MiR-1271 upregulated by saturated fatty acid palmitate provokes impaired insulin signaling by repressing INSR and IRS-1 expression in HepG2 cells

Yang, Won-Mo; Min, Kyung-Ho; Lee, Wan

doi:10.1016/j.bbrc.2016.09.029

Cited by 28 publications

(30 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…PA has been demonstrated to potently induce insulin resistance. PA impairs insulin signaling in HepG2 cells via a reduction in the expression of insulin receptors and insulin receptor substrate 1 (IRS-1) protein (27). Additionally, PA activates the ubiquitin-proteasome system and autophagy in human umbilical vein endothelial cells (28).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑29a is involved lipid metabolism dysfunction and insulin resistance in C2C12 myotubes by targeting PPARδ

Wang

Jiang

et al. 2018

Mol Med Report

View full text Add to dashboard Cite

MicroRNA‑29a (miR‑29a) expression has been reported to be closely associated with skeletal muscle insulin resistance and type 2 diabetes. The present study investigated the effect of miR‑29a on palmitic acid (PA)‑induced lipid metabolism dysfunction and insulin resistance in C2C12 myotubes via overexpressing or silencing of miR‑29a expression. Mouse C2C12 myoblasts were cultured, differentiated and transfected with miR‑29a or miR‑29a inhibitor lentiviral with or without subsequent palmitic acid (PA) treatment. Reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) and western blot analysis were performed to assess the mRNA and protein levels of related genes, respectively. PA treatment increased the expression of miR‑29a in a time‑ and dose‑ dependent manner. miR‑29a silencing improved insulin‑induced glucose uptake and increased glucose transporter‑4 (GLUT4) transportation to the plasma membrane by upregulating its target peroxisome proliferator‑activated receptor δ (PPARδ). Furthermore, it was observed that miR‑29a regulated the expression of genes associated with lipid metabolism, including pyruvate dehydrogenase kinase isoform, mitochondrial uncoupling protein (UCP)2, UCP3, long chain specific acyl‑CoA dehydrogenase, mitochondrial and fatty acid transport protein 2. The results confirmed that silencing miR‑29a induced a decrease in glucose transport and affected lipid metabolism in PA‑treated C2C12 cells, and therefore may be involved in insulin resistance by targeting PPARδ in skeletal muscle. Therefore, the inhibition of miR‑29a may be a potential novel strategy for treating insulin resistance and type 2 diabetes.

show abstract

Section: Discussionmentioning

confidence: 99%

MicroRNA‑29a is involved lipid metabolism dysfunction and insulin resistance in C2C12 myotubes by targeting PPARδ

Wang

Jiang

et al. 2018

Mol Med Report

View full text Add to dashboard Cite

show abstract

“…IRS is the substrate for the activation of the insulin receptor tyrosine kinase. IRS-1 plays a major role in glucose and lipid metabolism [32, 33]. The insulin receptor is phosphorylated and activates IRS-1 after it binds to insulin.…”

Section: Discussionmentioning

confidence: 99%

[Retracted] An ErChen and YinChen Decoction Ameliorates High‐Fat‐Induced Nonalcoholic Steatohepatitis in Rats by Regulating JNK1 Signaling Pathway

Xie

Mao

et al. 2017

Evidence-Based Complementary and Alternative Medicine

View full text Add to dashboard Cite

ErChen and YinChen decoction (ECYCD) is an effective traditional Chinese medicine and has been widely used in traditional Chinese medicine to treat nonalcoholic steatohepatitis (NASH), with good curative effects. However, the specific mechanisms underlying these effects are unclear. In this study, we determined the efficacy of ECYCD in a high-fat diet-induced NASH rat model, established by 8-week administration of a high-fat diet. ECYCD was administered daily for 4 weeks, after which the rats were euthanized. The results demonstrated that ECYCD ameliorated high-fat diet-induced NASH, as evidenced by decreased liver indexes, reduced hepatic lipid deposition and liver injury, lower serum biochemistry markers (including low-density lipoprotein), and reduced HOMA-IR scores. Moreover, levels of free fatty acids, tumor necrosis factor, and malondialdehyde were decreased, whereas glutathione was increased in the liver. Serum high-density lipoprotein was also increased in the liver, and ECYCD regulated the c-Jun N-terminal kinase 1 (JNK1) signaling pathway by decreasing the levels of JNK1 protein, JNK1 mRNA, activator protein- (AP-) 1 protein, AP-1 mRNA, and phospho-insulin receptor substrate- (IRS-) 1ser307 and increasing phopsho-PKBser473 levels. These results suggested that ECYCD could ameliorate high-fat diet-induced NASH in rats through JNK1 signaling. ECYCD may be a safe therapeutic option for the treatment of NASH.

show abstract

“…3). Among those differentially expressed miRNAs, upregulated miRNAs have implications on the reduction of INSR and IRS-1 observed in palmitate-treated HepG2 cells [1]. Further analysis of the data and insights into the implications of miRNAs, especially miR-1271, in HepG2 cells are reported in another publication [1].…”

Section: Datamentioning

confidence: 97%

“…The expression of certain miRNAs targeting the insulin signaling molecules is modulated aberrantly in diet-induced obesity, which participates actively in the pathogenesis of insulin resistance [3], [4]. A previous study reported that SFA palmitate induces miR-1271 in HepG2 hepatocytes, and the expression of INSR and IRS-1 is suppressed by targeting their 3’UTR directly [1]. This means that certain miRNA induced by SFA could be linked causally to the development of hepatic insulin resistance and further to type 2 diabetes.…”

Section: Datamentioning

confidence: 99%

Data for differentially expressed microRNAs in saturated fatty acid palmitate-treated HepG2 cells

2016

Self Cite

View full text Add to dashboard Cite

Certain microRNAs (miRNAs) targeting the molecules in the insulin signaling cascades are dysregulated by saturated fatty acids (SFA), which can lead to insulin resistance and type 2 diabetes. This article reports the accompanying data collected using miRNAs microarrays to identify the changes in miRNA expression in HepG2 cells treated with SFA palmitate. Differentially expressed miRNA analyses in HepG2 cells showed that a range of upregulated (>1.5-fold) or downregulated (<0.5-fold) miRNAs. Further extensive insights into the implications of miRNAs, particularly miR-1271, in HepG2 cells can be found in "MiR-1271 upregulated by saturated fatty acid palmitate provokes impaired insulin signaling by repressing INSR and IRS-1 expression in HepG2 cells" (W.M. Yang, K.H. Min, W. Lee, 2016) [1].

show abstract

MiR-1271 upregulated by saturated fatty acid palmitate provokes impaired insulin signaling by repressing INSR and IRS-1 expression in HepG2 cells

Cited by 28 publications

References 29 publications

MicroRNA‑29a is involved lipid metabolism dysfunction and insulin resistance in C2C12 myotubes by targeting PPARδ

MicroRNA‑29a is involved lipid metabolism dysfunction and insulin resistance in C2C12 myotubes by targeting PPARδ

[Retracted] An ErChen and YinChen Decoction Ameliorates High‐Fat‐Induced Nonalcoholic Steatohepatitis in Rats by Regulating JNK1 Signaling Pathway

Data for differentially expressed microRNAs in saturated fatty acid palmitate-treated HepG2 cells

Contact Info

Product

Resources

About