hyperphagia/obezitate

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Early hypothalamic FTO overexpression in response to maternal obesity--potential contribution to postweaning hyperphagia.

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BACKGROUND Intrauterine and postnatal overnutrition program hyperphagia, adiposity and glucose intolerance in offspring. Single-nucleotide polymorphisms (SNPs) of the fat mass and obesity associated (FTO) gene have been linked to increased risk of obesity. FTO is highly expressed in hypothalamic

Overeating phenotypes in overweight and obese children.

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The purpose of this study was to identify overeating phenotypes and their correlates in overweight and obese children. One hundred and seventeen treatment-seeking overweight and obese 8-12year-old children and their parents completed the study. Children completed an eating in the absence of hunger

Low-protein diet blocks development of hyperphagia and obesity in rats with hypothalamic knife cuts.

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The objective of this study was to examine the influence of dietary protein levels on development of hyperphagia and obesity in rats that had been given surgical knife cuts between the ventromedial and lateral areas of the hypothalamus. Under normal conditions, rats with this type of surgery exhibit

Putative neuropeptide Y antagonist failed to decrease overeating in obese Zucker rats.

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A central dysregulation of several neuropeptides could be at the origin of the marked hyperphagia of the obese Zucker rat, a well-known animal model used for the study of obesity. Neuropeptide Y (NPY), which stimulates food intake and increases early in life in obese rats, plays a major role in the

A novel form of ciliopathy underlies hyperphagia and obesity in Ankrd26 knockout mice.

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Human ciliopathies are genetic disorders caused by mutations in genes responsible for the formation and function of primary cilia. Some are associated with hyperphagia and obesity (e.g., Bardet-Biedl Syndrome, Alström Syndrome), but the mechanisms underlying these problems are not fully understood.

Diet-induced obesity attenuates fasting-induced hyperphagia.

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Obesity impairs arcuate (ARC) neuropeptide Y (NPY)/agouti-releated peptide (AgRP) neuronal function and renders these homeostatic neurones unresponsive to the orexigenic hormone ghrelin. In the present study, we investigated the effect of diet-induced obesity (DIO) on feeding behaviour, ARC neuronal

The role of hyperphagia and hypothyroidism in the development of the obese-hyperglycemic syndrome in mice (ob/ob).

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Obese-hyperglycemic mice show hyperphagia and hypothyroidism. The reduced body temperature can be normalized by injection of thyroxin. Limiting food intake to normal non-obese levels reduces blood sugar level, insulin content of the blood and body weight. However, reduction of all these parameters

Raising at thermoneutrality prevents obesity and hyperphagia in BAT-ablated transgenic mice.

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Transgenic mice with ablation of brown adipocytes induced by brown adipocyte-specific expression of diphtheria toxin A chain (DTA) driven by the uncoupling protein (UCP) promoter (UCP-DTA mice) become obese and hyperphagic (Lowell, B. B., V. S. Susulic, A. Hamann, J. A. Lawitts, J. Himms-Hagen, B.

Individual severity of dietary obesity in unselected Wistar rats: relationship with hyperphagia.

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We investigated the relative importance of overeating, thermogenesis, and uncoupling protein (UCP) expression in determining the severity of obesity in male Wistar rats fed a highly palatable diet. After 2 wk of feeding, body weight did not differ significantly from controls (248 +/- 4 vs. 229 +/- 3

Massive obesity and hyperphagia in posterior bilateral periventricular heterotopias: case report.

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BACKGROUND Bilateral posterior periventricular nodular heterotopia PNH is a complex malformation of cortical development with imaging features distinguishing it from classic bilateral PNH associated with filamin (FLNA) mutations. It distinctively consists of variably sized nodules of neurons along

Effect of factors besides hyperphagia on cellularity of adipose tissue in gold thioglucose-induced obese mice.

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Whether or not factors besides hyperphagia influence cellularity of adipose tissue in gold thioglucose (GTG)-treated mice was examined. The animals were treated with GTG (800 mg/kg body weight) or saline as control. Control and one of the GTG-treated groups were given a diet ad libitum and another

Can we apply the dual-pathway model of overeating to a population of weight-preoccupied overweight women?

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OBJECTIVE The aim of the study is to verify the applicability of the dual-pathway model among weight-preoccupied overweight women and to document the restraint pathway, the negative affect pathway, and the possibility of a direct pathway from body dissatisfaction to overeating. METHODS Structural

Robust Reductions of Excess Weight and Hyperphagia by Beloranib in Rat Models of Genetic and Hypothalamic Obesity.

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Hypothalamic lesions or deficient melanocortin (MC) signaling via MC4 receptor (MC4r) mutations often lead to hyperphagia and severe treatment-resistant obesity. We tested the methionine aminopeptidase 2-inhibitor beloranib (ZGN-440) in 2 male rat models of obesity, one modeling hypothalamic obesity

Stress-induced hyperphagia and obesity in rats: a possible model for understanding human obesity.

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Mild tail pinch administered to rats several times daily in the presence of sweetened mild induced immediate hyperphagia and led to considerable gain in body weight. Parallels are drawn with stress-induced hyperhagia and altered affective states in obese humans.

Hypothalamic hyperphagia and obesity in rats with jejunoileal bypass.

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Jejunoileal bypass or sham surgery was performed in adult female rats followed 35 days later by ventromedial hypothalamic (VMH) knife cut or sham surgery (forming groups Bypass-VMH, Bypass-Sham, Sham-VMH, and Sham-Sham). Bypassed rats receiving VMH cuts (Bypass-VMH group) ate more food and gained

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