Asprosin attenuates insulin signaling pathway through PKCδ‐activated ER stress and inflammation in skeletal muscle

内科学 内分泌学 胰岛素抵抗 骨骼肌 细胞生物学 内质网 心肌细胞 胰岛素 磷酸化 化学 生物 医学
作者
Tae Woo Jung,Hyoung‐Chun Kim,Ho Ung Kim,Taekwang Park,Jin‐Woo Park,Uiseok Kim,Min Kyoon Kim,Ji Hoon Jeong
出处
期刊:Journal of Cellular Physiology [Wiley]
卷期号:234 (11): 20888-20899 被引量:89
标识
DOI:10.1002/jcp.28694
摘要

Abstract It has been reported that asprosin is a novel adipokine which is augmented in mice and humans with type 2 diabetes (T2DM). Asprosin stimulates hepatic gluconeogenesis under fasting conditions. However, the roles of asprosin in inflammation, endoplasmic reticulum (ER) stress, and insulin resistance in skeletal muscle has not been studied. In the currents study, elevated levels of asprosin expression were observed in adipocytes under hyperlipidemic conditions. Treatment of C2C12 myocytes with asprosin‐induced ER stress markers (phosphorylated inositol‐requiring enzyme 1 and eukaryotic initiation factor 2, and CHOP expression) as well as inflammation markers (interleukin‐6 expression, phosphorylated IκB, and nuclear translocated nuclear factor‐κβ). Finally, asprosin treatment promoted exacerbation of insulin sensitivity as determined by levels of insulin receptor substrate 1 and Akt phosphorylation as well as glucose uptake. Moreover, treatment of asprosin augmented protein kinase C‐δ (PKCδ) phosphorylation and nuclear translocation, but suppressed messenger RNA expression of sarcoplasmic reticulum Ca 2+ ATPase 2b in both C2C12 myocytes and in mouse soleus skeletal muscle. These asprosin‐induced effects were markedly decreased in small interfering (si) RNA‐mediated PKCδ‐knockdown in C2C12 myocytes. These results suggest that asprosin results in impairment of insulin sensitivity in skeletal muscle through PKCδ‐associated ER stress/inflammation pathways and may be a valuable strategy for management of insulin resistance and T2DM.
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