Salans L B, Bray G A, Cushman S W, Danforth E, Glennon J A, Horton E S, Sims E A
J Clin Invest. 1974 Mar;53(3):848-56. doi: 10.1172/JCI107625.
[1-(14)C]glucose oxidation to CO(2) and conversion into glyceride by adipose tissue from nonobese and obese subjects has been studied in vitro in the presence of varying medium glucose and insulin concentrations as functions of adipose cell size, the composition of the diet, and antecedent weight gain or loss. Increasing medium glucose concentrations enhance the incorporation of glucose carbons by human adipose tissue into CO(2) and glyceride-glycerol. Insulin further stimulates the conversion of glucose carbons into CO(2), but not into glyceride-glycerol. Incorporation of [1-(14)C]glucose into glyceride-fatty acids by these tissues could not be demonstrated under any of the conditions tested. Both adipose cell size and dietary composition influence the in vitro metabolism of glucose in, and the response to insulin by, human adipose tissue. During periods of ingestion of weight-maintenance isocaloric diets of similar carbohydrate, fat, and protein composition, increasing adipose cell size is associated with (a) unchanging rates of glucose oxidation and increasing rates of glucose carbon incorporation into glyceride-glycerol in the absence of insulin, but (b) decreasing stimulation of glucose oxidation by insulin. On the other hand, when cell size is kept constant, increasing dietary carbohydrate intake is associated with an increased basal rate of glucose metabolism and response to insulin by both small and large adipose cells. Thus, the rate of glucose oxidation and the magnitude of the insulin response of large adipose cells from individuals ingesting a high carbohydrate diet may be similar to or greater than that in smaller cells from individuals ingesting an isocaloric lower carbohydrate diet.The alterations in basal glucose metabolism and insulin response observed in adipose tissue from patients with spontaneous obesity are reproduced by weight gain induced experimentally in nonobese volunteers; these metabolic changes are reversible with weight loss. The relationships among adipose cell size, dietary composition, and the metabolism of adipose tissue are similar in spontaneous and in experimental obesity.
在不同的培养基葡萄糖和胰岛素浓度条件下,研究了非肥胖和肥胖受试者的脂肪组织将[1-(14)C]葡萄糖氧化为二氧化碳并转化为甘油酯的过程,这些条件是脂肪细胞大小、饮食组成以及先前体重增加或减少的函数。培养基葡萄糖浓度的增加会增强人体脂肪组织将葡萄糖碳掺入二氧化碳和甘油-甘油的能力。胰岛素进一步刺激葡萄糖碳转化为二氧化碳,但不刺激其转化为甘油-甘油。在任何测试条件下,均未证明这些组织能将[1-(14)C]葡萄糖掺入甘油酯脂肪酸中。脂肪细胞大小和饮食组成均会影响人体脂肪组织中葡萄糖的体外代谢以及对胰岛素的反应。在摄入碳水化合物、脂肪和蛋白质组成相似的维持体重等热量饮食期间,脂肪细胞大小增加与以下情况相关:(a) 在无胰岛素时,葡萄糖氧化速率不变,葡萄糖碳掺入甘油-甘油的速率增加;(b) 胰岛素对葡萄糖氧化的刺激作用减弱。另一方面,当细胞大小保持恒定时,饮食中碳水化合物摄入量的增加与大小脂肪细胞的葡萄糖基础代谢率和对胰岛素的反应增加相关。因此,摄入高碳水化合物饮食个体的大脂肪细胞的葡萄糖氧化速率和胰岛素反应幅度可能与摄入等热量低碳水化合物饮食个体的小脂肪细胞相似或更大。在非肥胖志愿者中通过实验性体重增加可再现自发性肥胖患者脂肪组织中观察到的基础葡萄糖代谢和胰岛素反应的改变;这些代谢变化可随体重减轻而逆转。自发性肥胖和实验性肥胖中脂肪细胞大小与饮食组成以及脂肪组织代谢之间的关系相似。