Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Revital , a product containing 19 amino acids, was applied to experimental deep second degree burns in guinea-pigs for 24 days, in order to assess the effect of this form of hyperalimentation on the healing process. Silver sulphadiazine cream served as the contralateral control standard. Epithelialization was faster in the silver sulphadiazine treated burn wounds, while contraction of both tested wounds proceeded at a similar rate. Revital significantly enhanced the formation of granulation and scar tissue in this burn wound model. These observations indicate that topical wound hyperalimentation promotes granulation tissue formation of experimental deep second degree burns in guinea-pigs.
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PMID:The effect of topical hyperalimentation on wound healing rate and granulation tissue formation of experimental deep second degree burns in guinea-pigs. 671 39

Previous studies have shown that lesions of the posterodorsal amygdala result in hyperphagia and obesity in female rats. In the present study, lesions of the stria terminalis at its most dorsal point (before it separates into dorsal and ventral components) also resulted in hyperphagia and excessive weight gains in female rats compared to female rats with sham lesions, as did coronal knife cuts anterior to the ventromedial hypothalamus. Identical lesions and knife cuts did not elevate food intake or weight gains in male rats compared to male control animals. Examination of the anterograde degeneration with the amino-cupric-silver method in the brains of two female rats with hypothalamic knife cuts revealed degenerating terminals in the capsule of the ventromedial hypothalamus and in the premammillary nuclei, two classic indicators of damage to the dorsal component of the stria terminalis. No degenerating axon terminals were observed in the paraventricular nucleus. Differences from previous studies that used male rats were attributed to a sex difference for the effects of amygdaloid and ventromedial hypothalamic lesions. It is proposed that the posterodorsal amygdala, dorsal component of the stria terminalis, and ventromedial hypothalamus are part of an inhibitory pathway in the regulation of feeding behavior.
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PMID:Role of the stria terminalis in food intake and body weight in rats. 1684 29

The most prevalent disordered eating pattern described in overweight youth is loss of control (LOC) eating, during which individuals experience an inability to control the type or amount of food they consume. LOC eating is associated cross-sectionally with greater adiposity in children and adolescents and seems to predispose youth to gain weight or body fat above that expected during normal growth, thus likely contributing to obesity in susceptible individuals. No prior studies have examined whether LOC eating can be decreased by interventions in children or adolescents without full-syndrome eating disorders or whether programs reducing LOC eating prevent inappropriate weight gain attributable to LOC eating. Interpersonal psychotherapy, a form of therapy that was designed to treat depression and has been adapted for the treatment of eating disorders, has shown efficacy in reducing binge eating episodes and inducing weight stabilization among adults diagnosed with binge eating disorder. In this paper, we propose a theoretical model of excessive weight gain in adolescents at high risk for adult obesity who engage in LOC eating and associated overeating patterns. A rationale is provided for interpersonal psychotherapy as an intervention to slow the trajectory of weight gain in at-risk youth, with the aim of preventing or ameliorating obesity in adulthood.
Obesity (Silver Spring) 2007 Jun
PMID:Preventing excessive weight gain in adolescents: interpersonal psychotherapy for binge eating. 1755 71

The administration of antipsychotic drugs to human patients or experimental animals leads to significant weight gain, which is widely presumed to be driven by hyperphagia; however, the contribution from energy expenditure remains unclear. These studies aim to examine the contribution of shifts in energy expenditure, particularly those involving centrally mediated changes in thermogenesis, to the body weight gain associated with the administration of olanzapine to female Sprague Dawley rats. Olanzapine (6 mg/kg/day orally) caused a transient increase in food intake but a maintained increase in body weight. When pair-fed rats were treated with olanzapine, body weight continued to rise compared to vehicle-treated rats, consistent with a reduction in energy expenditure. Brown adipose tissue (BAT) temperature, measured using biotelemetry devices, decreased immediately after the onset of olanzapine treatment and remained depressed, as did physical activity. UCP1 expression in interscapular BAT was reduced following chronic olanzapine treatment. An acute injection of olanzapine was preceded by an injection of a retrograde tracer into the spinal cord to evaluate the nature of the olanzapine-activated neural pathway. Levels of Fos protein in a number of spinally projecting neurons within discrete hypothalamic and brainstem sites were elevated in olanzapine-treated rats. Some of these neurons in the perifornical region of the lateral hypothalamus (LHA) were also Orexin A positive. These data collectively show a significant impact of thermogenesis (and physical activity) on the weight gain associated with olanzapine treatment. The anatomical studies provide an insight into the central neuroanatomical substrate that may subserve the altered thermogenic responses brought about by olanzapine.
Obesity (Silver Spring) 2009 Jan
PMID:The role of thermogenesis in antipsychotic drug-induced weight gain. 1910 24

Oxytocin (Oxt) is secreted both peripherally and centrally and is involved in several functions including parturition, milk let-down reflex, social behavior, and food intake. Recently, it has been shown that mice deficient in Oxt receptor develop late-onset obesity. In this study, we characterized a murin model deficient in Oxt peptide (Oxt(-/-)) to evaluate food intake and body weight, glucose tolerance and insulin tolerance, leptin and adrenaline levels. We found that Oxt(-/-) mice develop late-onset obesity and hyperleptinemia without any alterations in food intake in addition to having a decreased insulin sensitivity and glucose intolerance. The lack of Oxt in our murin model also results in lower adrenalin levels which led us to hypothesize that the metabolic changes observed are associated with a decreased sympathetic nervous tone. It has been shown that Oxt neurons in the paraventricular nucleus (PVN) are a component of a leptin-sensitive signaling circuit between the hypothalamus and caudal brain stem for the regulation of food intake and energy homeostasis. Nevertheless, the lack of Oxt in these mice does not have a direct impact on feeding behavior whose regulation is probably dependent on the complex interplay of several factors. The lack of hyperphagia evident in the Oxt(-/-) mice may, in part, be attributed to the developmental compensation of other satiety factors such as cholecystokinin or bombesin-related peptides which merits further investigation. These findings identify Oxt as an important central regulator of energy homeostasis.
Obesity (Silver Spring) 2009 May
PMID:Low sympathetic tone and obese phenotype in oxytocin-deficient mice. 1924 73

Maternal obesity due to long-term high-fat diet (HFD) consumption leads to faster growth in offspring during suckling, and increased adiposity at 20 days of age. Decreased expression of the orexigenic neuropeptide Y (NPY) and increased anorexigenic proopiomelanocortin (POMC) mRNA expression were observed in the fed state. However, hunger is the major drive to eat and hypothalamic appetite regulators change in response to meals. Therefore, it is important to compare both satiated and fasting states. Female Sprague-Dawley rats (8 weeks old) were fed a cafeteria-style HFD (15.33 kJ/g) or chow for 5 weeks before mating, with the same diet continuing throughout gestation and lactation. At postnatal day 20, male pups were killed either after overnight fasting or in the fed state. Pups from obese dams were hyperphagic during both pre- and postweaning periods. Pups from obese dams had higher hypothalamic mRNA expression of POMC and NPY Y1 receptor, but lower hypothalamic melanocortin-4 receptor (MC4R) and its downstream target single-minded gene 1 (Sim1), in the fed state. Overnight fasting reduced circulating glucose, insulin, and leptin and increased hypothalamic NPY Y1 receptor mRNA in pups from both lean and obese dams. Hypothalamic NPY and agouti-related protein (AgRP) were only increased by fasting in pups from obese dams; reductions in MC4R and Sim1 were only seen in pups from lean dams. At weaning, the suppressed orexigenic signals in offspring from obese dams were normalized after overnight fasting, although anorexigenic signaling appeared impaired in these animals. This may contribute to their hyperphagia and faster growth.
Obesity (Silver Spring) 2009 Jul
PMID:Differential responses of orexigenic neuropeptides to fasting in offspring of obese mothers. 1928 28

To constitute a valuable resource to identify individual genes involved in the development of obesity, a novel mouse model, the Berlin Fat Mouse Inbred line 860 (BFMI860), was established. In order to characterize energy intake and energy expenditure in obese BFMI860 mice, we performed two independent sets of experiments in male BFMI860 and B6 control mice (10 per line). In experiment 1, we analyzed body fat content noninvasively by dual-energy X-ray absorptiometry and measured resting metabolic rate at thermoneutrality (RMRt) and respiratory quotient (RQ) in week 6, 10, and 18. In a second experiment, energy digested (energy intake minus fecal energy loss) was determined by bomb calorimetry from week 6 through week 12. BFMI860 mice were heavier and had higher fat mass (final body fat content was 24.7% compared with 14.6% in B6). They also showed fatty liver syndrome. High body fat accumulation in BFMI860 mice was restricted to weeks 6-10 and was accompanied by hyperphagia, higher energy digestion, higher RQs, and abnormally high blood triglyceride levels. Lean mass-adjusted RMRt was not altered between lines. These results indicate that in BFMI860 mice, the excessive accumulation of body fat is associated with altered lipid metabolism, high energy intake, and energy digestion. Assuming that BFMI860 mice and their obese phenotypes are of polygenic nature, this line is an excellent model for the study of obesity in humans, especially for juvenile obesity and hyperlipidemia.
Obesity (Silver Spring) 2009 Nov
PMID:High energy digestion efficiency and altered lipid metabolism contribute to obesity in BFMI mice. 1939 May 16

N-oleoylethanolamine (OEA) and N-palmitoylethanolamine (PEA) are endogenous lipids that activate peroxisome proliferator-activated receptor-alpha with high and intermediate potency, and exert anorectic and anti-inflammatory actions in rats, respectively. We investigated OEA and PEA tissue level regulation by the nutritional status in lean and obese rats. OEA and PEA levels in the brainstem, duodenum, liver, pancreas, and visceral (VAT) or subcutaneous (SAT) adipose tissues of 7-week-old wild-type (WT) and Zucker rats, fed ad libitum or following overnight food deprivation, with and without refeeding, were measured by liquid chromatography-mass spectrometry. In WT rats, duodenal OEA, but not PEA, levels were reduced by food deprivation and restored by refeeding, whereas the opposite was observed for OEA in the pancreas, and for both mediators in the liver and SAT. In ad lib fed Zucker rats, PEA and OEA levels were up to tenfold higher in the duodenum, slightly higher in the brainstem, and lower in the other tissues. Fasting/refeeding-induced changes in OEA levels were maintained in the duodenum, liver, and SAT, and lost in the pancreas, whereas fasting upregulated this compound also in the VAT. The observed changes in OEA levels in WT rats are relevant to the actions of this mediator on satiety, hepatic and adipocyte metabolism, and insulin release. OEA dysregulation in Zucker rats might counteract hyperphagia in the duodenum, but contribute to hyperinsulinemia in the pancreas, and to fat accumulation in adipose tissues and liver. Changes in PEA levels might be relevant to the inflammatory state of Zucker rats.
Obesity (Silver Spring) 2010 Jan
PMID:Basal and fasting/refeeding-regulated tissue levels of endogenous PPAR-alpha ligands in Zucker rats. 1952 49

Increasing neuropeptide Y (NPY) signaling in the paraventricular nucleus (PVN) by recombinant adeno-associated virus (rAAV)-mediated overexpression of NPY in rats, results in hyperphagia and obesity in rats. To determine the importance of hyperphagia in the observed obesity phenotype, we pair-fed a group of AAV-NPY-injected rats to AAV-control-injected rats and compared parameters of energy balance to ad libitum fed AAV-NPY-injected rats. For 3 weeks, AAV-NPY-injected rats, received the same amount of food as ad libitum-fed rats injected with control rAAV They did not gain more body weight than these controls. When allowed access to food ad libitum, these AAV-NPY-injected rats increased food intake, which subsequently decreased when rats reached the same body weight as AAV-NPY-injected rats that were fed ad libitum for the entire study. These data indicate that overexpression of NPY in the PVN results in obesity by increasing food intake until a certain body weight is achieved.
Obesity (Silver Spring) 2009 Jul
PMID:Sustained NPY overexpression in the PVN results in obesity via temporarily increasing food intake. 1955 28

One out of three adults in the United States is clinically obese. Excess food intake is associated with food motivation, which has been found to be higher in obese compared to healthy weight (HW) individuals. Little is known, however, regarding the neural mechanisms associated with food motivation in obese compared to HW adults. The current study used functional magnetic resonance imaging (fMRI) to examine changes in the hemodynamic response in obese and HW adults while they viewed food and nonfood images in premeal and postmeal states. During the premeal condition, obese participants showed increased activation, compared to HW participants, in anterior cingulate cortex (ACC) and medial prefrontal cortex (MPFC). Moreover, in the obese group, self-report measures of disinhibition were negatively correlated with premeal ACC activations and self-report measures of hunger were positively correlated with premeal MPFC activations. During the postmeal condition, obese participants also showed greater activation than HW participants in the MPFC. These results indicate that brain function associated with food motivation differs in obese and HW adults and may have implications for understanding brain mechanisms contributing to overeating and obesity, and variability in response to diet interventions.
Obesity (Silver Spring) 2010 Feb
PMID:Neural mechanisms associated with food motivation in obese and healthy weight adults. 1962 52


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