Kovanen P T, Nikkilä E A, Miettinen T A
J Lipid Res. 1975 May;16(3):211-23.
The fat cells of rat epididymal adipose tissue contain an average of 0.5 mg of cholesterol per gram of triglyceride. Of this cholesterol, 90% is nonesterified and 80% is located in the lipid storage compartment. The fat cell cholesterol content correlated positively with cell size. During fasting the free cholesterol of the adipocyte decreased in parallel with triglyceride, whereas the amount of esterified cholesterol did not change. The fat cell cholesterol content is independent of the amount of dietary cholesterol. On in vitro incubation of rat fat cells with radiolabeled acetate, mevalonate, glucose, leucine, or water, labeled cholesterol was synthesized. The rate of cholesterol synthesis increased with fat cell size. Fasting suppressed cholesterol synthesis by 90%, whereas refeeding stimulated the synthesis above values found in normally fed rats. Stimulation of lipolysis with theophylline or with dibutyryl cyclic AMP markedly inhibited cholesterol synthesis in fat cells. Insulin increased the incorporation of glucose and leucine into fat cell cholesterol. The cholesterol synthesis in fat cells was not suppressed by a high cholesterol diet. Addition of very low or low density lipoprotein into the incubation medium suppressed fat cell cholesterol synthesis whereas high density lipoprotein did not. The lipoprotein-free serum stimulated cholesterol synthesis compared with serum-free medium. The rate of cholesterol synthesis in total adipose tissue of rat was estimated to be 4% of that in the liver. It seems unlikely that the increased body cholesterol turnover present in obesity is accounted for by the enhanced cholesterol formation in the enlarged adipose tissue.
大鼠附睾脂肪组织的脂肪细胞每克甘油三酯平均含有0.5毫克胆固醇。其中，90%的胆固醇未酯化，80%位于脂质储存区。脂肪细胞胆固醇含量与细胞大小呈正相关。禁食期间，脂肪细胞的游离胆固醇与甘油三酯平行下降，而酯化胆固醇的量不变。脂肪细胞胆固醇含量与饮食胆固醇量无关。用放射性标记的乙酸盐、甲羟戊酸、葡萄糖、亮氨酸或水对大鼠脂肪细胞进行体外培养时，会合成标记的胆固醇。胆固醇合成速率随脂肪细胞大小增加而增加。禁食使胆固醇合成减少90%，而重新喂食则刺激合成速率高于正常喂食大鼠的水平。用茶碱或二丁酰环磷腺苷刺激脂肪分解可显著抑制脂肪细胞中的胆固醇合成。胰岛素增加葡萄糖和亮氨酸掺入脂肪细胞胆固醇的量。高脂肪饮食不会抑制脂肪细胞中的胆固醇合成。向孵育培养基中添加极低密度脂蛋白或低密度脂蛋白可抑制脂肪细胞胆固醇合成，而高密度脂蛋白则无此作用。与无血清培养基相比，无脂蛋白血清刺激胆固醇合成。据估计，大鼠总脂肪组织中的胆固醇合成速率为肝脏的4%。肥胖时体内胆固醇周转率增加似乎不太可能是由于增大的脂肪组织中胆固醇生成增加所致。
