The protective effect of high expression of mouse peroxisome proliferator activated receptor γ1 on free fatty acid induced β cell impairment
- VernacularTitle:小鼠过氧化物酶体增殖物激活受体γ1高表达对游离脂肪酸介导的β细胞损害的保护作用
- Author:
Yunfeng DU
;
Liyong YANG
- Publication Type:Journal Article
- Keywords:
Peroxisome proliferator activated receptor γ1;
Gene expression;
Islets of Langerhans transplantation;
Free fatty acid, nonesterified
- From:
Chinese Journal of Diabetes
2005;13(4):296-298,301
- CountryChina
- Language:Chinese
-
Abstract:
Objective To observe the protective effect of high expression of mouse proxisome proliferator activated receptor γ1(PPARγ1)on free fatty acid (FFA)-induced βTC3 cell impairment. Methods The recombinant plasmid pcDNA3.1/PPARγ1 was generated with cloning and was stably transfected into pancreatic β TC3 cells. The expression was detected with semi-quantitative RT-PCR. Then the cell viability of wild βTC3 cells was compared with that of the βTC3 cells with high expressed PPARγ1 by MTT viability assay after they were exposed to high-level FFA for 48 hours. Results The sequencing results for amplified target gene showed that the sequence of PPARγ1 from Chinese Kunming mouse is similar to that of mouse PPARγ1 in Genebank, only the codon coding Asp at the site of 421 amino acid changed from AAU to AAC. PPARγ1 was efficiently expressed in βTC3 cells in vitro. The cell viability of wild βTC3 cells reduced after being exposed to high-level FFA for 48 hours(P< 0.01). Higher the level of FFA was, more obvious the reduction of the cell viability was (r=-0.962, P<0.01). However, at the same condition, the cell viability of the βTC3 cells high expressing PPARγ1 had no significant change(P>0.05). Conclusion The high expression of PPARγ1 could protect βTC3 cells from FFA-induced impairment