Kyung-Ho Min

Induction of miR-96 by Dietary Saturated Fatty Acids Exacerbates Hepatic Insulin Resistance through the Suppression of INSR and IRS-1

Obesity is defined as the excessive accumulation of body fat that ultimately leads to chronic metabolic diseases. Diets rich in saturated fatty acids (SFA) exacerbate obesity and hepatic steatosis, which increase the risk of hepatic insulin resistance and type 2 diabetes (T2DM). Although microRNAs (miRNAs) play an important role in a range of biological processes, the implications of SFA-induced miRNAs in metabolic dysregulation, particularly in the pathogenesis of hepatic insulin resistance, are not well understood. This study investigated the implications of miR-96, which is induced strongly by SFA, in the development of hepatic insulin resistance. The liver of HFD mice and the palmitate-treated hepatocytes exhibited an impairment of insulin signaling due to the significant decrease in INSR and IRS-1 expression. According to expression profiling and qRT-PCR analysis of the miRNAs, the expression level of miR-96 was higher in hepatocytes treated with palmitate. Moreover, miR-96 was also upregulated in the liver of HFD mice. Interestingly, miR-96 targeted the 3’UTRs of INSR and IRS-1 directly, and repressed the expression of INSR and IRS-1 at the post-transcriptional level. Accordingly, the overexpression of miR-96 was found to cause a significant decrease in INSR and IRS-1 expression, thereby leading to an impairment of insulin signaling and glycogen synthesis in hepatocytes. These results reveal a novel mechanism whereby miR-96 promotes the pathogenesis of hepatic insulin resistance resulted from SFA or obesity.

C1q tumor necrosis factor α-related protein isoform 5 attenuates palmitate-induced DNA fragmentation in myocytes through an AMPK-dependent mechanism.

This article reports the data for the effects of C1q tumor necrosis factor α-related protein isoform 5 (CTRP5) on the palmitate-induced apoptosis in myocytes. The data obtained from in vitro cultured myocytes shows that the cellular treatment with the globular domain of CTRP5 (gCTRP5) significantly inhibits the palmitate-induced MTT reduction, caspase-3 activation, and DNA fragmentation in a time-dependent manner. The data presented in this article also shows that AraA, an inhibitor of AMPK, almost completely abolished the protective effect of gCTRP5 on the DNA fragmentation induced by palmitate in myocytes. Interpretation of our data and further extensive insights into the protective role of CTRP5 in palmitate-induced apoptosis in myocytes can be found in Yang and Lee (2014) [1].

Data on the effect of miR-15b on the expression of INSR in murine C2C12 myocytes

The ectopic expression of miR-15b is linked causally to impaired insulin signaling in human HepG2 hepatocytes through the suppression of INSR (Yang et al., 2015) [1]. In this data article, we further examined the effect of miR-15b on insulin signaling in a murine skeletal muscle cells, C2C12 myocytes. Although the 3’UTR of mouse INSR mRNA has an appropriate binding site for miR-15b based on TargetScan analysis, the ectopic expression of miR-15b did not suppress the expression and insulin-stimulated phosphorylation of insulin signaling intermediates in C2C12 myocytes. A more detailed understanding of the effects of miR-15b on hepatic insulin resistance can be found in “Obesity-induced miR-15b is linked causally to the development of insulin resistance through the repression of the insulin receptor in hepatocytes” (Yang et al., 2015) [1].