ABSTRACT
BACKGROUND: Our objective was to evaluate how various measures of obesity, such as body mass index(BMI), body roundness index(BRI), and weigh adjusted waist index(WWI), influence urate levels, prevalence of gout and to compare the disparities among these obesity indicators. METHODS: By analyzing the 2001-2018 National Health and Nutrition Examination Survey (NHANES), we assessed the relationship between BMI, WWI, and BRI indices and urate levels, hyperuricemia, and the prevalence of gout. Smoothed curve fitting was used to determine whether there was a nonlinear relationship between BMI,WWI, and BRI indices and urate levels, hyperuricemia, and the prevalence of gout, and threshold effects analysis was used to test this relationship. We also used ROC curves to determine the diagnostic efficacy of BMI, WWI, and BRI on the prevalence of hyperuricemia and gout. RESULTS: The study incorporated a total of 29,310 participants aged over 20 years, out of which 14,268 were male. Following the adjustment for the pertinent confounding factors, it was observed that higher levels of BMI, WWI, and BRI were significantly associated with a gradual and dose-dependent increase in urate levels. In the sensitivity analysis, each unit increment in BMI, WWI, and BRI levels exhibited an 8%, 72%, and 26% respective elevation in the risk of hyperuricemia, as well as a 5%, 31%, and 15% respective increase in the risk of gout. Dose-response curves provided evidence of a linear positive correlation between BMI, WWI, BRI, and urate levels, as well as the prevalence of hyperuricemia and gout. Based on the response from the ROC curve, overall, the diagnostic efficacy of BRI for hyperuricemia and gout surpasses that of BMI. CONCLUSION: The central obesity indices WWI and BRI levels are superior to BMI in detecting the prevalence of urate levels, hyperuricemia, and gout, and although a clear causal relationship has not yet been established, it is important to recognize the impact of central obesity on uric acid levels and to give it due attention.
ABSTRACT
Diabetic nephropathy (DN) is the second most common complication of diabetes mellitus after cardiovascular complications. Endoplasmic reticulum (ER) stress is known to be associated with DN. Resveratrol (RSV) exhibits antioxidative, antiinflammatory and cytoprotective effects. Therefore, the aims of the present study were to investigate the role of RSV in the inhibition of high concentration glucose (HG)induced apoptosis in renal tubular cells, as well as to examine the protective effects of RSV against diabetesmediated renal damage via inhibition of ER stress in DN. RSV was orally administered to diabetic db/db mice once a day for 12 consecutive weeks. Compared with untreated db/db mice, treating db/db mice with RSV significantly decreased urine albumin excretion and the urine albumin to creatinine ratio, and attenuated renal histopathological injury. Furthermore, RSV treatment resulted in decreased expression levels of glucoseregulated protein of 78 kDa and C/EBPhomologous protein (two ER stress markers) and caspase12 in murine kidneys. RSV administration also inhibited the apoptosis of NRK52E cells and activation of the ER stress signal transduction pathway induced by HG treatment in vitro. Collectively, the present results indicated that RSV protected renal tubular cells against HGinduced apoptosis in DN by suppressing ER stress.
