Palmitic acid causes insulin resistance in granulosa cells via activation of JNK. (May 2019)

• Record Type: Journal Article
• Authors: Xu, Lan; Wang, Wenting; Zhang, Xinyue; Ke, Hanni; Qin, Yingying; You, Li; Li, Weiping; Lu, Gang; Chan, Wai-Yee; Leung, Peter C K; Zhao, Shidou; Chen, Zi-Jiang
• Is Part Of: Journal of molecular endocrinology. Volume 62:Number 4(2019)
• Page Start: 197
• Page End: 206
• Publication Date: 2019-05
• Subjects: obesity -- free fatty acid -- granulosa cells -- insulin resistance; Molecular endocrinology -- Periodicals; Endocrinology -- Periodicals; 616.407
• DOI: 10.1530/JME-18-0214
• Languages: English
• ISSNs: 0952-5041

Abstract

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.