Correlation analysis of microribonucleic acid‐155 and microribonucleic acid‐29 with type 2 diabetes mellitus, and the prediction and verification of target genes

Abstract

Aims/Introduction Microribonucleic acid‐155 (microRNA155) and microRNA29 are reported to inhibit glucose metabolism in some cell and animal models, but no evidence from susceptible populations that examines the relationship between microRNA155 or microRNA29 and type 2 diabetes mellitus currently exists. Furthermore, target genes regulated by microRNA155 and microRNA29 that affect glucose and lipid metabolism remain unknown. Materials and Methods Human participants were divided into normal weight (n = 72), obesity (n = 120) and type 2 diabetes (n = 59) groups. The contents of microRNA155 and microRNA29 abundance in serum were measured, and candidate genes potentially related to glucose and lipid metabolism targeted by either microRNA155 or microRNA29 were screened. Overexpression of microRNA155 and microRNA29 in HepG2 cells was used to verify candidate gene expression, and measure the effects on glucose and lipid metabolism. Results Serum levels of microRNA155 and microRNA29 show a significant increase in individuals with obesity and type 2 diabetes compared with normal weight individuals. Identified target genes for microRNA155 were MAPK14, MAP3K10, DUSP14 and PRKAR2B. Identified target genes for microRNA29 were PEX11A and FADS1. Overexpression of microRNA155 or microRNA29 in HepG2 cells was found to downregulate the expression of identified target genes, and result in inhibition of triglyceride synthesis and glucose incorporation. Conclusions MicroRNA155 and microRNA29 were significantly higher in type 2 diabetes patients compared with the control patients, their levels were also positively correlated with fasting plasma glucose levels, and over‐expression of microRNA155 or microRNA29 were found to downregulate glucose and lipid metabolism target genes, and reduce lipid synthesis and glucose incorporation in HepG2 cells.

Investigation of umbilical cord serum miRNAs associated with childhood obesity: A pilot study from a birth cohort study

“…In addition, Marcondes et al 16 demonstrated that altered miR-181a in umbilical cord blood cells could be adopted as a biomarker for childhood obesity. Moreover, in the past few years, it has been reported that circulating miRNAs may also play a variety of biological roles, such as in energy homeostasis and metabolic processes 6,17,18 . Three of the candidate miRNAs in this study have been reported to be associated with metabolism.…”

Cherry juice alleviates high-fat diet-induced obesity in C57BL/6J mice by resolving gut microbiota dysbiosis and regulating microRNA

“…These microRNAs include miR-27a-5p, miR-27b-5p, miR-146a-5p, miR-378a-3p, miR-155a, miR-223-3p, miR-132-3p, miR-200c-3p, miR181a and miR-125a, which have previously been linked to obesity. 15–20…”

“…These microRNAs include miR-27a-5p, miR-27b-5p, miR-146a-5p, miR-378a-3p, miR-155a, miR-223-3p, miR-132-3p, miR-200c-3p, miR181a and miR-125a, which have previously been linked to obesity. [15][16][17][18][19][20] Previous research has linked dysregulation of the gut microbiota to obesity and other metabolic syndromes. 21 The richness of the gut microbiota in obese hosts is lower than that of the normal microflora, and anthocyanin-rich fruit intervention can increase the richness of the gut microbiota and reduce body weight.…”

miR‐4431 targets TRIP10/PRKD1 and impairs glucose metabolism

“…Moreover, obesity‐associated microRNAs, such as miR‐192, miR‐27a‐3p, and miR‐27b‐3p, can modulate glucose and lipid metabolism in mice 9 . Recent studies have demonstrated that miR‐155 and miR‐29 levels are elevated in the serum of obese and type 2 diabetes mellitus patients, and an overexpression of miR‐155 and miR‐29 in HepG2 cells negatively impacts glucose and lipid metabolism 10 . These results suggest the important role of miRNAs in obesity and related metabolic disorders.…”