Poehlman E T, Després J P, Marcotte M, Tremblay A, Thériault G, Bouchard C
Am J Physiol. 1986 Apr;250(4 Pt 1):E480-5. doi: 10.1152/ajpendo.1986.250.4.E480.
The present study investigated the interaction of genotype and short-term overfeeding on adipose tissue metabolism of six pairs of male monozygotic twins. The sedentary nonobese twins were submitted to a 22-day overfeeding period in which their normal daily intake was supplemented by an additional 1,000 kcal/day. A fat tissue biopsy was performed in the suprailiac region before and after overfeeding to determine fat cell diameter and basal and maximal stimulated epinephrine, norepinephrine, and isoproterenol lipolysis from collagenase-isolated fat cells. Fat cell basal and maximal insulin-stimulated glucose conversion into triglycerides (basal and stimulated lipogenesis) were measured using [14C]glucose. Adipose tissue heparin-releasable lipoprotein lipase activity (LPL) was also determined. A repeated measures analysis of variance revealed overfeeding induced significant elevations in basal lipogenesis (P less than 0.05) and fat cell diameter (P less than 0.05). No significant group changes were noted in basal, epinephrine-, norepinephrine-, and isoproterenol-stimulated lipolysis, insulin-stimulated lipogenesis, and LPL activity due to large individual variation in the response to overfeeding. However, significant intrapair resemblance was noted in the changes of the aforementioned variables, suggesting a coherent within-twin pair response, despite large between-pair variation in response. Less within-pair similarity was noted in changes in basal lipogenesis and fat cell diameter. The results of the present study suggest that overfeeding induced a large range of adipose tissue metabolic responses and that the genotype plays a role in determining the sensitivity of adipose tissue adaptation to caloric affluence.
本研究调查了六对男性同卵双胞胎的基因型与短期过量进食对脂肪组织代谢的相互作用。久坐不动的非肥胖双胞胎接受了为期22天的过量进食期,在此期间,他们的正常每日摄入量额外增加1000千卡/天。在过量进食前后,在髂上区域进行脂肪组织活检,以确定脂肪细胞直径以及胶原酶分离的脂肪细胞的基础和最大刺激肾上腺素、去甲肾上腺素和异丙肾上腺素的脂解作用。使用[14C]葡萄糖测量脂肪细胞基础和最大胰岛素刺激的葡萄糖转化为甘油三酯(基础和刺激的脂肪生成)。还测定了脂肪组织肝素可释放脂蛋白脂肪酶活性(LPL)。重复测量方差分析显示,过量进食导致基础脂肪生成(P<0.05)和脂肪细胞直径(P<0.05)显著升高。由于对过量进食的反应存在较大个体差异,基础、肾上腺素、去甲肾上腺素和异丙肾上腺素刺激的脂解作用、胰岛素刺激的脂肪生成和LPL活性未观察到显著的组间变化。然而,上述变量的变化存在显著的同对内相似性,表明尽管双胞胎对之间的反应存在较大差异,但同卵双胞胎对之间的反应是一致的。基础脂肪生成和脂肪细胞直径变化的同对内相似性较低。本研究结果表明,过量进食会引发一系列广泛的脂肪组织代谢反应,并且基因型在决定脂肪组织对热量充裕的适应敏感性方面发挥作用。