Obestatin is a 23-residue peptide, obtained after posttranslational modification of preproghrelin. It has been shown, in Swiss albino mice, to upregulate glycerolipid metabolism and PPARγ signaling. It was opined that the by-products of increased glycerolipid metabolism triggered PPARγ signaling. It was hypothesized that obestatin upon co-administration with a full agonist of PPARγ should reveal the comparative significance or possible synergy in PPARγ signaling. We postulated they would act synergistically by obestatin increasing PPARγ expression and rosiglitazone enhancing PPARγ activity. We evaluated the combination in DIO-C57BL/6 mice and observed that obestatin completely reversed the increase in subcutaneous fat brought about by rosiglitazone. To understand their role at the adipocyte level, 3T3-L1 cells were treated with a combination of obestatin and rosiglitazone during (1) initiation of differentiation and (2) after 14 days from initiation of differentiation when the adipocytes were mature. Interestingly, their influence was mainly adipogenic and showed double lipid accumulation when estimated 14 days after initiation of differentiation. There was an upregulation of Pparγ by fourfold, Hsl by eightfold, Glut4 by fourfold, Leptin by 2.7-fold, Atgl by sixfold, Fasn by sixfold, and Fabp4 by sevenfold at the mRNA level, whereas in mature adipocytes there was a significant decrease in fat accumulation by 20%. There was downregulation of Pparγ, Hsl, Lpl, and Fasn by 0.5-fold at the mRNA level. These results show that the combined influence of obestatin and rosiglitazone is significant and the outcome is dependent on the metabolic stage of the adipocyte.

Obestatin是一种23个残基的肽，在前proghrelin的翻译后修饰后获得。在瑞士的白化病小鼠中，它已被证明可上调甘油脂代谢和PPARγ信号传导。认为甘油脂代谢增加的副产物触发了PPARγ信号传导。假设与完整的PPARγ激动剂共同使用时，抑素应显示PPARγ信号传导的比较意义或可能的协同作用。我们推测它们将通过Obestatin增加PPARγ表达和罗格列酮增强PPARγ活性而协同发挥作用。我们在DIO-C57BL / 6小鼠中评估了该组合，并观察到Obestatin完全逆转了罗格列酮引起的皮下脂肪增加。要了解它们在脂肪细胞水平上的作用，在脂肪细胞成熟的过程中，在（1）分化开始和（2）分化开始后14天后，用Obestatin和Rosiglitazone联合处理3T3-L1细胞。有趣的是，它们的影响主要是成脂作用，并且在分化开始后14天估计显示出双倍的脂质蓄积。在mRNA水平上，Pparγ上调四倍，Hsl上调八倍，Glut4上调四倍，瘦素上调2.7倍，Att1上调六倍，Fasn上调六倍，Fabp4上调七倍，而在成熟的脂肪细胞中上调脂肪积聚了20％。在mRNA水平上，Pparγ，Hsl，Lpl和Fasn的表达下调了0.5倍。