Yingzhong Yang, Droma Yunden, Rili Ge, Kubo Keishi
The Research Center for High Altitude Medicine, Qinghai University.
Intern Med. 2006;45(16):941-6. doi: 10.2169/internalmedicine.45.1733. Epub 2006 Sep 15.
Since first cloned and reported by Zhang et al in 1994 (Nature 372:425), the obese gene and its product-leptin has been studied profoundly. Our knowledge in body weight regulation and the role played by leptin has increased substantially. Leptin serves as an adiposity signal to inform the brain of the adipose tissue mass in a negative feedback loop regulating food intake and energy expenditure. Many articles have reported weight loss at high altitude, but the explanation has been limited to loss of appetite. New ideas were highlighted after studies by Grosfeld et al and Ambrosini et al on the obese gene under hypoxia condition. Cells with hypoxia treatment upregulated obese gene transcription and suggested that enhancement of leptin secretion in vivo under hypoxia environment may be one of the potential therapeutic methods for obesity treatment.
自1994年张等人首次克隆并报道（《自然》372:425）以来，肥胖基因及其产物瘦素得到了深入研究。我们对体重调节以及瘦素所起作用的认识有了大幅提高。瘦素作为一种肥胖信号，通过负反馈回路向大脑传递脂肪组织量的信息，从而调节食物摄入和能量消耗。许多文章报道了在高海拔地区体重减轻的情况，但其解释仅限于食欲不振。在格罗斯费尔德等人和安布罗西尼等人对缺氧条件下肥胖基因的研究之后，新的观点被凸显出来。经过缺氧处理的细胞上调了肥胖基因转录，这表明在缺氧环境下增强体内瘦素分泌可能是治疗肥胖症的潜在方法之一。
