Freeth Amy, Udupi Vidya, Basile Robin, Green Allan
University of Vermont, Endocrinology Clinic, FAHC-UHC Campus, 1 South Prospect Street, Burlington, VT 05401, USA.
Life Sci. 2003 Jun 13;73(4):393-401. doi: 10.1016/s0024-3205(03)00313-8.
Prolonged treatment of adipocytes with certain inhibitors of lipolysis, including N(6)-phenylisopropyl adenosine (PIA) and prostaglandin E(1) (PGE(1)) leads to down-regulation of G(i). Prolonged treatment with PIA increases the rate of lipolysis, and we have reported that tumor necrosis factor-alpha (TNF alpha) stimulates lipolysis by down-regulating G(i). To determine the relationship between G(i) concentration and lipolysis, we have investigated the effect of two other acute inhibitors of lipolysis; PGE(1), which down-regulates G(i), and nicotinic acid (NA), which does not down-regulate G(i). Rat adipocytes were incubated with PIA (300 nM), PGE(1) (3 microM) or nicotinic acid (1 mM) for 24 h. The rate of lipolysis (glycerol release) was increased approximately 2 to 3-fold in PIA-treated cells, and in PGE(1)-treated cells. Conversely, the rate of lipolysis was not altered by the prolonged nicotinic acid treatment. These findings support the hypothesis that the rate of lipolysis in adipocytes is determined, at least partly, by the cellular concentration of G(i) proteins.
用某些脂解抑制剂，包括N(6)-苯基异丙基腺苷（PIA）和前列腺素E(1)（PGE(1)）对脂肪细胞进行长时间处理会导致G(i)下调。用PIA长时间处理会增加脂解速率，并且我们已经报道肿瘤坏死因子-α（TNFα）通过下调G(i)来刺激脂解。为了确定G(i)浓度与脂解之间的关系，我们研究了另外两种急性脂解抑制剂的作用；下调G(i)的PGE(1)和不下调G(i)的烟酸（NA）。将大鼠脂肪细胞与PIA（300 nM）、PGE(1)（3 μM）或烟酸（1 mM）孵育24小时。在PIA处理的细胞和PGE(1)处理的细胞中，脂解速率（甘油释放）增加了约2至3倍。相反，长时间的烟酸处理并未改变脂解速率。这些发现支持了这样的假设，即脂肪细胞中的脂解速率至少部分由G(i)蛋白的细胞浓度决定。
