猪上普遍存在的宫内发育迟缓（IUGR）导致脂肪过度沉积，严重影响畜产品品质。申请人前期研究发现IUGR可增强大鼠脂肪组织PPARγ表达，改变mTOR通路，增强脂肪细胞自噬，促进脂肪沉积；IUGR肥育猪也有PPARγ表达增强和脂肪过度沉积现象，但有待从自噬角度深入研究PPARγ调控IUGR猪脂肪沉积的机制。本项目拟以脂肪细胞自噬为靶点，系统研究IUGR对肥育猪脂肪组织PPARγ、mTOR通路、脂肪细胞自噬、脂肪沉积及肉品质的影响，揭示PPARγ、自噬及脂肪沉积间的联系。再结合细胞试验，通过抑制和增强PPARγ表达，明确PPARγ对脂肪细胞自噬及mTOR通路的影响；并通过抑制和增强PPARγ时改变mTOR的表达，揭示PPARγ通过mTOR通路调控脂肪细胞自噬影响脂代谢的机制。从转录因子调控自噬角度，阐明PPARγ介导细胞自噬调控IUGR肥育猪脂肪沉积的机理，为猪肉品质的改善提供理论依据。

With a high incidence in pigs, intrauterine growth retardation (IUGR) leads to excess fat deposition, and affects meat quality. Our previous study indicated that IUGR rats showed increased PPARγ expression, alerted mTOR signalling, enhanced autophagy in adipose tissue and increased fat deposition. In addtion, IUGR finishing pigs also showed enhanced PPARγ expression and increased fat deposition. However, the mechnism of adipocyte autophagy mediated by PPARγ which regulates fat deposition in IUGR finishing pigs should be studied further. Centering on adipocyte autophagy, this project intends to investigate effects of IUGR on expression of PPARγ, mTOR signalling, adipocyte autophagy, fat deposition, lipid metabolism and meat quality in finishing pigs, and the relations among PPARγ, mTOR\ULK1\Beclin1 pathway, adipocyte autophagy and fat deposition will also be analyzed. In vitro, effects of PPARγ on adipocyte autophagy and the expression of mTOR signalling through inhibition and activition of PPARγ. Subsequently, the mechnism that PPARγ regulates lipid metabolim by adipocyte autophagy throught mTOR signal pathway will be studied by using alerting mTOR expression as well as inhibition and activation of PPARγ. Therefore, the mechnism of adipocyte autophagy mediated by PPARγ which regulates fat deposition in IUGR finishing pigs could be explored very well. This will be beneficial for improving and studying meat quality.