RRC ID 72477
著者 Xu L, Wang W, Zhang X, Ke H, Qin Y, You L, Li W, Lu G, Chan WY, Leung PCK, Zhao S, Chen ZJ.
タイトル Palmitic acid causes insulin resistance in granulosa cells via activation of JNK.
ジャーナル J Mol Endocrinol
Abstract Obesity is a worldwide health problem with rising incidence and results in reproductive difficulties. Elevated saturated free fatty acids (FFAs) in obesity can cause insulin resistance (IR) in peripheral tissues. The high intra-follicular saturated FFAs may also account for IR in ovarian granulosa cells (GCs). In the present study, we investigated the relationship between saturated FFAs and IR in GCs by the use of palmitic acid (PA). We demonstrated that the glucose uptake in cultured GCs and lactate accumulation in the culture medium were stimulated by insulin, but the effects of insulin were attenuated by PA treatment. Besides, insulin-induced phosphorylation of Akt was reduced by PA in a dose- and time-dependent manner. Furthermore, PA increased phosphorylation of JNK and JNK blockage rescued the phosphorylation of Akt which was downregulated by PA. These findings highlighted the negative effect of PA on GCs metabolism and may partially account for the obesity-related reproductive disorders.
巻・号 62(4)
ページ 197-206
公開日 2019-5-1
DOI 10.1530/JME-18-0214
PII JME-18-0214.R3
PMID 30913535
MeSH Animals Apoptosis / drug effects Cell Line, Tumor Cell Survival / drug effects Fatty Acids / metabolism Female Glucose / metabolism Granulosa Cells / drug effects Granulosa Cells / metabolism* Humans Insulin / metabolism Insulin Resistance* JNK Mitogen-Activated Protein Kinases / genetics JNK Mitogen-Activated Protein Kinases / metabolism* Lactic Acid / metabolism MAP Kinase Signaling System / drug effects Mice Obesity / etiology Obesity / metabolism Palmitic Acid / pharmacology* Phosphorylation Proto-Oncogene Proteins c-akt / metabolism
IF 3.562
リソース情報
ヒト・動物細胞 KGN(RCB1154)