Fisher M H, Amend A M, Bach T J, Barker J M, Brady E J, Candelore M R, Carroll D, Cascieri M A, Chiu S H, Deng L, Forrest M J, Hegarty-Friscino B, Guan X M, Hom G J, Hutchins J E, Kelly L J, Mathvink R J, Metzger J M, Miller R R, Ok H O, Parmee E R, Saperstein R, Strader C D, Stearns R A, MacIntyre D E
Department of Medicinal Chemistry, Merck Research Laboratories, Rahway, New Jersey 07065, USA.
J Clin Invest. 1998 Jun 1;101(11):2387-93. doi: 10.1172/JCI2496.
Activation of beta3 adrenergic receptors on the surface of adipocytes leads to increases in intracellular cAMP and stimulation of lipolysis. In brown adipose tissue, this serves to up-regulate and activate the mitochondrial uncoupling protein 1, which mediates a proton conductance pathway that uncouples oxidative phosphorylation, leading to a net increase in energy expenditure. While chronic treatment with beta3 agonists in nonprimate species leads to uncoupling protein 1 up-regulation and weight loss, the relevance of this mechanism to energy metabolism in primates, which have much lower levels of brown adipose tissue, has been questioned. With the discovery of L-755,507, a potent and selective partial agonist for both human and rhesus beta3 receptors, we now demonstrate that acute exposure of rhesus monkeys to a beta3 agonist elicits lipolysis and metabolic rate elevation, and that chronic exposure increases uncoupling protein 1 expression in rhesus brown adipose tissue. These data suggest a role for beta3 agonists in the treatment of human obesity.
脂肪细胞表面β3肾上腺素能受体的激活会导致细胞内cAMP增加并刺激脂肪分解。在棕色脂肪组织中,这有助于上调并激活线粒体解偶联蛋白1,该蛋白介导质子传导途径,使氧化磷酸化解偶联,从而导致能量消耗净增加。虽然在非灵长类动物中用β3激动剂进行长期治疗会导致解偶联蛋白1上调和体重减轻,但这种机制与棕色脂肪组织水平低得多的灵长类动物能量代谢的相关性受到了质疑。随着L-755,507(一种对人和恒河猴β3受体均有效的选择性部分激动剂)的发现,我们现在证明恒河猴急性暴露于β3激动剂会引发脂肪分解和代谢率升高,而长期暴露会增加恒河猴棕色脂肪组织中解偶联蛋白1的表达。这些数据表明β3激动剂在治疗人类肥胖症中具有作用。