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Prolonged treatment with prostaglandin E1 increases the rate of lipolysis in rat adipocytes.

机译:前列腺素E1的延长治疗可增加大鼠脂肪细胞中脂解的速率。

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摘要

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.
机译: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)))对脂肪细胞的长期治疗会导致G(i)的下调。 PIA的长期治疗会增加脂肪分解的速率,并且我们已经报道肿瘤坏死因子-α(TNF alpha)通过下调G(i)刺激脂肪分解。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 microM)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,脂解的速率(甘油释放)增加了大约2到3倍。相反,延长的烟酸处理不会改变脂肪分解的速率。这些发现支持以下假设:脂肪细胞中脂解的速率至少部分地由G(i)蛋白的细胞浓度决定。

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