Effects of leptin on mitochondrial 'proton leak' and uncoupling proteins: implications for mammalian energy metabolism

摘要

Since the discovery of the ob gene (Zhang et al. 1994), much research has focused on its product leptin and its role in energy balance and metabolism (Campfield et al. 1996; Caro et al. 1996; Trayhurn, 1996; Flier, 1997; Lonnqvist & Schalling, 1997). The leptin gene is expressed in white adipose tissue (WAT; and brown adipose tissue (BAT)) under conditions when high energy surplus leads to triacylglycerol accumulation (Zhang et al. 1994; Trayhurn, 1996). Such conditions include obesity, feeding, increased glucose and insulin concentrations, and also administration of cytokines and endotoxins. Conversely, leptin expression is decreased by weight reduction, fasting, cold exposure and #beta#_3-receptor agonists, thiazolidinediones, and in insulin-dependent diabetes (Lonnqvist & Schalling, 1997). Leptin administration to ob/ob mice reduces appetite, increases metabolic rate and decreases fat mass (Pelleymounter et al. 1995; Hwa et al. 1997).