Hyperthyroidism is characterized in rats by increased energy expenditure and marked hyperphagia.
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Development of obesity was concomitant with hyperphagia, increased food efficiency, and decreased activity.
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Key findings: GPR61-deficient mice exhibited marked hyperphagia and heavier body weight than wild-type mice.
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Calorie-rich diets induce hyperphagia and promote obesity, although the underlying mechanisms remain poorly defined.
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Upon presentation of a calorically dense diet, rats display hyperphagia driven by increased meal size.
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These results may account for the hyperphagia and obesity produced by selective lesions of the V-NA bundle.
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The aggravated obesity of LepRbeKO mice was due to hyperphagia and a higher sensitivity to food reward.
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OLETF rats are hyperphagic with the hyperphagia expressed as a significant increase in the size of meals.
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We characterize PNOCARC neurons as a novel ARC neuron population activated upon palatable food consumption to promote hyperphagia.
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There have been no new cases of postoperative hyperphagia, morbid obesity, or behavioral dysfunction in this prospective cohort.
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OLETF rat obesity is secondary to the hyperphagia and has been proposed to derive from two regulatory deficits.
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The inhibition of early hyperinsulinemia and adult hyperphagia may be associated with decreased metabolic disease risk in these animals.
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However, this deficiency caused neither hyperphagia nor obesity in mice fed on either a standard or a high-fat diet.
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Both the obesity and the hyperphagia of UCP-DTA mice appear to be due to their deficit in BAT thermogenesis.
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Before hibernation many animals experience hyperphagia: increased appetite leading to the laying down of abundant adipose tissue, or fat.
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Mutant males and females developed severe obesity with hyperphagia, impaired thermal regulation in response to cold, hyperleptinemia and insulin resistance.