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• W2065272607 abstract "Some C57Bl/6 mice become obese, whereas others remain lean when raised on a high-fat diet. The mechanisms underlying this interindividual susceptibility to diet-induced obesity remain unknown. Because hypothalamus plays a major role in the regulation of body weight, this study was conducted to identify the differences of hypothalamic neuronal activity between diet-induced obese and diet-resistant mice. Using c-fos as a marker, this study showed that diet-induced obese mice significantly increased c-fos-like immunoreactive neurons in the dorsal part of lateral hypothalamus (+183%) and dorsomedial hypothalamic nucleus (+87.5%) compared with diet-resistant mice. Furthermore, switching from high fat to low fat, or high n-3 polyunsaturated fatty acid diet, significantly decreased body weight gain (-35.7% and -31.0%), overall fat storage (-63.4% and -59.6%), and c-fos-like immunoreactive neurons in the dorsal part of lateral hypothalamus (-76.5% and -64.7%) and dorsomedial hypothalamic nucleus (-73.3% and -56.7%) in diet-induced obese mice, respectively. The present study also showed that the ratio of serum leptin/fat mass was threefold higher in the diet-resistant mice than in the diet-induced obese mice, which may be responsible for the less fat storage in the diet-resistant mice. The current data further confirm that the increased neuronal activity in the key autonomic regulatory centers may contribute to the excessive fat storage in diet-induced obese mice. Moreover, both high-fat diet-induced excessive fat storage and the altered hypothalamic neuronal activity may be largely corrected by reducing dietary fat content or replacing it with non-obesogenic fat." @default.
• W2065272607 created "2016-06-24" @default.
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• W2065272607 date "2000-07-01" @default.
• W2065272607 modified "2023-10-13" @default.
• W2065272607 title "Hypothalamic c-fos-like immunoreactivity in high-fat diet-induced obese and resistant mice" @default.
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• W2065272607 doi "https://doi.org/10.1016/s0361-9230(00)00228-8" @default.
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