Lee Woo Je, Koh Eun Hee, Won Jong Chul, Kim Min-Seon, Park Joong-Yeol, Lee Ki-Up
Department of Internal Medicine, University of Ulsan College of Medicine, Asan Medical Center, Song-Pa P.O. Box 145, Seoul 138-600, Republic of Korea.
Int J Biochem Cell Biol. 2005 Nov;37(11):2254-9. doi: 10.1016/j.biocel.2005.06.019.
Obesity is rapidly increasing and is of great public health concern worldwide. Although there have been remarkable developments in obesity research over the past 10 years, the molecular mechanism of obesity is still not completely understood. Body weight results from the balance between food intake and energy expenditure. Recent studies have found that hypothalamic AMP-activated protein kinase plays a key role in regulating these processes. Leptin, insulin, glucose and alpha-lipoic acid have been shown to reduce food intake by lowering hypothalamic AMP-activated protein kinase activity, whereas ghrelin and glucose depletion increase food intake by increasing hypothalamic AMP-activated protein kinase activity. In addition, this enzyme plays a role in the central regulation of energy expenditure. These findings indicate that hypothalamic AMP-activated protein kinase is an important signal molecule, which integrates nutritional and hormonal signals and modulates feeding behavior and energy expenditure.
肥胖症正在迅速增加，是全球范围内重大的公共卫生问题。尽管在过去十年里肥胖症研究取得了显著进展，但肥胖症的分子机制仍未完全明确。体重取决于食物摄入与能量消耗之间的平衡。最近的研究发现，下丘脑AMP激活的蛋白激酶在调节这些过程中起关键作用。已证实，瘦素、胰岛素、葡萄糖和α-硫辛酸通过降低下丘脑AMP激活的蛋白激酶活性来减少食物摄入，而胃饥饿素和葡萄糖耗竭则通过增加下丘脑AMP激活的蛋白激酶活性来增加食物摄入。此外，这种酶在能量消耗的中枢调节中发挥作用。这些发现表明，下丘脑AMP激活的蛋白激酶是一个重要的信号分子，它整合营养和激素信号并调节进食行为和能量消耗。
