Nonalcoholic fatty liver disease is associated with obesity and insulin resistance. Factors that regulate the disposal of hepatic triglycerides contribute to the development of hepatic steatosis. G0/G1 switch gene 2 (G0S2) is a target of peroxisome proliferator-activated receptors and plays an important role in regulating lipolysis in adipocytes. Therefore, we investigated whether G0S2 plays a role in hepatic lipid metabolism. Adenovirus-mediated expression of G0S2 (Ad-G0S2) potently induced fatty liver in mice. The liver mass of Ad-G0S2-infected mice was markedly increased with excess triglyceride content compared to the control mice. G0S2 did not change cellular cholesterol levels in hepatocytes. G0S2 was found to be co-localized with adipose triglyceride lipase at the surface of lipid droplets. Hepatic G0S2 overexpression resulted in an increase in plasma Low-density lipoprotein (LDL)/Very-Low-density (VLDL) lipoprotein cholesterol level. Plasma High-density lipoprotein (HDL) cholesterol and ketone body levels were slightly decreased in Ad-G0S2 injected mice. G0S2 also increased the accumulation of neutral lipids in cultured HepG2 and L02 cells. However, G0S2 overexpression in the liver significantly improved glucose tolerance in mice. Livers expressing G0S2 exhibited increased 6-(N-(7-nitrobenz-2-oxa-1-3-diazol-4-yl) amino)-6-deoxyglucose uptake compared with livers transfected with control adenovirus. Taken together, our results provide evidence supporting an important role for G0S2 as a regulator of triglyceride content in the liver and suggest that G0S2 may be a molecular target for the treatment of insulin resistance and other obesity-related metabolic disorders.

BackgroundRed cell distribution width (RDW) is associated with a poor prognosis and adverse events in cardiovascular diseases. The aims of this study were to investigate the relationship between serum RDW levels and outcomes after percutaneous coronary intervention and to identify potential novel laboratory markers for evaluating the risk of in-stent restenosis (ISR) with stable angina pectoris.MethodsA total of 261 patients with coronary heart disease from Dongfeng General Hospital implanted with a coronary drug-eluting stent (DES) were enrolled in the study. We retrospectively analysed the role and prognosis values of serum parameters that were measured before angiography at the first admission. According to the results of the second angiogram, the patients were divided into two groups as follows: the non-ISR group (n=143) and the ISR group (n=118). The clinical characteristics and all laboratory data were considered for univariate and multivariate logistic regression analyses.ResultsThe white cell count, RDW, neutrophil count, C-reactive protein (CRP), total cholesterol, low-density lipoprotein cholesterol (LDL-C), blood urea nitrogen and uric acid levels were higher in the ISR group than in the non-ISR group. There were no differences in the rates of hypertension, fasting plasma glucose, red cell count, neutrophil to lymphocyte ratio, platelet count, triglyceride, high-density lipoprotein cholesterol and creatinine levels. In the univariate regression analysis, age, diabetes, white cell count, neutrophil count, RDW, CRP, total cholesterol, LDL-C, blood urea nitrogen, Gensini score and number of stents were predictors of ISR. According to the multiple logistic regression analysis, age, RDW and number of stents were independent predictors of ISR.ConclusionsPreprocedural blood parameters can independently predict ISR. Our study results demonstrated that a high preprocedural RDW is an independent predictor of DES restenosis.

BackgroundCoronary artery disease (CAD) is the most frequent multifactorial disease worldwide and is characterised by endothelial injury, lipid deposition and coronary artery calcification. The purpose of this study was to determine the allelic and genotypic frequencies of two loci (rs2026458 and rs9349379) of phosphatase and actin regulator 1 (PHACTR1) to the risk of developing CAD in the Chinese Han population.MethodsA case–control study was conducted including 332 patients with CAD and 119 controls. Genotype analysis was performed by PCR and Sanger sequencing. Genetic model analysis was performed to evaluate the association between single nucleotide polymorphisms and CAD susceptibility using Pearson’s χ2 test and logistic regression analysis.ResultsThe GG genotype of rs9349379 represented 50% and 29% of patients with CAD and controls, respectively (p<0.001). The CC genotype of rs2026458 was more prevalent in the controls than in patients with CAD compared with TT genotype (OR=0.548, 95% CI 0.351 to 0.856, p=0.008). Logistic regression analyses revealed that PHACTR1 rs9349379 GG genotype was significantly associated with increased risk of CAD in the recessive model (OR=2.359, 95% CI 1.442 to 3.862, p=0.001), even after adjusting for age gender, hypertension, type 2 diabetes, hyperlipidaemia and smoking habit. Heterogeneity test proved that rs9349379’s risk effects on CAD were more significant among women.ConclusionsOur study indicate that the PHACTR1 rs9349379 polymorphism is associated with the increased risk for CAD in the female Chinese Han population.

Glucagon-like peptide-1 (GLP-1) is a 30-amino acid hormone secreted by L cells in the distal ileum, colon, and pancreatic α cells, which participates in blood sugar regulation by promoting insulin release, reducing glucagon levels, delaying gastric emptying, increasing satiety, and reducing appetite. GLP-1 specifically binds to the glucagon-like peptide-1 receptor (GLP-1R) in the body, directly stimulating the secretion of insulin by pancreatic β-cells, promoting proliferation and differentiation, and inhibiting cell apoptosis, thereby exerting a glycemic lowering effect. The glycemic regulating effect of GLP-1 and its analogues has been well studied in human and murine models in the circumstance of many diseases. Recent studies found that GLP-1 is able to modulate innate immune response in a number of inflammatory diseases. In the present review, we summarize the research progression of GLP-1 and its analogues in immunomodulation and related signal pathways.