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We developed two different ketogenic diets, which will allow us to understand the mechanisms of ketosis in lean and obese female and male Zucker rats. The obese Zucker rat has a point mutation in the long form of the leptin receptor causing these rats to be refractory to endogenous leptin, hyperinsulinemic, and obese (perhaps analogous to some states of human obesity). Leptin is currently believed to control body composition largely via hypothalamic receptors that regulate food intake and thermogenesis. In this study, 50 lean and obese female Zucker rats and 48 lean and obese male Zucker rats were offered ad libitum three different diets. A high protein (50% casein by calories, 43% hydrogenated fat, 7% polyunsaturated, no carbohydrate ketogenic diet), a high fat (76% hydrogenated fat, 13% polyunsaturated fat, 11% casein, no carbohydrate ketogenic diet), and AIN93-G, a normal rat chow (all diets provided the required vitamins and minerals for normal growth and maintenance for rats). Food intake and body weights were recorded every other day. Animals were placed in respiration chambers where oxygen consumption, carbon dioxide production, and heat production were recorded for 48 hours. There was a statistically significant difference (p |
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