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Archives of Physiology and Biochemistry
The Journal of Metabolic Diseases
Volume 128, 2022 - Issue 2
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Original Articles

Metformin reduces lipid accumulation in HepG2 cells via downregulation of miR-33b

, , , & ORCID Icon
Pages 333-340 | Received 30 Jul 2019, Accepted 09 Oct 2019, Published online: 05 Nov 2019

Reference

  • Alrob, O.A., et al., 2017. MicroRNAs 33, 122, and 208: a potential novel targets in the treatment of obesity, diabetes, and heart-related diseases. Journal of physiology and biochemistry, 73(2), 307–314.
  • Arias, N., et al., 2016. MicroRNAs involved in the browning process of adipocytes. Journal of physiology and biochemistry, 72(3), 509–521.
  • Azimova, K., et al., 2014. Cardiovascular safety profile of currently available diabetic drugs. Ochsner journal, 14(4), 616–632.
  • Baselga-Escudero, L., et al., 2014. Resveratrol and EGCG bind directly and distinctively to miR-33a and miR-122 and modulate divergently their levels in hepatic cells. Nucleic acids research, 42(2), 882–892.
  • Bhagat, N. and Zarbin, M. A., 2019. Epidemiology, risk factors, and pathophysiology of diabetic retinopathy. In: Clinical strategies in the management of diabetic retinopathy. Springer. p. 1–19.
  • Blandino, G., et al., 2012. Metformin elicits anticancer effects through the sequential modulation of DICER and c-MYC. Nature communications, 3(1), 865.
  • Bugianesi, E., et al., 2005. A randomized controlled trial of metformin versus vitamin E or prescriptive diet in nonalcoholic fatty liver disease. The American journal of gastroenterology, 100(5), 1082.
  • Chaudhury, A., et al., 2017. Clinical review of antidiabetic drugs: implications for type 2 diabetes mellitus management. Frontiers in endocrinology, 8, 6.
  • Dávalos, A., et al., 2011. miR-33a/b contribute to the regulation of fatty acid metabolism and insulin signaling. Proceedings of the national academy of sciences, 108(22), 9232–9237.
  • Dyson, J. and Day, C., 2014. Treatment of non-alcoholic fatty liver disease. Digestive diseases, 32(5), 597–604.
  • Gerin, I., et al., 2010. Expression of miR-33 from an SREBP2 intron inhibits cholesterol export and fatty acid oxidation. Journal of biological chemistry, 285(44), 33652–33661.
  • Goedeke, L., et al., 2013. A regulatory role for microRNA 33* in controlling lipid metabolism gene expression. Molecular and cellular biology, 33(11), 2339–2352.
  • Gorgani-Firuzjaee, S. and Meshkani, R., 2015. SH2 domain-containing inositol 5-phosphatase (SHIP2) inhibition ameliorates high glucose-induced de-novo lipogenesis and VLDL production through regulating AMPK/mTOR/SREBP1 pathway and ROS production in HepG2 cells. Free radical biology and medicine, 89, 679–689.
  • Iliopoulos, D., et al., 2010. MicroRNA-370 controls the expression of microRNA-122 and Cpt1α and affects lipid metabolism. Journal of lipid research, 51(6), 1513–1523.
  • Ipsen, D.H., et al., 2018. Molecular mechanisms of hepatic lipid accumulation in non-alcoholic fatty liver disease. Cellular and molecular life sciences, 75(18), 3313–3327.
  • Kaiser, A.B., et al., 2018. Global prevalence of type 2 diabetes over the next ten years (2018-2028). Diabetes, 67(Supplement 1), 202-LB.
  • Li, Z., et al., 2019. Transcriptional regulation of early growth response gene-1 (EGR1) is associated with progression of nonalcoholic fatty liver disease (NAFLD) in patients with insulin resistance. Medical science monitor, 25, 2993.
  • Liu, F., et al., 2014. Metformin prevents hepatic steatosis by regulating the expression of adipose differentiation-related protein. International journal of molecular medicine, 33(1), 51–58.
  • Loomba, R., et al., 2009. Clinical trial: pilot study of metformin for the treatment of non‐alcoholic steatohepatitis. Alimentary pharmacology & therapeutics, 29(2), 172–182.
  • Luthra, R., et al., 2008. MicroRNA-196a targets annexin A1: a microRNA-mediated mechanism of annexin A1 downregulation in cancers. Oncogene, 27(52), 6667.
  • Marquart, T.J., et al., 2010. miR-33 links SREBP-2 induction to repression of sterol transporters. Proceedings of the national academy of sciences, 107(27), 12228–12232.
  • Mazloom, H., et al., 2015. Downregulated microRNA-155 expression in peripheral blood mononuclear cells of type 2 diabetic patients is not correlated with increased inflammatory cytokine production. Cytokine, 76(2), 403–408.
  • McMurry, H.S., et al., 2019. Coprevalence of type 2 diabetes mellitus and tuberculosis in low‐income and middle‐income countries: a systematic review. Diabetes/metabolism research and reviews, 35(1), e3066.
  • Meshkani, R., and Adeli, K., 2009. Hepatic insulin resistance, metabolic syndrome and cardiovascular disease. Clinical biochemistry, 42(13-14), 1331–1346.
  • Montvida, O., et al., 2018. Treatment with incretins does not increase the risk of pancreatic diseases compared to older anti‐hyperglycaemic drugs, when added to metformin: real world evidence in people with Type 2 diabetes. Diabetic medicine, 36(4), 491–498.
  • Najafi-Shoushtari, S.H., et al., 2010. MicroRNA-33 and the SREBP host genes cooperate to control cholesterol homeostasis. Science, 328(5985), 1566–1569.
  • Ono, K., 2016. Functions of microRNA-33a/b and microRNA therapeutics. Journal of cardiology, 67(1), 28–33.
  • Palumbo, P.J., 1998. Metformin: effects on cardiovascular risk factors in patients with non-insulin-dependent diabetes mellitus. Journal of diabetes and its complications, 12(2), 110–119.
  • Panahi, G., et al., 2018a. High glucose induces inflammatory responses in HepG2 cells via the oxidative stress-mediated activation of NF-kappaB, and MAPK pathways in HepG2 cells. Archives of physiology and biochemistry, 124(5), 468–474.
  • Panahi, G., et al., 2018b. MCU-knockdown attenuates high glucose-induced inflammation through regulating MAPKs/NF-kappaB pathways and ROS production in HepG2 cells. PLoS one, 13(4), e0196580.
  • Perry, R.J., et al., 2014. The role of hepatic lipids in hepatic insulin resistance and type 2 diabetes. Nature, 510(7503), 84.
  • Price, N.L., et al., 2018. Genetic ablation of miR-33 increases food intake, enhances adipose tissue expansion, and promotes obesity and insulin resistance. Cell reports, 22(8), 2133–2145.
  • Rawshani, A., et al., 2017. Mortality and cardiovascular disease in type 1 and type 2 diabetes. New England journal of medicine, 376(15), 1407–1418.
  • Rouabhia, S., et al., 2014. Metformin in the treatment of non-alcoholic fatty liver disease: safety, efficacy and mechanism. Expert review of gastroenterology & hepatology, 8(4), 343–349.
  • Sanchez-Rangel, E., and Inzucchi, S.E., 2017. Metformin: clinical use in type 2 diabetes. Diabetologia, 60(9), 1586–1593.
  • Tokubuchi, I., et al., 2017. Beneficial effects of metformin on energy metabolism and visceral fat volume through a possible mechanism of fatty acid oxidation in human subjects and rats. PLoS one, 12(2), e0171293.
  • Tolman, K.G., et al., 2007. Spectrum of liver disease in type 2 diabetes and management of patients with diabetes and liver disease. Diabetes care, 30(3), 734–743.
  • Wang, C., et al., 2014. Metformin suppresses lipid accumulation in skeletal muscle by promoting fatty acid oxidation. Clinical laboratory, 60(6), 887–896.
  • Yang, Z., et al., 2015. Emerging role of microRNAs in lipid metabolism. Acta pharmaceutica sinica B, 5(2), 145–150.
  • Zhu, M., et al., 2018. Integrated analysis of hepatic mRNA and miRNA profiles identified molecular networks and potential biomarkers of NAFLD. Scientific reports, 8(1), 7628.

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