Intracerebroventricular injection of leptin increases thermogenesis and mobilizes fat metabolism in ob/ob mice
Intracerebroventricular injection of leptin increases thermogenesis and mobilizes fat metabolism in ob/ob mice
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DOI：
10.1055/s-2007-979873
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发表时间：
1996-12-01
影响因子：
2.2
通讯作者：
Strader, CD
中科院分区：
文献类型：
--
作者：
Hwa, JJ;Ghibaudi, L;Strader, CD
遗传性肥胖（ob/ob）小鼠表现出许多代谢改变，包括产热减少、摄食过多、高血糖和体脂增加。单次侧脑室（i. c. v.）给这些小鼠注射瘦素（0.01 - 1 μ g）在24小时内降低了食物摄入和体重。此外，i. c. v.管理瘦素增加22小时的能量消耗，同时降低呼吸商（RQ）的剂量依赖性的方式。瘦素诱导的RQ减少表明来自碳水化合物氧化的总能量的分数减少，来自脂肪氧化的能量相应增加。我们的数据表明，瘦素通过激活中枢神经系统（CNS）中调节食物摄入和能量代谢的受体来控制能量稳态。
Genetically obese (ob/ob) mice display a number of metabolic alterations, including decreased thermogenesis, hyperphagia, hyperglycemia and increased body fat. A single intracerebroventricular (i.c.v.) injection of these mice with leptin (0.01 to 1 mu g) lowered food intake and body weight within 24 h. In addition, i.c.v. administration of leptin increased 22 h energy expenditure while reducing the respiratory quotient (RQ) in a dose-dependent manner. The leptin-induced decrease in RQ suggests a reduction in the fraction of total energy derived from carbohydrate oxidation and a corresponding increase in energy derived from fat oxidation. Our data suggest that leptin controls energy homeostasis through activation of receptor(s) in the central nervous system (CNS) that regulate both food intake and energy metabolism.