Department of Animal Physiology and Biochemistry, Poznan University of Life Sciences, Wolynska, Poznan, Poland.
J Biol Regul Homeost Agents. 2013 Jan-Mar;27(1):23-33.
Ghrelin and obestatin are encoded by the preproghrelin gene and originate from post-translational processing of the preproghrelin peptide. Obestatin is mainly present in the stomach, but its action is focused on appetite inhibition in opposition to ghrelin function. Recently, it has been presented that obestatin may regulate adipocyte metabolism and influence fat content. However, obestatin action is still poorly understood. Therefore, we aimed to investigate obestatin function on adipocyte metabolism in the rat. We studied changes in the mRNA expression of active and inactive isoforms of obestatin receptors. In addition, we analyzed influence of obestatin on lipogenesis, lipolysis and glucose transport in isolated adipocytes. Moreover, we also performed analysis of obestatin action on lipolysis in differentiated rat preadipocytes with silenced obestatin receptor. We found significantly higher expression of the obestatin receptor Gpr39-1a active form at an mRNA level following adipocytes incubation with obestatin. We did not observe expression changes in the inactive form of obestatin receptor Gpr39-1b. Additionally, we found significant changes in Gpr39-1a expression following obestatin receptor silencing in cells incubated with obestatin in comparison to control. Obestatin inhibited both, basal and insulin-stimulated lipogenesis and glucose transport in adipocytes. Furthermore, obestatin potentiated adrenalin-stimulated lipolysis. We also found reduced glycerol release following obestatin incubation in adipocytes with silenced Gpr39 gene. Our results indicate that obestatin acts via the GPR39 receptor in isolated adipocytes, and that through this mechanism obestatin influences lipid accumulation, glucose uptake and lipolysis.
胃饥饿素和肥胖抑制素由前胃饥饿素基因编码，来源于前胃饥饿素肽的翻译后加工。肥胖抑制素主要存在于胃中，但它的作用是抑制食欲，与胃饥饿素的功能相反。最近，已经发现肥胖抑制素可能调节脂肪细胞代谢并影响脂肪含量。然而，肥胖抑制素的作用仍知之甚少。因此，我们旨在研究肥胖抑制素对大鼠脂肪细胞代谢的作用。我们研究了活性和非活性肥胖抑制素受体同工型的 mRNA 表达变化。此外，我们分析了肥胖抑制素对分离的脂肪细胞中脂肪生成、脂肪分解和葡萄糖转运的影响。此外，我们还对沉默肥胖抑制素受体的分化大鼠前脂肪细胞中的脂肪分解进行了肥胖抑制素作用分析。我们发现，在与肥胖抑制素孵育后，脂肪细胞中肥胖抑制素受体 Gpr39-1a 的活性形式的 mRNA 水平显著升高。我们没有观察到肥胖抑制素受体 Gpr39-1b 的非活性形式的表达变化。此外，我们发现，与对照组相比，在与肥胖抑制素孵育的细胞中沉默肥胖抑制素受体后，Gpr39-1a 的表达发生了显著变化。肥胖抑制素抑制了脂肪细胞中的基础和胰岛素刺激的脂肪生成和葡萄糖转运。此外，肥胖抑制素增强了肾上腺素刺激的脂肪分解。我们还发现，在沉默 Gpr39 基因的脂肪细胞中孵育肥胖抑制素后，甘油释放减少。我们的结果表明，肥胖抑制素在分离的脂肪细胞中通过 GPR39 受体起作用，通过这种机制，肥胖抑制素影响脂质积累、葡萄糖摄取和脂肪分解。
