胰高血糖素、环磷酸腺苷和肾上腺素可刺激培养的大鼠肝细胞对低密度脂蛋白的降解。
Glucagon, cyclic AMP and adrenaline stimulate the degradation of low-density lipoprotein by cultured rat hepatocytes.
作者信息
Brown N F, Salter A M, Fears R, Brindley D N
机构信息
Department of Biochemistry, University of Alberta, Edmonton, Canada.
出版信息
Biochem J. 1989 Sep 1;262(2):425-9. doi: 10.1042/bj2620425.
Abstract
Rat hepatocytes were preincubated for 16 h with hormones or drugs and then for a further 8 h with 125I-human low-density lipoprotein (LDL). Glucagon (via cyclic AMP) and adrenaline (via cyclic AMP and alpha-effects) increased the binding of 125I-LDL to the LDL receptor, and the degradation of LDL to [125I]iodotyrosine. The effects on degradation were antagonized by dexamethasone, and the action of cyclic AMP on binding and degradation was inhibited by actinomycin D. The results are discussed in relation to the control of lipoprotein metabolism in diabetes.
摘要
将大鼠肝细胞先用激素或药物预孵育16小时，然后再与125I-人低密度脂蛋白（LDL）一起孵育8小时。胰高血糖素（通过环磷酸腺苷）和肾上腺素（通过环磷酸腺苷和α效应）增加了125I-LDL与LDL受体的结合，以及LDL降解为[125I]碘酪氨酸。地塞米松可拮抗对降解的影响，放线菌素D可抑制环磷酸腺苷对结合和降解的作用。结合糖尿病中脂蛋白代谢的控制对结果进行了讨论。
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本文引用的文献
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