miR-29a levels are elevated in the db/db mice liver and its overexpression leads to attenuation of insulin action on PEPCK gene expression in HepG2 cells

Pandey, Amit Kumar; Verma, Gaurav; Vig, Saurabh; Srivastava, Suman; Srivastava, Arvind K.; Datta, Malabika

doi:10.1016/j.mce.2010.10.004

Cited by 104 publications

(81 citation statements)

References 47 publications

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“…and miR-29b, have been linked to insulin resistance, through the down-regulation of proteins that promote insulin signaling like caveolin 2 and phosphatidylinositol 3-kinase (PI3K) regulatory subunit-α [62,63]. The inhibition of insulin receptor substrate-1 (IRS1) by miR-126 also promotes insulin resistance [64], while miR-33a and miR-33b affect insulin signaling and glucose regulation by targeting IRS2, SIRT6 and AMPKα1 [65].…”

Section: Mirna Regulation Of Insulin Secretion and Signalingmentioning

confidence: 99%

miRNAs link metabolic reprogramming to oncogenesis

Hatziapostolou¹,

Polytarchou²,

Iliopoulos

2013

Trends in Endocrinology & Metabolism

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Section: Mirna Regulation Of Insulin Secretion and Signalingmentioning

confidence: 99%

miRNAs link metabolic reprogramming to oncogenesis

Hatziapostolou¹,

Polytarchou²,

Iliopoulos

2013

Trends in Endocrinology & Metabolism

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“…Many members of the PI3K/AKT pathway are regulated by miRNAs. miR-29a and miR-126 target the p85α and p85β subunits of PI3K [74,75] , respectively. The down-regulation of miR-126 in colon cancer is associated with the up-regulation of the p85β subunit, which induces the phosphorylation of AKT and promotes the proliferation of colon cancer cells [75] .…”

Section: Pi3k/akt Pathwaymentioning

confidence: 99%

Macro-management of microRNAs in cell cycle progression of tumor cells and its implications in anti-cancer therapy

Liang

2011

Acta Pharmacol Sin

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The cell cycle, which is precisely controlled by a number of regulators, including cyclins and cyclin-dependent kinases (CDKs), is crucial for the life cycle of mammals. Cell cycle dysregulation is implicated in many diseases, including cancer. Recently, compelling evidence has been found that microRNAs play important roles in the regulation of cell cycle progression by modulating the expression of cyclins, CDKs and other cell cycle regulators. Herein, the recent findings on the regulation of the cell cycle by microRNAs are summarized, and the potential implications of miRNAs in anti-cancer therapies are discussed.

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“…In adipocytes, miR-320 induces insulin resistance by inhibiting the insulin-phosphoinositide 3-kinase (PI3K) signalling pathway [22]. miR-29, which has been found to be elevated in the skeletal muscle of diabetic rats and the liver of db/db mice, negatively regulates insulin signalling via inhibiting the p85α subunit of PI3K [23,24]. In muscle cells, miR-7 downregulates IRS-1 levels as well as inhibiting insulin-stimulated Akt phosphorylation and glucose uptake [25].…”

Section: Introductionmentioning

confidence: 99%

Downregulation of miR-181a upregulates sirtuin-1 (SIRT1) and improves hepatic insulin sensitivity

et al. 2012

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Aims/hypothesis Sirtuin-1 (SIRT1) is a potential therapeutic target to combat insulin resistance and type 2 diabetes. This study aims to identify a microRNA (miRNA) targeting SIRT1 to regulate hepatic insulin sensitivity. Methods Luciferase assay combined with mutation and immunoblotting was used to screen and verify the bioinformatically predicted miRNAs. miRNA and mRNA levels were measured by real-time PCR. Insulin signalling was detected by immunoblotting and glycogen synthesis. Involvement of SIRT1 was studied with adenovirus, inhibitor and SIRT1-deficient hepatocytes. The role of miR-181a in vivo was explored with adenovirus and locked nucleic acid antisense oligonucleotides. Results miR-181a targets the 3′ untranslated region (3′UTR) of Sirt1 mRNA through a miR-181a binding site, and downregulates SIRT1 protein abundance at the translational level. miR-181a is increased in insulin-resistant cultured hepatocytes and liver, and in the serum of diabetic patients. Overexpression of miR-181a decreases SIRT1 protein levels and activity, and causes insulin resistance in hepatic cells. Inhibition of miR-181a by antisense oligonucleotides increases SIRT1 protein levels and activity, and improves insulin sensitivity in hepatocytes. Ectopic expression of SIRT1 abrogates the effect of miR-181a on insulin sensitivity, and inhibition of SIRT1 activity or SIRT1 deficiency markedly attenuated the improvement in insulin sensitivity induced by antisense miR-181a. In addition, overexpression of miR181a by adenovirus impairs hepatic insulin signalling, and intraperitoneal injection of locked nucleic acid antisense oligonucleotides for miR-181a improves glucose homeostasis in diet-induced obesity mice. Conclusions/interpretation miR-181a regulates SIRT1 and improves hepatic insulin sensitivity. Inhibition of miR-181a might be a potential new strategy for treating insulin resistance and type 2 diabetes.

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miR-29a levels are elevated in the db/db mice liver and its overexpression leads to attenuation of insulin action on PEPCK gene expression in HepG2 cells

Cited by 104 publications

References 47 publications

miRNAs link metabolic reprogramming to oncogenesis

miRNAs link metabolic reprogramming to oncogenesis

Macro-management of microRNAs in cell cycle progression of tumor cells and its implications in anti-cancer therapy

Downregulation of miR-181a upregulates sirtuin-1 (SIRT1) and improves hepatic insulin sensitivity

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