Shimada M, Ishibashi S, Yamamoto K, Kawamura M, Watanabe Y, Gotoda T, Harada K, Inaba T, Ohsuga J, Yazaki Y
Third Department of Internal Medicine, University of Tokyo, Japan.
Biochem Biophys Res Commun. 1995 Jun 26;211(3):761-6. doi: 10.1006/bbrc.1995.1878.
An elevation of lipoprotein lipase (LPL) activity in adipose tissue is considered a possible cause of obesity. However, transgenic mice that overexpress the human LPL gene showed no increase in fat deposition as compared with controls. In the present study, we investigated effects of LPL on fat accumulation. Respiratory quotients and uptake of [3H] triolein by tissues (white and brown adipose tissue, and skeletal muscles) did not differ significantly for transgenic and non-transgenic mice. The mRNA levels of hormone-sensitive lipase (HSL) and HSL activity in adipose tissue during feeding were higher in LPL transgenic mice than in controls. Results suggest that the overexpression of LPL does not induce obesity by enhancing the hydrolysis of triglycerides in adipose tissue.
脂肪组织中脂蛋白脂肪酶（LPL）活性升高被认为是肥胖的一个可能原因。然而，与对照组相比，过度表达人LPL基因的转基因小鼠脂肪沉积并未增加。在本研究中，我们调查了LPL对脂肪积累的影响。转基因小鼠和非转基因小鼠的呼吸商以及组织（白色和棕色脂肪组织以及骨骼肌）对[3H]甘油三油酸酯的摄取没有显著差异。喂食期间，LPL转基因小鼠脂肪组织中激素敏感性脂肪酶（HSL）的mRNA水平和HSL活性高于对照组。结果表明，LPL的过度表达不会通过增强脂肪组织中甘油三酯的水解来诱发肥胖。
