β-Lapachone Prevents Diet-Induced Obesity by Increasing Energy Expenditure and Stimulating the Browning of White Adipose Tissue via Downregulation of miR-382 Expression

Choi, Won Hee; Ahn, Jiyun; Jung, Chang Hwa; Jang, Young Jin; Ha, Tae Youl

doi:10.2337/db15-1423

Cited by 36 publications

(20 citation statements)

References 42 publications

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“…Therefore, we proposed that increased expression of miR-382 may promote LPCs differentiation. Occasionally, according to previous reports, miR-382 affect various lineage conversion, including adipocytes differentiation [32], osteogenic differentiation [33] and hematopoietic stem cell differentiation [34]. Together with our findings, we speculate that miR-382 is always involved in various stem cell differentiation.…”

Section: Discussionsupporting

confidence: 57%

Mir-382 Promotes Differentiation of Rat Liver Progenitor Cell WB-F344 by Targeting Ezh2

Zheng

Zhou

et al. 2018

Cell Physiol Biochem

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Background/Aims: Liver progenitor cells (LPCs) were considered as a promising hepatocyte source of cell therapy for liver disease due to their self-renewal and differentiation capacities, while little is known about the mechanism of LPC differentiate into hepatocytes. This study aims to explore the effect of miR-382, a member of Dlk1-Dio3 microRNA cluster, during hepatic differentiation from LPCs. Methods: In this study, we used rat liver progenitor cell WB-F344 as LPC cell model and HGF as inducer to simulate the process of LPCs hepatic differentiation, then microRNAs were quantified by qPCR. Next, WB-F344 cell was transfected with miR-382 mimics, then hepatocyte cell trait was characterized by multiple experiments, including that periodic acid schiff staining and cellular uptake and excretion of indocyanine green to evaluate the hepatocellular function, qPCR and Western Blotting analysis to detect the hepatocyte-specific markers (ALB, Ttr, Apo E and AFP) and transmission electron microscopy to observe the hepatocellular morphology. Moreover, Luciferase reporter assay was used to determine whether Ezh2 is the direct target of miR-382. Results: We found that miR-382 increased gradually and was inversely correlated with the potential target, Ezh2, during WB-F344 hepatic differentiation. In addition, functional studies indicated that miR-382 increased the level of hepatocyte-specific genes. Conclusions: This study demonstrates that miR-382 may be a novel regulator of LPCs differentiation by targeting Ezh2.

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Section: Discussionsupporting

confidence: 57%

Mir-382 Promotes Differentiation of Rat Liver Progenitor Cell WB-F344 by Targeting Ezh2

Zheng

Zhou

et al. 2018

Cell Physiol Biochem

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“…We found that the expression of Dio2 and PPARγ was increased in the epididymal fat of CTS-, COST-, and COSM-treated rats compared with the rats in the HF group ( Supplementary Figure S2D,E). Another argument is that Dio2 and PPARγ also play an important role in promoting browning [36], as PPARγ is essential for maintaining WAT and BAT differentiation [37] and Dio2 activation promotes adrenergic response and energy expenditure [38].…”

Section: Discussionmentioning

confidence: 99%

Beneficial Metabolic Effects of Chitosan and Chitosan Oligosaccharide on Epididymal WAT Browning and Thermogenesis in Obese Rats

Wang

Yang

et al. 2019

Molecules

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Many anti-obesity chemicals have been withdrawn from the market due to serious adverse reactions, and the researchers have turned their attention to low-toxic natural products. Previous studies have demonstrated that chitosan (CTS) and chitosan oligosaccharide (COS) were low-toxic natural products for the use of weight loss. However, it is still unclear whether CTS and COS have positive effects on the thermogenesis. In this study, CTS and COS significantly reduced the weight gain of rats without affecting food intake and effectively inhibited adipose tissue hypertrophy and hyperplasia. Consistently, CTS and COS significantly increased the thermogenic capacity of obese rats induced by high-fat diet (HFD) and increased the expression of browning genes and proteins (UCP1, PGC1α, PRMD16, and ATF2) in white adipose tissue (WAT) and brown adipose tissue (BAT). In vitro, COS inhibited the formation of mature adipocytes and increased the expression of browning genes. In conclusion, COS and CTS was used to explore the function and mechanism on thermogenesis, and CTS and COS can increase the browning of WAT and the thermogenesis of BAT to inhibit obesity. This effect may be achieved by promoting the expression of browning and thermogenic genes, providing new ideas for the utilization of COS and CTS.

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“…miR-378 is increased during brown adipocyte differentiation, promoting brown adipogenesis and protecting against both genetic and high-fat diet-induced obesity. Upregulation of miR-382 inhibited beige differentiation of mice WAT stromal vascular fractions, thereby reducing UCP1 mRNA and protein levels (18). On the other hand, miR-196a induced the beigening of mice WAT with characteristic appearance and gene expression profile of brown adipocytes (Prdm16 and Ucp1) (74).…”

Section: Mirs Involved In Nonshivering Thermogenesismentioning

confidence: 99%

MicroRNAs as regulators of mitochondrial dysfunction and obesity

Murri

Azzouzi

2018

American Journal of Physiology-Heart and Circulatory Physiology

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Obesity, which has become a major global epidemic, is associated with numerous comorbidities and nearly every chronic condition. Mitochondria play a central role in this disorder, as they control cell metabolism, regulating important processes, such as ATP production, lipid β-oxidation, oxidative stress, and inflammation. MicroRNAs (miRs) have been shown to regulate many biological processes associated with obesity, comprising adipocyte differentiation, insulin action, and fat metabolism. In addition, recent studies have confirmed that miRs are important regulators of mitochondrial function by either directly modulating mitochondrial proteins or targeting mitochondrial regulators, thereby modulating metabolic process in the context of obesity. In this review, we describe the different roles of mitochondria in obesity, specifically in adipose tissue, and those miRs that are involved in mitochondrial dysfunction in this disease.

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β-Lapachone Prevents Diet-Induced Obesity by Increasing Energy Expenditure and Stimulating the Browning of White Adipose Tissue via Downregulation of miR-382 Expression

Cited by 36 publications

References 42 publications

Mir-382 Promotes Differentiation of Rat Liver Progenitor Cell WB-F344 by Targeting Ezh2

Mir-382 Promotes Differentiation of Rat Liver Progenitor Cell WB-F344 by Targeting Ezh2

Beneficial Metabolic Effects of Chitosan and Chitosan Oligosaccharide on Epididymal WAT Browning and Thermogenesis in Obese Rats

MicroRNAs as regulators of mitochondrial dysfunction and obesity

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