Waldbillig D, Desautels M
Department of Physiology, College of Medicine, University of Saskatchewan, Saskatoon, Canada.
Am J Physiol. 1992 Nov;263(5 Pt 2):R1003-12. doi: 10.1152/ajpregu.1992.263.5.R1003.
Rat brown adipocytes were incubated for 24 h with or without norepinephrine (NE) in Dulbecco's modified Eagle's medium with albumin, calf serum, and antibiotics. Brown fat cells were viable as defined by unchanged cell morphology, ATP content, or basal and NE-stimulated respiration. However, a 24-h exposure to NE led to a decline in NE-stimulated respiration that was not due to loss of thermogenic capacity. Brown fat cells incubated with or without NE had similar protein, succinate dehydrogenase, and uncoupling protein (UCP) content. These results differ from those observed after food deprivation in rats where loss of mitochondrial proteins occurs within 24 h, suggesting that reduced exposure to NE is not the only factor responsible for brown fat atrophy. NE increased [35S]methionine incorporation into cellular proteins, mitochondrial proteins, and UCP. The effect of NE on cell protein synthesis was inhibited by propranolol but not by prazosin. It was also inhibited 95% by cycloheximide but only partially (50%) by actinomycin D in contrast to NE stimulation of UCP labeling, which required RNA transcription. Chloramphenicol-sensitive protein synthesis was stimulated by NE. These results indicate a trophic action of NE in brown adipocytes exerted both at the level of RNA transcription and translation.
将大鼠棕色脂肪细胞在含有白蛋白、小牛血清和抗生素的杜尔贝科改良伊格尔培养基中，分别在有无去甲肾上腺素（NE）的情况下孵育24小时。根据细胞形态、ATP含量或基础及NE刺激的呼吸作用未改变来定义，棕色脂肪细胞是有活力的。然而，24小时暴露于NE会导致NE刺激的呼吸作用下降，这并非由于产热能力的丧失。在有无NE的情况下孵育的棕色脂肪细胞具有相似的蛋白质、琥珀酸脱氢酶和解偶联蛋白（UCP）含量。这些结果与在大鼠禁食后观察到的结果不同，在禁食大鼠中，24小时内会发生线粒体蛋白质的丢失，这表明减少NE暴露不是棕色脂肪萎缩的唯一原因。NE增加了[35S]甲硫氨酸掺入细胞蛋白质、线粒体蛋白质和UCP中。NE对细胞蛋白质合成的作用被普萘洛尔抑制，但不被哌唑嗪抑制。与NE刺激UCP标记需要RNA转录相反，它也被放线菌酮抑制95%，但仅被放线菌素D部分抑制（50%）。氯霉素敏感的蛋白质合成受到NE的刺激。这些结果表明NE在棕色脂肪细胞中具有营养作用，在RNA转录和翻译水平上均有发挥。
