Harris R B, Martin R J
Department of Foods and Nutrition, University of Georgia, Athens 30602.
Am J Physiol. 1990 Jul;259(1 Pt 2):R45-52. doi: 10.1152/ajpregu.1990.259.1.R45.
Obesity due to overfeeding in one parabiotic rat results in mild hypophagia and specific loss of fat from its partner. Studies were conducted to determine whether the changes in body composition were reversible and whether the nonsignificant reduction in food intake was a primary response to a humoral lipostatic factor. Tube feeding partners of overfed rats 0.5 g more food per day than eaten voluntarily prevented loss of fat, although hepatic and adipose glucose-6-phosphate dehydrogenase activities were depressed. Glucose flux through the pentose phosphate pathway was inhibited in both adipose and hepatic tissue from thin partners of obese rats, although fatty acid synthesis was depressed only in adipose tissue. Response to insulin by adipocytes from ad libitum partners of obese rats appeared to be blunted, but insulin sensitivity was normal. When overfeeding stopped, both partners returned to control body composition, suggesting that the changes observed in parabiotic partners of obese rats were physiological responses to a putative circulating lipostatic factor rather than a nonspecific consequence of parabiosis.
联体大鼠中一只因过度喂食而肥胖，会导致其轻度食欲减退，且其伙伴会出现特定的脂肪流失。开展了多项研究以确定身体成分的变化是否可逆，以及食物摄入量的轻微减少是否是对体液性脂肪稳态因子的主要反应。给过度喂食大鼠的联体伙伴每天通过管饲多提供0.5克食物（超过其自愿进食量），可防止脂肪流失，尽管肝脏和脂肪组织中的葡萄糖-6-磷酸脱氢酶活性受到抑制。肥胖大鼠瘦伙伴的脂肪组织和肝脏组织中，通过磷酸戊糖途径的葡萄糖通量均受到抑制，不过脂肪酸合成仅在脂肪组织中受到抑制。肥胖大鼠自由进食伙伴的脂肪细胞对胰岛素的反应似乎减弱，但胰岛素敏感性正常。当停止过度喂食后，两个伙伴的身体成分都恢复到对照水平，这表明在肥胖大鼠联体伙伴中观察到的变化是对一种假定的循环脂肪稳态因子的生理反应，而非联体的非特异性后果。
