CircRNF111 Protects Against Insulin Resistance and Lipid Deposition via Regulating miR-143-3p/IGF2R Axis in Metabolic Syndrome

Lin, Xihua; Du, Ying; Lu, Weina; Gui, Weiwei; Sun, Shuiya; Zhu, Yiyi; Wang, Gangliang; Eserberg, Daniel Turunen; Zheng, Fenping; Zhou, Jiaheng; Wu, Fang; Li, Hong

doi:10.3389/fcell.2021.663148

Cited by 17 publications

(16 citation statements)

References 61 publications

(78 reference statements)

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“…6). miR-143-3p was involved in protection of against insulin resistance and lipid deposition in liver metabolic syndrome [30]. The miRNA-mRNA-pathway regulatory network indicated PME miRNA may function as a critical regulator involved in the metabolic disorder of mice.…”

Section: Discussionmentioning

confidence: 99%

Cooked pork-derived exosome nanovesicles mediate metabolic disorder—microRNA could be the culprit

Shen

Yang

et al. 2022

Preprint

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In this study, we extracted exosomes from cooked meat by ultra-high-speed centrifugation. Exosome had an average of size of 70.29 nm. Flow cytometry demonstrated that the positive rate of exosomal surface marker CD63 and CD81 were 84.5% and 95.9%. microRNA sequencing revealed the exosomal microRNA were differences among porcine muscle, fat and liver. The mice plasma levels of miR-1, miR-133a-3p, miR-206 and miR-99a were increase with varying degrees after drinking water with exosomes. GTT and ITT suggest that abnormal glucose metabolism and insulin resistance in mice. Moreover, the lipid droplets were significant increased in the liver were also observed. Transcriptome analysis identified 446 differentially expressed genes in liver. Functional enrichment analysis found that metabolic pathway were most significantly enriched. microRNA may function as a critical regulator involved in the metabolic disorder of mice. This study suggests that the exosomal microRNAs from meat products has the potential to adversely affect health.

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Section: Discussionmentioning

confidence: 99%

Cooked pork-derived exosome nanovesicles mediate metabolic disorder—microRNA could be the culprit

Shen

Yang

et al. 2022

Preprint

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“…In addition, miR-143-3p overexpression has been demonstrated to alleviate the pulmonary inflammatory response and suppress alveolar epithelial cell apoptosis in mice with mycoplasmal pneumonia (37). miR-143-3p was also found to at least partially reverse obesity-induced insulin resistance by downregulating insulin-like growth factor 2 receptor expression in differentiated hADSCs (50). However, the role of miR-143-3p in GDM remains elusive and requires further investigation.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑143‑3p levels are reduced in the peripheral blood of patients with gestational diabetes mellitus and influences pancreatic β‑cell function and viability

et al. 2022

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Pancreatic β-cell dysfunction has been demonstrated to mediate key roles in the pathogenesis of gestational diabetes mellitus (GDM). Accumulating evidence has supported the functional involvement of microRNAs (miRNAs) in various types of diabetes, including GDM. However, the detailed biological effect of miRNAs in pancreatic β-cell dysfunction remains poorly understood. In the present study, microarray data of miRNAs in the blood plasma of patients with GDM were retrieved from the Gene Expression Omnibus dataset under the accession number GSE98043. Reverse transcription-quantitative PCR (RT-qPCR) was performed to measure the expression levels of miR-143-3p in the blood plasma isolated from 30 female patients with GDM women and 30 healthy female individuals. Subsequently, murine pancreatic β-cell line, MIN6 cells were treated with high glucose (HG) to construct in vitro cell models of GDM. miR-143-3p in HG-treated MIN6 cells was overexpressed or knocked down using miR-143-3p mimics and miR-143-3p inhibitor. Cell viability, insulin secretion and proinflammatory cytokine production were examined using CCK-8 and ELISA, respectively Cell apoptosis was measured by flow cytometry assay. The protein expression levels of proteins involved in the TAK1/NF-κB pathway were also assessed using western blot. The levels of miR-143-3p were found to be markedly lower in samples from patients with GDM, which were in turn negatively correlated with blood glucose levels. Overexpression of miR-143-3p in MIN6 cells significantly reversed HG-induced cell apoptosis and impairments in cell viability and insulin secretion. In addition, miR-143-3p overexpression attenuated HG-induced proinflammatory cytokine production by MIN6 cells. Subsequently, TGFβ-activated kinase 1 (TAK1), an upstream regulator of the NF-κB pathway, was found to be a direct target of miR-143-3p in pancreatic β cells through luciferase assays and western blot. Overexpression of TAK1 was revealed to abolish the curative effects of miR-143-3p on insulin secretion, cell viability and inflammatory response in HG-treated MIN6 cells. In addition, miR-143-3p could inactivate the NF-κB pathway by inhibiting TAK1 expression. Collectively, these results suggest that miR-143-3p levels are downregulated in the peripheral blood of patients with GDM. Therefore, miR-143-3p overexpression may serve as a method for preventing pancreatic β cell dysfunction by inhibiting the TAK1/NF-κB pathway.

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“…Another circRNA deep sequencing analysis of sera from patients with metabolic syndrome (MetS) identified the presence of a novel circRNA, circRNF111, involved in MetS progression. 278 CircRNF111 inhibition enhances IR and lipid deposition in MetS by regulating the miR-143-3p/ IGF2R pathway.…”

Section: The Insulin Signaling and Irmentioning

confidence: 99%

Trends in insulin resistance: insights into mechanisms and therapeutic strategy

Chi²,

Wang

et al. 2022

Sig Transduct Target Ther

246

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The centenary of insulin discovery represents an important opportunity to transform diabetes from a fatal diagnosis into a medically manageable chronic condition. Insulin is a key peptide hormone and mediates the systemic glucose metabolism in different tissues. Insulin resistance (IR) is a disordered biological response for insulin stimulation through the disruption of different molecular pathways in target tissues. Acquired conditions and genetic factors have been implicated in IR. Recent genetic and biochemical studies suggest that the dysregulated metabolic mediators released by adipose tissue including adipokines, cytokines, chemokines, excess lipids and toxic lipid metabolites promote IR in other tissues. IR is associated with several groups of abnormal syndromes that include obesity, diabetes, metabolic dysfunction-associated fatty liver disease (MAFLD), cardiovascular disease, polycystic ovary syndrome (PCOS), and other abnormalities. Although no medication is specifically approved to treat IR, we summarized the lifestyle changes and pharmacological medications that have been used as efficient intervention to improve insulin sensitivity. Ultimately, the systematic discussion of complex mechanism will help to identify potential new targets and treat the closely associated metabolic syndrome of IR.

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CircRNF111 Protects Against Insulin Resistance and Lipid Deposition via Regulating miR-143-3p/IGF2R Axis in Metabolic Syndrome

Cited by 17 publications

References 61 publications

Cooked pork-derived exosome nanovesicles mediate metabolic disorder—microRNA could be the culprit

Cooked pork-derived exosome nanovesicles mediate metabolic disorder—microRNA could be the culprit

MicroRNA‑143‑3p levels are reduced in the peripheral blood of patients with gestational diabetes mellitus and influences pancreatic β‑cell function and viability

Trends in insulin resistance: insights into mechanisms and therapeutic strategy

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