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We determined if the increasing trend in hypertension can be partly attributed to increasing prevalence of overweight/obesity in China over the past two decades. Data were collected from 1991 to 2011 and the population attributable risk (PAR), which is used to estimate the intervention effect on hypertension if overweight/obese, were eliminated. Linear regression was used to evaluate the secular trends. The age-standardized prevalence of overweight and obesity increased by 26.32% with an overall slope of 1.27% (95% CI: 1.12–1.43%) per year. Hypertension also increased by 12.37% with an overall slope of 0.65% (95% CI: 0.51–0.79%) per year. The adjusted ORs of overweight/obesity for hypertension across the survey years remained unchanged; however, the trend in PAR increased steadily from 27.1 to 44.6% with an overall slope of 0.81% (95% CI: 0.34–1.28%) per year (P = 0.006). There was no significant gender difference in the slopes of increasing PAR, as measured by regression coefficients (β = 0.95% vs. β = 0.63% per year, P = 0.36). Over the past two decades, the increase in the prevalence of hypertension in China was partly attributed to the overweight/obesity epidemic, which highlights the importance of controlling weight and further reducing the burden of hypertension.

IntroductionIntrauterine malnutrition impairs embryo kidney development and leads to kidney disease and hypertension in adulthood, yet the underlying mechanism remains unclear.MethodsWith a maternal protein restriction (MPR) rat model, we investigated the critical ciliogenesis factors and β-catenin pathway in FGR fetal kidneys and analyzed the impact of aberrant primary cilia on renal tubular epithelium.ResultsThe data showed decreased nephron number and renal tubular dysgenesis in FGR fetus. FGR fetus showed deregulated expression of ciliogenesis factors including upregulation of IFT88 and downregulation of DYNLT1, accompanied with cilia elongation in renal tubular epithelial cells. Wnt7b, the key ligand for Wnt/β-catenin signaling, was downregulated and nuclear translocation of β-catenin was decreased. The proapoptotic protein was upregulated. In vitro study with HK-2 cells showed that overexpression of IFT88 lengthened the cilia, inhibited β-catenin signaling. Besides, IFT88 overexpression suppressed cell proliferation, activated autophagy, and induced cell apoptosis. Inhibition of autophagy partly restored the cilia length and cell viability. Likewise, knockdown of DYNLT1 led to cilia elongation, suppressed cell proliferation, and promoted apoptosis in HK-2 cell. However, the cilia elongation induced by DYNLT1 knockdown was not autophagy-dependent, but associated with reactive oxygen species (ROS) accumulation.DiscussionWe elucidated that intrauterine protein malnutrition led to deregulation of ciliogenesis factors and cilia elongation in renal tubular epithelial, inhibited β-catenin signaling, and induced cell apoptosis and ultimately, compromised kidney development.