Okuda H, Tsujita T, Sumida M, Takahashi Y, Shimizu D, Fujii S
J Biochem. 1983 Feb;93(2):575-82. doi: 10.1093/oxfordjournals.jbchem.a134212.
Endogenous lipid droplets were prepared by subjecting fat cells to hypotonic shock and to Triton X-100 treatment. The structure of the endogenous lipid droplet fraction was examined by scanning and transmission electron microscopies. Neither intact fat cells nor disrupted cell membranes were detectable in the endogenous lipid droplet fraction. With this endogenous substrate, epinephrine elicited lipolysis with either hormone-sensitive lipase or lipoprotein lipase, but no cyclic AMP-protein kinase mediated stimulation of lipolysis was observed. On the other hand, epinephrine did not stimulate lipolysis when triolein emulsified with arabic gum was used as substrate. With the latter exogenous substrate, however, cyclic AMP-protein kinase was found to stimulate lipolysis with hormone-sensitive lipase as enzyme. These results agree with the proposal of Wise and Jungas that the epinephrine-stimulated increase of hydrolysis of endogenous fat is not mediated through cyclic AMP-protein kinase. A possible mechanism of hydrolysis of endogenous fat by induction of lipolysis by epinephrine in fat cells is discussed.
通过对脂肪细胞进行低渗休克和用Triton X-100处理来制备内源性脂滴。通过扫描电子显微镜和透射电子显微镜检查内源性脂滴部分的结构。在内源性脂滴部分中未检测到完整的脂肪细胞或破裂的细胞膜。利用这种内源性底物，肾上腺素可通过激素敏感性脂肪酶或脂蛋白脂肪酶引发脂解作用，但未观察到环磷酸腺苷-蛋白激酶介导的脂解刺激作用。另一方面，当使用用阿拉伯胶乳化的三油酸甘油酯作为底物时，肾上腺素不会刺激脂解作用。然而，对于后一种外源性底物，发现环磷酸腺苷-蛋白激酶可通过激素敏感性脂肪酶作为酶来刺激脂解作用。这些结果与怀斯和荣加斯的提议一致，即肾上腺素刺激的内源性脂肪水解增加不是通过环磷酸腺苷-蛋白激酶介导的。讨论了脂肪细胞中肾上腺素诱导脂解作用从而水解内源性脂肪的可能机制。
