Reitman M L, Gavrilova O
Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892-1770, USA.
Int J Obes Relat Metab Disord. 2000 Nov;24 Suppl 4:S11-4. doi: 10.1038/sj.ijo.0801493.
The A-ZIP/F-1 mouse is lacking virtually all white adipose tissue. Like humans with extensive deficiencies of adipose tissue, the A-ZIP/F-1 mice develop a severe form of insulin resistant diabetes. We have studied the physiology of the A-ZIP/F-1 mice. Their adaptation to fasting is notable for its rapidity and the use of torpor, a hibernation-like state, to minimize energy needs. Transplantation of adipose tissue reversed the metabolic manifestations in the mice, demonstrating that the lack of adipose tissue is the cause of the insulin resistance. Leptin replacement is not very effective in reversing the diabetes of the A-ZIP/F-1 mice, which contrasts with its efficacy in the aP2-SREBP-lc mouse.
A-ZIP/F-1小鼠几乎没有所有的白色脂肪组织。与脂肪组织严重缺乏的人类一样,A-ZIP/F-1小鼠会发展出严重形式的胰岛素抵抗性糖尿病。我们已经研究了A-ZIP/F-1小鼠的生理学。它们对禁食的适应以其快速性以及利用类似冬眠状态的蛰伏来尽量减少能量需求而著称。脂肪组织移植逆转了小鼠的代谢表现,表明脂肪组织的缺乏是胰岛素抵抗的原因。瘦素替代在逆转A-ZIP/F-1小鼠的糖尿病方面效果不佳,这与其在aP2-SREBP-1c小鼠中的疗效形成对比。