Gorman R R, Tepperman H M, Tepperman J
J Lipid Res. 1973 May;14(3):279-85.
Fat feeding results in a progressive loss of epineph-rine- and glucagon-stimulated adenylate cyclase activity in adipocyte plasma membrane sacs (ghosts). Basal and NaF-stimulated adenylate cyclase activities in fat-fed animals are not significantly different from those in preparations obtained from chow-fed rats. The high fat diet increases the mean adipocyte diameter rapidly, but increased cell size, at least in the case of epinephrine stimulation, is not responsible for the decreased hormone-stimulated adenylate cyclase activity. Diet shifts to high carbohydrate or high protein regimens result in the restoration of the epinephrine-stimulated, but not the glucagon-stimulated, activity without a significant reduction in mean cell diameter. Both hormone-resistant adipocyte ghosts from fat-fed animals and ghosts obtained from hormone-sensitive adipocytes bind the same amount of [(3)H]epinephrine per milligram of membrane protein. These data indicate that the fat diet inhibits epinephrine-stimulated adenylate cyclase activity at a point between the hormone receptor and the catalytic unit of adenylate cyclase.
喂食脂肪会导致脂肪细胞质膜囊泡（空壳）中肾上腺素和胰高血糖素刺激的腺苷酸环化酶活性逐渐丧失。喂食高脂肪饮食的动物的基础腺苷酸环化酶活性和氟化钠刺激的腺苷酸环化酶活性与从喂食普通饲料的大鼠获得的制剂中的活性没有显著差异。高脂肪饮食会迅速增加脂肪细胞的平均直径，但细胞大小增加，至少在肾上腺素刺激的情况下，并不是激素刺激的腺苷酸环化酶活性降低的原因。饮食改为高碳水化合物或高蛋白饮食会使肾上腺素刺激的活性恢复，但胰高血糖素刺激的活性不会恢复，且平均细胞直径没有显著减小。来自喂食高脂肪饮食动物的抗激素脂肪细胞空壳和来自激素敏感脂肪细胞的空壳每毫克膜蛋白结合的[³H]肾上腺素量相同。这些数据表明，高脂肪饮食在激素受体和腺苷酸环化酶催化单元之间的某个点抑制了肾上腺素刺激的腺苷酸环化酶活性。
