This study aims to examine the relationship between high birth weight (HBW) and blood pressure and assess whether HBW leads to increased hypertension during childhood and adolescence. All the participants aged 6-18 years with HBW were selected from a cross-sectional study from seven provinces in China. Nine thousand nine hundred and sixty-two children were randomly sampled with matched data. Basic information of students was collected with a standardized student and guardian questionnaire. High blood pressure was defined according to sex-, age- and height-specific references. Multi-variance logistic regression was used to estimate the odds ratio (OR) of high blood pressure and HBW after adjustment for confounding factors. The overall mean of systolic BP and diastolic BP in HBW group were significantly higher than normal group in both genders and urban/rural area. Corresponding overall prevalence of high BP, elevated SBP and elevated DBP in HBW group were also higher than normal group in both genders, respectively (boys: 19.41% vs 16.16%; 10.12% vs 8.16%; 14.86% vs 12.71%; girls: 14.95% vs 12.66%; 8.19% vs 6.56%; 11.13% vs 9.86%). In addition, birth weight was positively associated with high BP, elevated SBP and elevated DBP in children and adolescents of both sexes (boys: OR 1.25, 1.27, 1.20; girls: OR 1.21, 1.27, 1.15). However, the positive association was attenuated and even reversed after adjustment for potential confounding variables. In this study, HBW may lead to higher childhood blood pressure, but no association between HBW and childhood hypertension was observed.

The present work provides evidence that mouse miR-20a promotes adipocyte progenitor cells to differentiate and this function may depend upon its inhibitory effects on Kdm6b and TGF-β signaling.

Background Oxidative stress contributes to adverse atrial remodeling in diabetes mellitus. This can be prevented by the PPAR-γ agonist pioglitazone through its anti-oxidant and anti-inflammatory effects. Purpose In this study, the molecular mechanisms underlying these effects were investigated. Methods Rabbits were randomly divided into control (C), diabetic (DM), and pioglitazone-treated DM (Pio) groups. Echocardiographic, hemodynamic, electrophysiological, intracellular Ca2+ properties were measured. Serum PPAR-γ levels, serum and tissue oxidative stress and inflammatory markers, mitochondrial morphology, reactive oxygen species (ROS) production rate, respiratory function, and mitochondrial membrane potential (MMP) levels were measured. Protein expression of pro-fibrotic marker transforming growth factor β1 (TGF-β1), and the mitochondrial proteins (PGC-1α, fission and fusion-related proteins) were measured. Results Compared with controls, the DM group demonstrated larger left atrial diameter and fibrosis area associated with a higher incidence of inducible AF. Lower serum PPAR-γ level was associated with lower PGC-1α, higher NF-κB and higher TGF-β1 expression. Mn-SOD protein was not different but lower mitochondrial fission- and fusion-related proteins were detected. Mitochondrial swelling, higher mitochondrial ROS, lower respiratory control rate, lower MMP and higher intracellular Ca2+ transients were observed. In the Pio group, reversal of structural remodeling and lower inducible AF incidence were associated with higher PPAR-γ and PGC-1α. NF-κB and TGF-β1 were lower and biogenesis, fission and fusion-related protein were higher. Mitochondrial structure and function, and intracellular Ca2+ transients were improved. In HL-1 cell line, transfected with PGC-1α siRNA blunted the effect of pioglitazone on Mn-SOD protein expression and MMP collapse in H2O2-treated cells. Conclusion Diabetes mellitus induces adverse atrial structural and electrophysiological remodeling, abnormal Ca2+ handling and mitochondrial damage and dysfunction. Pioglitazone prevented these abnormalities through the PPAR-γ/PGC-1α pathway. Acknowledgement/Funding National Natural Science Foundation of China (No 81570298, 81270245, 30900618 to T.L.)