Schwartz R S, Brunzell J D
J Clin Invest. 1981 May;67(5):1425-30. doi: 10.1172/jci110171.
Obese subjects have elevated adipose tissue lipoprotein lipase activity per fat cell when compared with lean control subjects. This enzyme, which is rate limiting for the uptake and storage of lipoprotein triglyceride in adipose tissue, has been shown to be further elevated in a group of previously obese subjects who had been weight stable at a reduced weight for 4-28 mo. In the present prospective study of eight obese subjects, adipose tissue lipoprotein lipase activity was demonstrated to increase after weight stabilization at a reduced weight (0.33 mU/10(6) cells). In three subjects who lost weight and subsequently regained their lost weight, the enzyme activity increased after weight loss and then returned toward the original basal level with weight gain. One subject who maintained his weight loss for 10 mo. continued to have an elevated level of enzyme activity. Because adipose tissue lipoprotein lipase activity does not "normalize" after weight loss, we hypothesize that this enzyme may play a counterregulatory role in resisting deviation from a "set point" for fat mass or fat cell size and thereby predispose to reattainment of the original obese state.
与瘦的对照受试者相比,肥胖受试者每个脂肪细胞的脂肪组织脂蛋白脂肪酶活性升高。这种酶是脂肪组织中脂蛋白甘油三酯摄取和储存的限速酶,在一组先前肥胖但体重已稳定减轻4至28个月的受试者中,该酶活性进一步升高。在目前对8名肥胖受试者的前瞻性研究中,脂肪组织脂蛋白脂肪酶活性在体重稳定减轻后增加(0.33 mU/10(6) 个细胞)。在3名体重减轻后又恢复体重的受试者中,酶活性在体重减轻后增加,然后随着体重增加又回到原来的基础水平。一名体重减轻并维持10个月的受试者,其酶活性持续升高。由于体重减轻后脂肪组织脂蛋白脂肪酶活性并未“正常化”,我们推测这种酶可能在抵抗脂肪量或脂肪细胞大小偏离“设定点”方面发挥反调节作用,从而易导致恢复到原来的肥胖状态。