MicroRNA-193b Controls Adiponectin Production in Human White Adipose Tissue

Belarbi, Yasmina; Mejhert, Niklas; Lorente‐Cebrián, Silvia; Dahlman, Ingrid; Arner, Peter; Kulyté, Agné

doi:10.1210/jc.2015-1530

Cited by 54 publications

(45 citation statements)

References 19 publications

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“…Nine of these miRNAs significantly reduced the secretion of pro-inflammatory chemokine (C–C motif) ligand 2 (CCL2), which was in line with the observation that they were downregulated in AT in human obesity (Arner et al, 2012). More-over three of these downregulated miRNAs were recently found to increase ApN secretion in conditioned media (Belarbi et al, 2015). The previous study of Ge et al also identified that miR-883b-5p, which was upregulated by ApN and downregulated in omental AT of obese human repressed the lipopolysaccharide-binding protein (LBP) and TLR4 signaling (Ge et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

miR-1934, downregulated in obesity, protects against low-grade inflammation in adipocytes

Liu

Xiao

et al. 2016

Molecular and Cellular Endocrinology

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It has been previously demonstrated that miR-1934 was specially regulated by adiponectin, an anti-inflammatory adipokine, in adipose tissue (AT) in vivo. Herein we investigated the role of miR1934 in the regulation of inflammatory response. Compared with chow-diet fed mice, miR1934 expression was down-regulated in epididymal AT of high-fat diet-induced obese mice. miR1934 expression was down-regulated as well in omental AT of obese subjects in comparison with lean subjects. The circulating miR-1934 was also lower in obese subjects and its levels were correlated negatively with body mass index (BMI), waist circumference (WC), low-density lipoprotein cholesterol (LDL-c), insulin resistance and high-sensitivity C-reactive protein (hs-CRP). The down-regulation of miR1934 in obesity was mimicked by TNF-α treatment of 3T3-L1 adipocytes. Moreover, overexpression of miR1934 suppressed the TNF-α-induced gene expression of interleukin-6 (IL-6) and monocyte chemotactic protein-1 (MCP-1) in 3T3-L1 adipocytes. De novo formed AT in nude mice transplanted with 3T3-L1 preadipocytes overexpressing miR1934 displayed a reduction in IL-6, TNF-α, IL-1β and an enhancement in IL-10 gene expression when compared with transplant with 3T3-L1 preadipocytes overexpressing miR1934 scrambled control sequence. These results suggest that miR1934 is an important anti-inflammatory factor and may represent a novel mechanism for controlling AT inflammation.

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Section: Discussionmentioning

confidence: 99%

miR-1934, downregulated in obesity, protects against low-grade inflammation in adipocytes

Liu

Xiao

et al. 2016

Molecular and Cellular Endocrinology

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“…As for the human WAT, numerous miRs exist but only a few number is altered in obesity and type 2 diabetes mellitus such as miR-193b, whose expression correlates positively with adiponectin gene expression and negatively with homeostasis model assessment of insulin-resistance [26].…”

Section: Introductionmentioning

confidence: 99%

MicroRNAs: Decoders of Dysbiosis into Metabolic Diseases?

Sérino¹

2016

J Diabetes Metab

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The identification of molecular factors bridging gut microbiota dysbiosis to alterations of host metabolism still remains a major goal in biomedical research. In fact, on one hand, there is a worldwide consensus about the systemic impact, from brain to liver, from heart to adipose tissue, of gut microbiota dysbiosis. On the other hand, beyond the microbial production of short chain fatty acids and their vast metabolic properties, little is known about the molecular mechanisms linking a change in the activity of gut microbes to a modification of host cell metabolism. In this context, microRNAs (also known as miRs) are promising molecules which could allow explaining how dysbiosis is converted into metabolic outcomes since: 1-miRs are pleiotropic regulators of gene expression, targeting multiple mRNAs at once; 2-miRs expression in specific organs such as the intestine has been demonstrated to be under the control of gut microbiota; 3-alterations in miRs expression have been found in the majority of tissues targeted by gut microbiota dysbiosis during metabolic diseases such as liver, adipose tissue, pancreas, skeletal muscle, intestine, heart and also the brain. In this review publications in the growing field of miRsbased metabolic control at a systemic level will be discussed together with a putative link with gut microbiota dysbiosis.

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“…Further, overexpression of miR-378 in 3T3L1 cells decreased mRNA and protein levels of adiponectin (Ishida et al 2014). A similar study in humans have shown significant association of serum adiponectin level with increased expression of miR-193b in white adipose tissue (Belarbi et al 2015). Few studies have implicated miRNA in degradation of adiponectin receptor.…”

Section: Introductionmentioning

confidence: 98%

“…The potential role of miRNA in insulin resistance (IR) and type 2 diabetes has been explored although there is potential for further investigation. Few recent studies indicate their potential as diagnostic and prognosis biomarkers (Ling et al 2012, Chakraborty et al 2014, Belarbi et al 2015, Chuang et al 2015.…”

Section: Introductionmentioning

confidence: 99%

“…A comprehensive study toward expression profile of miRNA in adipocytes during IR would be important to understand the pathophysiology of IR and type 2 diabetes. Recently, several miRNAs such as miR-378 and miR-193b have been shown to regulate the expression of adiponectin (Belarbi et al 2015, Gao et al 2015, Li et al 2016. miR-378 has been shown to regulate adiponectin level by binding to the 3′UTR of the adiponectin.…”

Section: Introductionmentioning

confidence: 99%

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miR-876-3p regulates glucose homeostasis and insulin sensitivity by targeting adiponectin

Rajan

Panzade

Srivastava

et al. 2018

Journal of Endocrinology

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miRNA have been known to regulate diverse cellular and molecular functions. In the earlier study, we have reported that adipocytes differentiated from human mesenchymal stem cells (hMSC) on 72hr chronic insulin (CI) treatment exhibit insulin resistance (IR). Present study has further explored above model to investigate the role of early expressed miRNAs within human adipocytes to modulate differential adipokine expression as observed during IR. Our results highlight that miR-876-3p regulate glucose homeostasis and its dysregulation lead to IR. We found that miR-876-3p level is a critical determinant of adiponectin expression by virtue of its target within adiponectin 3'UTR. Regulatory effect of miR-876-3p impacts crosstalk between adiponectin and insulin signaling. Rosiglitazone treatment in CI induced IR adipocytes drastically reduced miR-876-3p expression and increased adiponectin level. In line with this, lentiviral mediated inhibition of miR-876-3p expression ameliorated CI and high fat diet (HFD) induced insulin resistance in adipocytes differentiated from hMSC and C57BL/6 mice. Our findings thus suggest that modulating miR-876-3p expression could provide novel opportunities for therapeutic intervention of obesity-associated metabolic syndrome.

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MicroRNA-193b Controls Adiponectin Production in Human White Adipose Tissue

Abstract: In human adipocytes, miR-193b controls adiponectin production via pathways involving nuclear transcription factor Yα and possibly nuclear receptor interacting protein 1.

Cited by 54 publications

References 19 publications

miR-1934, downregulated in obesity, protects against low-grade inflammation in adipocytes

miR-1934, downregulated in obesity, protects against low-grade inflammation in adipocytes

MicroRNAs: Decoders of Dysbiosis into Metabolic Diseases?

miR-876-3p regulates glucose homeostasis and insulin sensitivity by targeting adiponectin

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