Adipose HuR protects against diet-induced obesity and insulin resistance

Li, Jingyuan; Gong, Lei; Liu, Shaozhuang; Zhang, Yujie; Zhang, Chunmei; Tian, Mi; Lu, Huixia; Bu, Peili; Yang, Jianmin; Chen, Ouyang; Jiang, Xiuxin; Wu, Jiliang; Zhang, Yun; Qi, Min; Cheng, Zhenshun; Zhang, Wencheng

doi:10.1038/s41467-019-10348-0

Cited by 63 publications

(49 citation statements)

References 47 publications

(49 reference statements)

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“…* p<0.05; ** p<0.01; *** p<0.001; **** p<0.0001; ns, not statistically significant. Many studies have indicated that HFD can induce adipocyte expansion in size and number, which aims to accommodate the need for excessive TG storage and the anabolic force of hyperinsulinemia [32][33][34]. Our study shown that RD reduced visceral fat accumulation, adipocyte hypertrophy and serum TG.…”

Section: Discussionsupporting

confidence: 54%

Resistant dextrin reduces obesity and attenuates adipose tissue inflammation in high-fat diet-fed mice

et al. 2020

Int. J. Med. Sci.

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Resistant dextrin (RD), a short chain glucose polymer, has been shown to improve type 2 diabetes mellitus (T2DM) in clinical studies. However, the improvement of adipose tissue inflammation and specific mechanisms of RD supplementation in obesity have not been fully investigated. Therefore, we examined whether RD attenuates obesity and adipose tissue inflammation in high-fat diet (HFD)-fed mice. Male C57BL/6 mice were fed a chow diet, a HFD or a HFD with RD supplementation for 12 weeks. Body weight (BW), fasting blood glucose (FBG), epididymal fat accumulation, serum total triglyceride (TG), free fatty acid (FFA) and inflammatory cytokine levels (TNF-α, IL-1β, IL-6, IL-10) were measured. Inflammation markers and macrophage infiltration in epididymal adipose tissue were observed. After 12 weeks of intervention, the body weight gain of mice in RD supplementation group was less than that in HFD group. FBG, epididymal fat accumulation, serum TG and FFA levels were reduced in RD supplementation group compared with HFD group. Moreover, serum and mRNA levels of IL-6 were significantly reduced in the RD supplementation group. In addition, RD supplementation reduced macrophage infiltration, regulated polarization of macrophage and inhibited NF-κB signaling in epididymal adipose tissue. In conclusion, RD reduces obesity and attenuates adipose tissue inflammation in HFD-fed mice, and the inhibition of NF-κB signaling may be a presumed mechanism for its effects.

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Section: Discussionsupporting

confidence: 54%

Resistant dextrin reduces obesity and attenuates adipose tissue inflammation in high-fat diet-fed mice

et al. 2020

Int. J. Med. Sci.

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“…We next probed lipolytic activity and fatty acid oxidation enhancement by analyzing serum glycerol levels, adipose lipolytic/lipogenic protein levels, and fatty acid catabolic pathways in the treated mice. We found that the treated obese mice demonstrated increases in serum glycerol levels linked to lipolysis [ 29 ] ( Figure S2 ). We also evaluated the effects of hormone-sensitive lipase (HSL) expression on lipolysis, fatty acid oxidation [ 30 , 31 ], and patatin-like phospholipid domain containing protein 3 (PNPLA3) expression in lipogenesis [ 32 ] ( Figure S3 ).…”

Section: Discussionmentioning

confidence: 99%

Mirtazapine Reduces Adipocyte Hypertrophy and Increases Glucose Transporter Expression in Obese Mice

Hou

Mao

et al. 2020

Animals

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Metabolic syndrome is known to engender type 2 diabetes as well as some cardiac, cerebrovascular, and kidney diseases. Mirtazapine—an atypical second-generation antipsychotic drug with less severe side effects than atypical first-generation antipsychotics—may have positive effects on blood glucose levels and obesity. In our executed study, we treated male high-fat diet (HFD)-fed C57BL/6J mice with mirtazapine (10 mg/kg/day mirtazapine) for 4 weeks to understand its antiobesity effects. We noted these mice to exhibit lower insulin levels, daily food efficiency, body weight, serum triglyceride levels, aspartate aminotransferase levels, liver and epididymal fat pad weight, and fatty acid regulation marker expression when compared with their counterparts (i.e., HFD-fed control mice). Furthermore, we determined a considerable drop in fatty liver scores and mean fat cell size in the epididymal white adipose tissue in the treated mice, corresponding to AMP-activated protein kinase expression activation. Notably, the treated mice showed lower glucose tolerance and blood glucose levels, but higher glucose transporter 4 expression. Overall, the aforementioned findings signify that mirtazapine could reduce lipid accumulation and thus prevent HFD-induced increase in body weight. In conclusion, mirtazapine may be useful in body weight control and antihyperglycemia therapy.

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“…However, accumulating evidence has shed light on how RNA networks dynamically affect metabolic, developmental, and inflammatory mechanisms in the pathogenesis of obesity-associated disorders. Indeed, functional changes of additional RBPs, including but not limited to LIN28A, IGF2BP2/IMP2, and HuR, are linked to the development of metabolic diseases (213–215). RNA methylation influences and fate maps RNA toward translation, degradation, or even sequestration inside cellular compartments.…”

Section: Discussionmentioning

confidence: 99%

RNAs and RNA-Binding Proteins in Immuno-Metabolic Homeostasis and Diseases

Salem

Vonberg

Borra

et al. 2019

Front. Cardiovasc. Med.

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The increasing prevalence of worldwide obesity has emerged as a major risk factor for type 2 diabetes (T2D), hepatosteatosis, and cardiovascular disease. Accumulating evidence indicates that obesity has strong inflammatory underpinnings tightly linked to the development of metabolic diseases. However, the molecular mechanisms by which obesity induces aberrant inflammation associated with metabolic diseases are not yet clearly defined. Recently, RNAs have emerged as important regulators of stress responses and metabolism. RNAs are subject to changes in modification status, higher-order structure, and cellular localization; all of which could affect the affinity for RNA-binding proteins (RBPs) and thereby modify the RNA-RBP networks. Proper regulation and management of RNA characteristics are fundamental to cellular and organismal homeostasis, as well as paramount to health. Identification of multiple single nucleotide polymorphisms (SNPs) within loci of fat mass- and obesity-associated protein (FTO) gene, an RNA demethylase, through genome-wide association studies (GWAS) of T2D, and functional assessments of FTO in mice, support the concept that disruption in RNA modifications leads to the development of human diseases including obesity and metabolic disorder. In obesity, dynamic alterations in modification and localization of RNAs appear to modulate the RNA-RBP networks and activate proinflammatory RBPs, such as double-stranded RNA (dsRNA)-dependent protein kinase (PKR), Toll-like receptor (TLR) 3 and TLR7, and RNA silencing machinery. These changes induce aberrant inflammation and the development of metabolic diseases. This review will describe the current understanding of the underlying causes of these common and altered characteristics of RNA-RBP networks which will pave the way for developing novel approaches to tackle the pandemic issue of obesity.

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Adipose HuR protects against diet-induced obesity and insulin resistance

Cited by 63 publications

References 47 publications

Resistant dextrin reduces obesity and attenuates adipose tissue inflammation in high-fat diet-fed mice

Resistant dextrin reduces obesity and attenuates adipose tissue inflammation in high-fat diet-fed mice

Mirtazapine Reduces Adipocyte Hypertrophy and Increases Glucose Transporter Expression in Obese Mice

RNAs and RNA-Binding Proteins in Immuno-Metabolic Homeostasis and Diseases

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