The prevalence of the metabolic syndrome in the Yan-an region was significantly higher than that in other regions of China, and participants with the metabolic syndrome were much younger than those in other Chinese regions.

Pancreatic β cells undergo significant expansion and maturation during human and rodent postnatal development. Here, we used single-cell RNA-seq to characterize gene expression patterns at various stages of mouse islet cell development and uncovered a population of cells that is most abundant during the early postnatal period. This cell population lacks expression of FLTP and expresses PDGF receptors. Each of these conditions have previously been associated with proliferative capacity in β cells suggesting that we have identified the proliferative competent of β cell mass expansion. The subpopulation co-express many endocrine lineage-specific genes and exhibits a downregulation of genes associated with mitochondrial oxidative phosphorylation and global protein synthesis. It has upregulated activity of genes in the Wnt, Hippo, PDGF, and Notch pathways and has a significantly higher proliferation potential than the more mature β population. We show that activity of the Notch pathway is required in postnatal β cell expansion where it serves to maintain an undifferentiated endocrine state in the polyhormonal cell population. Collectively, our study identifies a proliferative, progenitor-like cell subpopulation in the postnatal islet as the source of postnatal β cell expansion.

ABSTRACT. The aim of this study was to investigate the correlation between the A1166C polymorphism in the angiotensin II type 1 receptor (AT1R) gene and heart failure (HF) risk using meta-analysis. The PubMed database was searched, and data were extracted independently by two reviewers. Odds ratios (ORs) with corresponding 95% confi dence intervals (CIs) were used to assess the strength of the associations. Statistical analysis was performed using the STATA 12.0 software. The results of the metaanalysis showed no significant association between the AT1R A1166C polymorphism and HF risk (AA vs CC: OR = 0.72, 95%CI = 0.31-1.68; AA vs AC: OR = 0.78, 95%CI = 0.52-1.18; dominant model: OR = 1.37, 95%CI = 0.92-2.04; recessive model: OR = 0.73, 95%CI = 0.30-1.75). In the subgroup analysis by ethnicity, the results also showed no significant association between A1166C polymorphism and susceptibility to HF in both Caucasian and Asian populations. In conclusion, this meta-analysis suggests that the A1166C polymorphism in AT1R may not be associated with susceptibility to HF. J.A. Zhang et al. 9164©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 14 (3): 9163-9170 (2015) Further large and welldesigned studies are needed to confirm these conclusions.

A number of studies have previously assessed the impact of antibiotic exposure in early life on the risk of childhood obesity, but no systematic assessment is currently available. A systematic review and meta-analysis was performed to comprehensively and quantitatively elucidate the risk of childhood obesity caused by antibiotic exposure in early life. Literature search was performed in PubMed, Embase, and Web of Science. Random-effect meta-analysis was used to pool the statistical estimates. Fifteen cohort studies involving 445,880 participants were finally included, and all those studies were performed in developed countries. Antibiotic exposure in early life significantly increased risk of childhood overweight [relative risk (RR) = 1.23, 95% confidence interval (CI) 1.13-1.35, P < 0.001] and childhood obesity (RR = 1.21, 95% CI 1.13-1.30, P < 0.001). Antibiotic exposure in early life also significantly increased the z-score of childhood body mass index (mean difference: 0.07, 95% CI 0.05-0.09, P < 0.00001). Importantly, there was an obvious dose-response relationship between antibiotic exposure in early life and childhood adiposity, with a 7% increment in the risk of overweight (RR = 1.07, 95% CI 1.01-1.15, P = 0.03) and a 6% increment in the risk of obesity (RR = 1.06, 95% CI 1.02-1.09, P < 0.001) for each additional course of antibiotic exposure. In conclusion, antibiotic exposure in early life significantly increases risk of childhood obesity. Moreover, current analyses are mainly taken from developed countries, and therefore the impact of antibiotic exposure on risk of childhood obesity in vulnerable populations or developing countries still needs to be evaluated in future studies.