of glutamate- and GABA-markers revealed a possible contributory role of both glutamate and GABA in functional output of MCH and orexin neurons. 4. This method allowed differential screening at mRNA level after immunocytochemical neuron identification and analysis in heterogeneous brain regions, which can further specify functioning of the individual neurons. With respect to MCH and orexin neurons, this study emphasizes that these neurons are targets for stimulatory and inhibitory signals from other brain regions including the arcuate nucleus and the general circulation. Additionally, both glutamate and GABA appear to be involved in MCH and orexin neuronal functioning related to feeding and regulation of the energy balance.

Animals↗