Pedersen R C, Brownie A C
Mol Cell Endocrinol. 1987 Mar;50(1-2):157-64. doi: 10.1016/0303-7207(87)90088-8.
Gamma 3-melanotropin (gamma 3-MSH) exhibits a marked dose-dependent synergism with ACTH1-24 on corticosterone production by cells isolated from the inner zones of the rat adrenal cortex. This phenomenon is demonstrated to best advantage when donor animals are killed after stress or pretreatment with ACTH. If adrenal cells are prepared from quiescent or hypophysectomized animals, the inclusion of high density lipoprotein (HDL) in the incubation medium is required for a significant gamma 3-MSH response. Dibutyryl cAMP can successfully substitute for ACTH1-24 in these incubations but rat low density lipoprotein does not reproduce the HDL effect. These data are consistent with our in vivo studies demonstrating that gamma 3-MSH potentiation is a product of increased cholesterol mobilization within the adrenal cortex and suggest that in the rat, a significant source of the cholesteryl ester pool which is responsive to gamma 3-MSH may derive from circulating HDL.
γ3-促黑素（γ3-MSH）与促肾上腺皮质激素1-24（ACTH1-24）在由大鼠肾上腺皮质内层分离出的细胞生成皮质酮的过程中呈现出显著的剂量依赖性协同作用。当供体动物在应激或用促肾上腺皮质激素预处理后处死时，这一现象表现得最为明显。如果从静止或垂体切除的动物制备肾上腺细胞，孵育培养基中需要加入高密度脂蛋白（HDL）才能产生显著的γ3-MSH反应。在这些孵育实验中，二丁酰环磷腺苷（dibutyryl cAMP）能够成功替代促肾上腺皮质激素1-24，但大鼠低密度脂蛋白不能重现高密度脂蛋白的作用。这些数据与我们的体内研究结果一致，表明γ3-MSH增强作用是肾上腺皮质内胆固醇动员增加的结果，并提示在大鼠中，对γ3-MSH有反应的胆固醇酯池的一个重要来源可能来自循环中的高密度脂蛋白。
