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Hyperthyroidism is characterized in rats by increased energy expenditure and marked hyperphagia.
2
Development of obesity was concomitant with hyperphagia, increased food efficiency, and decreased activity.
3
Key findings: GPR61-deficient mice exhibited marked hyperphagia and heavier body weight than wild-type mice.
4
Calorie-rich diets induce hyperphagia and promote obesity, although the underlying mechanisms remain poorly defined.
5
Upon presentation of a calorically dense diet, rats display hyperphagia driven by increased meal size.
6
These results may account for the hyperphagia and obesity produced by selective lesions of the V-NA bundle.
7
The aggravated obesity of LepRbeKO mice was due to hyperphagia and a higher sensitivity to food reward.
8
OLETF rats are hyperphagic with the hyperphagia expressed as a significant increase in the size of meals.
9
We characterize PNOCARC neurons as a novel ARC neuron population activated upon palatable food consumption to promote hyperphagia.
10
There have been no new cases of postoperative hyperphagia, morbid obesity, or behavioral dysfunction in this prospective cohort.
11
OLETF rat obesity is secondary to the hyperphagia and has been proposed to derive from two regulatory deficits.
12
The inhibition of early hyperinsulinemia and adult hyperphagia may be associated with decreased metabolic disease risk in these animals.
13
However, this deficiency caused neither hyperphagia nor obesity in mice fed on either a standard or a high-fat diet.
14
Both the obesity and the hyperphagia of UCP-DTA mice appear to be due to their deficit in BAT thermogenesis.
15
Before hibernation many animals experience hyperphagia: increased appetite leading to the laying down of abundant adipose tissue, or fat.
16
Mutant males and females developed severe obesity with hyperphagia, impaired thermal regulation in response to cold, hyperleptinemia and insulin resistance.