F Wen1,2, Y Yang2, C Sun2, H Fang2, L Nie2, L Li1, Y Liu1, Z Yang2. 1. Henan University of Science and Technology, College of Animal Science and Technology, Luoyang, Henan, PR China. 2. Huazhong Agricultural University, College of Life Science and Technology, Breeding and Reproduction of Ministry of Education, Key Laboratory of Agricultural Animal Genetics, Wuhan, Hubei, PR China.
Abstract
AIMS: Resistin has been reported to impair the pancreatic beta cells and associated with insulin resistance. MicroRNAs (miRNAs) are short, endogenously produced non-coding ribonucleotides that bind mRNAs and function mainly as negative regulators in mammals. MiRNAs have been implicated in many diseases, including insulin resistance and diabetes. A considerable body of evidence has indicated an important function for miRNAs in insulin secretion. The current study was designed to investigate the effects of miR-494 in the reductions in insulin secretion attributable to resistin. METHODS: Insulin secretion was determined by ELISA, and expressions of genes were identified using quantitative RT-PCR (qRT-PCR) or Western blot analysis. RESULTS: Insulin secretion was significantly reduced by resistin. Overexpression of miR-494 inhibited insulin secretion both in diet culture and high glucose medium in MIN6 cell lines. MiR-494 down-regulated the protein level of STXBP5 by pairing with sites in the 3'UTR. CONCLUSION: miR-494 is involved in the insulin secretion regulated by resistin via its effects on STXBP5 in MIN6 cells.
AIMS: Resistin has been reported to impair the pancreatic beta cells and associated with insulin resistance. MicroRNAs (miRNAs) are short, endogenously produced non-coding ribonucleotides that bind mRNAs and function mainly as negative regulators in mammals. MiRNAs have been implicated in many diseases, including insulin resistance and diabetes. A considerable body of evidence has indicated an important function for miRNAs in insulin secretion. The current study was designed to investigate the effects of miR-494 in the reductions in insulin secretion attributable to resistin. METHODS: Insulin secretion was determined by ELISA, and expressions of genes were identified using quantitative RT-PCR (qRT-PCR) or Western blot analysis. RESULTS: Insulin secretion was significantly reduced by resistin. Overexpression of miR-494 inhibited insulin secretion both in diet culture and high glucose medium in MIN6 cell lines. MiR-494 down-regulated the protein level of STXBP5 by pairing with sites in the 3'UTR. CONCLUSION: miR-494 is involved in the insulin secretion regulated by resistin via its effects on STXBP5 in MIN6 cells.
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