Emodin improves glucose metabolism by targeting microRNA-20b in insulin-resistant skeletal muscle

Xiao, Dan; Hu, Yingying; Fu, Yujie; Wang, Rui; Zhang, Haiying; Li, Mingqi; Li, Zhange; Zhang, Ying; Xuan, Lina; Li, Xin; Xu, Chaoqian; Zhang, Yong; Yang, Baofeng

doi:10.1016/j.phymed.2018.11.018

Cited by 25 publications

(17 citation statements)

References 27 publications

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“…Secondly, emodin upregulates the levels of GLP-1R and PPAR- γ decreased in HFD mice in our experiment. However, emodin also protects individuals from weight gain, hyperglycemia, and hyperlipidemia in this work and others [ 43 , 44 ]. To exclude these potential mechanisms of beneficial effect from emodin, mice with hyperglycemia were removed from this experiment.…”

Section: Discussionsupporting

confidence: 62%

Emodin Attenuated the Kidney Damage of High-Fat-Diet Mice via the Upregulation of Glucagon-Like Peptide-1 Receptor

Liu¹,

Sun

Zheng³

et al. 2021

BioMed Research International

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Objective. Secretion of glucagon-like peptide 1 (GLP-1) and its effect on target organs were impaired in individuals with obesity. However, its mechanism needs to be further studied. We aim to explore the roles of the receptor of GLP-1 (GLP-1R) involved in high-fat-diet- (HFD-) induced kidney damage improved by emodin. Methods. Male C57bl/6 mice were fed with HFD diet and therapied by emodin. NRK-52E cells were cultured and treated with palmitic acid or low-density lipoprotein cholesterol (LDL-C). Emodin was used to remedy the NRK-52E cell damage. GW9662 was administrated to block the function of peroxisome proliferator-activated receptor γ (PPAR-γ). GLP-1 in the plasma was measured by ELISA. PPAR-γ and GLP-1R in the kidney and NRK-52E cells were detected by western blotting. The interaction between PPAR-γ protein and GLP-1R promoter regions was observed by chromatin immunoprecipitation (ChIP). Results. Postprandial GLP-1 levels in plasma, as well as PPAR-γ and GLP-1R, decreased in kidney tissue of HFD mice, while they were reserved by emodin treatment. Although PPAR-γ and GLP-1R were not downregulated by LDL-C, they were suppressed by palmitic acid. Interestingly, GLP-1R mRNA was detected by PCR in the mixture pulled down with PPAR-γ antibody. Additionally, downregulation of PPAR-γ and GLP-1R by palmitic acid was remanded by emodin. Moreover, GW9662, an inhibitor of PPAR-γ, abolished the protective effect of emodin. Conclusion. The kidney damage of HFD mice seems to be alleviated by emodin via the upregulation of GLP-1R in kidney tissue.

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Section: Discussionsupporting

confidence: 62%

Emodin Attenuated the Kidney Damage of High-Fat-Diet Mice via the Upregulation of Glucagon-Like Peptide-1 Receptor

Liu¹,

Sun

Zheng³

et al. 2021

BioMed Research International

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“…Let-7c, miR-20b, and miR-22 show relatively greater variance compared to others. Preliminary evidence supports associations between miR-20b and risk for T2DM, including insulin uptake in skeletal muscle [ 39 ] and T2DM-related complications including diabetic retinopathy [ 40 ] and endothelial cell function [ 41 ]. Similarly, miR-22 has been associated with adipose tissue mass, insulin sensitivity, and glucose homeostasis [ 42 ] and diabetic cardiomyopathy [ 43 ].…”

Section: Discussionmentioning

confidence: 99%

Circulating MicroRNAs predict glycemic improvement and response to a behavioral intervention

et al. 2021

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Background MicroRNAs may be important regulators of risk for type 2 diabetes. The purpose of this longitudinal observational study was to assess whether circulating microRNAs predicted improvements in fasting blood glucose, a major risk factor for type 2 diabetes, over 12 months. Methods The study included participants (n = 82) from a previously completed trial that tested the effect of restorative yoga on individuals with prediabetes. Circulating microRNAs were measured using a flow cytometry miRNA assay. Linear models were used to determine the optimal sets of microRNA predictors overall and by intervention group. Results Subsets of microRNAs were significant predictors of final fasting blood glucose after 12-months (R2 = 0.754, p < 0.001) and changes in fasting blood glucose over 12-months (R2 = 0.731, p < 0.001). Three microRNAs (let-7c, miR-363, miR-374b) were significant for the control group only, however there was no significant interaction by intervention group. Conclusions Circulating microRNAs are significant predictors of fasting blood glucose in individuals with prediabetes. Among the identified microRNAs, several have previously been associated with risk for type 2 diabetes. This is one of the first studies to use a longitudinal design to assess whether microRNAs predict changes in fasting blood glucose over time. Further exploration of the function of the microRNAs included in these models may provide new insights about the complex etiology of type 2 diabetes and responses to behavioral risk reduction interventions. Trial registration This study was a secondary analysis of a previously completed clinical trial that is registered at clinicaltrials.gov (NCT01024816) on December 3, 2009.

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“…Moreover, miR-214 was further proved to be a regulator of DPP4 in the adipocytes. Accumulated evidence demonstrate that miRNAs could exist pivotal regulatory effects in the pathogenesis of various diseases mediated by the target genes [24][25][26][27]. In the disease progression of IR, some members of miRNAs with critical roles have also been reported [28].…”

Section: Discussionmentioning

confidence: 99%

Aberrant expression of miR-214 is associated with obesity-induced insulin resistance as a biomarker and therapeutic

Cheng

Yuan

et al. 2020

Diagn Pathol

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Background: Insulin resistance (IR) in obesity is associated with the occurrence of metabolic and cardiovascular diseases. Dipepidyl peptidase 4 (DPP4) plays a pivotal role during the development of IR, and was found to be a target gene of microRNA-214 (miR-214) in our study. This study sought to assess the expression and clinical value of miR-214 in obese patients with IR, and investigate its therapeutic potential in obese rats and adipocytes with IR. Methods: Serum expression of miR-214 in obese patients with or without IR was estimated by quantitative realtime-PCR. A receiver operating characteristic curve was plotted to evaluate the diagnostic value of miR-214 in the patients. Obesity-induced IR animal and cell models were constructed, and the therapeutic ability of miR-214 was explored. Results: Serum expression of miR-214 was decreased in obese patients compared with the healthy controls, and the lowest expression was observed in the cases with IR. Downregulation of miR-214 was significantly correlated with the serum DPP4 levels and HOMA-IR of the patients upon IR conditions, and was demonstrated to perform diagnostic accuracy for distinguishing obese patients with IR from those without IR. In obesity-associated IR animal and cell models, the downregulation of miR-214 was also been detected. According to the measurement of glucose and insulin tolerance and glucose uptake abilities, we found that the overexpression of miR-214 could be used to alleviate IR in the IR models, especially when collaboratively used with DPP4 inhibitor vildagliptin. Conclusion: All data revealed that miR-214, as a regulator of DPP4, is decreased in obese patients with IR and may serve as a diagnostic biomarker. The upregulation of miR-214 could improve IR in obese rats and adipocytes, indicating that miR-214 has the therapeutic potential for obesity and IR.

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Emodin improves glucose metabolism by targeting microRNA-20b in insulin-resistant skeletal muscle

Cited by 25 publications

References 27 publications

Emodin Attenuated the Kidney Damage of High-Fat-Diet Mice via the Upregulation of Glucagon-Like Peptide-1 Receptor

Emodin Attenuated the Kidney Damage of High-Fat-Diet Mice via the Upregulation of Glucagon-Like Peptide-1 Receptor

Circulating MicroRNAs predict glycemic improvement and response to a behavioral intervention

Aberrant expression of miR-214 is associated with obesity-induced insulin resistance as a biomarker and therapeutic

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