Role of miR-383 and miR-146b in different propensities to obesity in male mice

Xia, Shufang; Duan, Xiaoling; Cheng, Xiang‐Rong; Chen, Limei; Kang, Yijun; Wang, Peng; Tang, Xue; Shi, Yonghui; Li, Guowei

doi:10.1530/joe-17-0044

Cited by 18 publications

(10 citation statements)

References 38 publications

(40 reference statements)

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“…Overall, our results suggest that miR-592 may play an important role in the regulation of hepatic lipid metabolism. Interestingly, a recent study showed that miR-592 was significantly reduced in the liver of mice fed a high-fat-diet for 7 weeks [43], which is consistent our results. However, they further found that miR-592 was not changed in the liver of mice fed a high-fat-diet for 17 weeks.…”

Section: Discussionsupporting

confidence: 92%

Down-regulation of MicroRNA-592 in obesity contributes to hyperglycemia and insulin resistance

Song

et al. 2019

EBioMedicine

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Background Many studies have demonstrated that microRNAs, a class of small and non-coding RNA molecules, play an important role in the regulation of glucose and lipid homeostasis. In the present study, we sought to investigate the function of miR-592 in the development of obesity-associated metabolic disorders, including hyperglycemia andinsulin resistance. Methods The expression levels of miR-592 were measured in the liver of obese mice and humans by quantitative reverse transcription PCR. Loss- and gain-of function experiments were employed to explore the metabolic function of miR-592 using locked nucleic acids and adenovirus in lean and obese mice, respectively. The molecular target of miR-592 was determined by western blotting and luciferase reporter assays. Findings We found a significant decreased expression of miR-592 in the liver of obese mice and humans. Inhibition of miR-592 led to elevated blood glucose levels, enhanced gluconeogenesis and reduced insulin sensitivity in lean mice. In contrast, adenovirus-mediated overexpression of hepatic miR-592 improved metabolic disorders in obese mice. Mechanistically, we found that the transcription factor forkhead box O1 (FOXO1) is a direct target gene of miR-592 to mediate its metabolic functions. miR-592 was able to inhibit the mRNA and protein expression of FOXO1 by binding to its 3′-untranslated region. Interpretations Our findings demonstrate that obesity-associated down-regulation of miR-592 plays an important role in the progression of metabolic diseases. Restoration of hepatic miR-592 could improve glucose and lipid metabolism in obese mice. Fund This work is supported by the (No. 2016YFC1304805 to Dr. Chen), Natural Science Foundation of China (No. 81771574 to Dr. Wu), Shanghai Science Foundation (No. 18ZR1437800 to Dr. Li), Science and Technology Commission of Shanghai Municipality (Nos.18dz2304400 and 15,411,970,700 to Dr. Yang).

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Section: Discussionsupporting

confidence: 92%

Down-regulation of MicroRNA-592 in obesity contributes to hyperglycemia and insulin resistance

Song

et al. 2019

EBioMedicine

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“…Notably, the upregulation of miR-146b in obese individuals correlates with a reduction of glucose metabolism and fatty acids mobilization [86]. In line with this observation, miR-146b inhibition in free fatty acids-treated primary hepatocytes displays a decreased accumulation of cellular lipids [85]. Finally, miR-146 exerts a tumor suppressive role in liver cancer cells in vitro and in vivo, through the inhibition of AKT activation mediated by TRAF6 [87].…”

Section: Resultsmentioning

confidence: 97%

“…Intriguingly, ablation of miR-146 in mice leads to severe liver steatosis and hepatitis by the upregulation of TNF-α and IL-6 [82]. Conversely, elevated hepatic level of miR-146b has been found in rats and mice treated with HFD as well as in obese subjects with NAFLD [84,85,86]. Notably, the upregulation of miR-146b in obese individuals correlates with a reduction of glucose metabolism and fatty acids mobilization [86].…”

Section: Resultsmentioning

confidence: 99%

Hepatic MicroRNA Expression by PGC-1α and PGC-1β in the Mouse

Piccinin

Arconzo

Graziano

et al. 2019

IJMS

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The fine-tuning of liver metabolism is essential to maintain the whole-body homeostasis and to prevent the onset of diseases. The peroxisome proliferator-activated receptor-γ coactivators (PGC-1s) are transcriptional key players of liver metabolism, able to regulate mitochondrial function, gluconeogenesis and lipid metabolism. Their activity is accurately modulated by post-translational modifications. Here, we showed that specific PGC-1s expression can lead to the upregulation of different microRNAs widely implicated in liver physiology and diseases development and progression, thus offering a new layer of complexity in the control of hepatic metabolism.

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“…For example, mice with a high-fat diet exhibited in the epididymal AT significant downregulation of miR-1247 compared to mice with regular diet [57]. And more, the miR-1247 was upregulated in the liver of obesity-resistant mice compared to prone-obesity subjects raised with high-fat diet [58]. Therefore, the ENSSSCG00000041577 can be the source of miR-1247 that plays a significant role in the counteraction of obesity effects.…”

Section: Validation Of Rna-seq Resultsmentioning

confidence: 99%

Long-non Coding RNAs Related to Fat Deposition in Pigs Included lncRNA Corresponding to Human MALAT1

Piórkowska¹,

Żukowski²,

Ropka‐Molik³

et al. 2021

Preprint

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Obesity is a problem in the last decades since the development of different technologies forced the submission of a faster pace of life, resulting in nutrition style changes. In turn, domestic pigs are an excellent animal model in recognition of adiposity-related processes, corresponding to the size of individual organs, the distribution of body fat in the organism, and similar metabolism. The present study applied the next-generation sequencing method to identify adipose tissue (AT) transcriptomic signals related to increased fat content by identifying differentially expressed genes (DEGs), included long-non coding RNA molecules. The Freiburg RNA tool was applied to recognise predicting hybridisation energy of RNA-RNA interactions. The results indicated several long non-coding RNAs (lncRNAs) whose expression was significantly positively or negatively associated with fat deposition. lncRNAs play an essential role in regulating gene expression by sponging miRNA, binding transcripts, facilitating translation, or coding other smaller RNA regulatory elements. In the pig fat tissue of obese group, increased expression of lncRNAs corresponding to human MALAT1 was observed that previously recognised in the obesity-related context. Moreover, hybridisation energy analyses pinpointed numerous potential interactions between identified differentially expressed lncRNAs, and obesity-related genes and miRNAs expressed in AT.

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Role of miR-383 and miR-146b in different propensities to obesity in male mice

Cited by 18 publications

References 38 publications

Down-regulation of MicroRNA-592 in obesity contributes to hyperglycemia and insulin resistance

Down-regulation of MicroRNA-592 in obesity contributes to hyperglycemia and insulin resistance

Hepatic MicroRNA Expression by PGC-1α and PGC-1β in the Mouse

Long-non Coding RNAs Related to Fat Deposition in Pigs Included lncRNA Corresponding to Human MALAT1

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