• Charles V Mobbs, Jason Mastaitis, Kelvin Yen, Joseph Schwartz, Vinuta Mohan, Michal Poplawski, and Fumiko Isoda.
• Mt. Sinai School of Medicine, Department of Neuroscience and Geriatrics, Mt. Sinai School of Medicine, New York, NY 10029, USA. Charles.mobbs@mssm.edu
• Appetite. 2007 Mar 1; 48 (2): 135-8.

AbstractHigh-fat diets produce obesity in part because, per calorie, glucose produces greater post-prandial thermogenesis than lipids, an effect probably mediated by glucose-sensing neurons. A very low-carbohydrate/high-fat/high-protein Atkins-type diet produces obesity but is marginally ketogenic in mice. In contrast, high-sucrose/low-fat diets, and very low-carbohydrate/high-fat/low-protein (anti-epileptic) ketogenic diets reverse diet-induced obesity independent of caloric intake. We propose that a non-ketogenic high-fat diet reduces glucose metabolism and signaling in glucose-sensing neurons, thereby reducing post-prandial thermogenesis, and that a ketogenic high-fat diet does not reduce glucose signaling, thereby preventing and/or reversing obesity.

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