The initial characterization of SSAT-overexpressing mice revealed, in addition to hairlessness, practically a total lack of subcutaneous fat depots (7). Subsequently, we found that these animals also lacked visceral fat depots and thus were severely lipo-atrophic. In contrast to other lipoatrophic mouse models, SSAT transgenics did not show any triglyceride accumulation in nonadipose tissues and they fully retained insulin sensitivity (21). On fasting, the transgenic animals showed severely impaired ketogenesis, very low plasma leptin level, and significantly reduced triglyceride, glucose, and insulin levels. The transgenic animals also exhibited significantly elevated basal metabolic rate in comparison with the wild-type animals, indicating a greater expenditure of energy (21). It thus appears that generalized SSAT overexpression causes lipoatrophy, but also protects the animals from the accumulation of fats in nonadipose tissues, insulin resistance, and lipoatrophic diabetes.
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