Yang Won-Mo, Min Kyung-Ho, Son Yi-Seul, Park Se-Whan, Lee Wan
Department of Biochemistry, Dongguk University College of Medicine, Gyeongju-si, Gyeongsangbuk-do 38067, Republic of Korea.
Endocrine Channelopathy, Channelopathy Research Center, Dongguk University College of Medicine, Goyang-si, Gyeonggi-do 10326, Republic of Korea.
Data Brief. 2017 Oct 28;15:728-732. doi: 10.1016/j.dib.2017.10.054. eCollection 2017 Dec.
Diets containing a high saturated fatty acid (SFA) increase the risk of metabolic diseases, and microRNAs (miRNAs) induced by SFA have been implicated in the pathogenesis of insulin resistance and type 2 diabetes. In a previous report, miR-96 is found to be upregulated by SFA and involved in the suppression of insulin signaling intermediates, leading to insulin resistance in hepatocytes (Yang et al., 2016) [1]. This article presents the accompanying data collected from L6-GLUT4myc myocytes to determine the effects of miR-96 on insulin signaling in skeletal muscle cells. The transfection of miR-96 decreased the expression of IRS-1 in myocytes. Accordingly, miR-96 inhibited the insulin-stimulated phosphorylation of IRS-1, which led to an impairment of insulin signaling. More detailed analysis and understanding of the roles of miR-96 in diet-induced insulin resistance can be found in "Induction of miR-96 by dietary saturated fatty acids exacerbates hepatic insulin resistance through the suppression of INSR and IRS-1" (Yang et al., 2016) [1].
含有高饱和脂肪酸（SFA）的饮食会增加患代谢性疾病的风险，由SFA诱导的微小RNA（miRNA）与胰岛素抵抗和2型糖尿病的发病机制有关。在之前的一份报告中，发现miR-96受SFA上调，并参与抑制胰岛素信号中间体，导致肝细胞出现胰岛素抵抗（Yang等人，2016年）[1]。本文展示了从L6-GLUT4myc肌细胞收集的相关数据，以确定miR-96对骨骼肌细胞中胰岛素信号的影响。miR-96的转染降低了肌细胞中IRS-1的表达。因此，miR-96抑制了胰岛素刺激的IRS-1磷酸化，导致胰岛素信号受损。关于miR-96在饮食诱导的胰岛素抵抗中的作用的更详细分析和理解可在“膳食饱和脂肪酸诱导miR-96通过抑制INSR和IRS-1加重肝脏胰岛素抵抗”（Yang等人，2016年）[1]中找到。
