Mohsen Mazidi1, Niki Katsiki2, Dimitri P Mikhailidis3, Maciej Banach4. 1. Key State Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Chaoyang, Beijing, China; Institute of Genetics and Developmental Biology, International College, University of Chinese Academy of Science (IC-UCAS), West Beichen Road, Chaoyang, China. Electronic address: moshen@genetics.ac.cn. 2. Second Propedeutic Department of Internal Medicine, Medical School, Aristotle University of Thessaloniki, Hippokration Hospital, Thessaloniki, Greece. 3. Department of Clinical Biochemistry, Royal Free Campus, University College London Medical School, University College London (UCL), London, UK. 4. Department of Hypertension, Chair of Nephrology and Hypertension, Medical University of Lodz, Poland; Polish Mother's Memorial Hospital Research Institute (PMMHRI), Lodz, Poland; Cardiovascular Research Centre, University of Zielona Gora, Zielona Gora, Poland.
Abstract
BACKGROUND AND AIMS: Conflicting results suggest a link between serum uric acid (SUA), inflammation and glucose/insulin homeostasis; however, the role of adiposity in this relationship is not clear. Therefore, we evaluated the role of different adiposity factors, including central body mass index (BMI), peripheral waist circumference (WC), and visceral adiposity [visceral adipose tissue (apVAT)], on the association between SUA, inflammation and glucose/insulin homeostasis among US adults. METHODS: Data were extracted from the 2005-2010 US National Health and Nutrition Examination Surveys. Overall, 16,502 participants were included in the analysis (mean age = 47.1 years, 48.2% men). Analysis of co-variance and "conceptus causal mediation" models were applied, while accounting for survey design. RESULTS: Corrected models showed that subjects with higher SUA levels have a less favorable profile of inflammation and glucose/insulin homeostasis parameters (all p < 0.001). We found that all our potential mediators (BMI, WC and apVAT) had an impact (to various extents) on the link between variables, including serum C-reactive protein (CRP), apolipoprotein-B (apoB), insulin resistance markers, 2-h blood glucose (2hG) and triglyceride, and fasting blood glucose (FBG) (TyG) index (all p < .001), while none of the potential mediators (BMI, apVAT, WC) had an impact on the link between FBG and glycated hemoglobin with SUA (all p > 0.05). We have found that all of our mediators partially mediated the link between inflammation and glucose/insulin homeostasis parameters and SUA. Of note, apVAT fully mediated the association between SUA and 2hG. CONCLUSIONS: By applying advanced statistical techniques, we shed light on the complex link of SUA with inflammation and glucose/insulin homeostasis and quantify the role of adiposity factors in that link.
BACKGROUND AND AIMS: Conflicting results suggest a link between serum uric acid (SUA), inflammation and glucose/insulin homeostasis; however, the role of adiposity in this relationship is not clear. Therefore, we evaluated the role of different adiposity factors, including central body mass index (BMI), peripheral waist circumference (WC), and visceral adiposity [visceral adipose tissue (apVAT)], on the association between SUA, inflammation and glucose/insulin homeostasis among US adults. METHODS: Data were extracted from the 2005-2010 US National Health and Nutrition Examination Surveys. Overall, 16,502 participants were included in the analysis (mean age = 47.1 years, 48.2% men). Analysis of co-variance and "conceptus causal mediation" models were applied, while accounting for survey design. RESULTS: Corrected models showed that subjects with higher SUA levels have a less favorable profile of inflammation and glucose/insulin homeostasis parameters (all p < 0.001). We found that all our potential mediators (BMI, WC and apVAT) had an impact (to various extents) on the link between variables, including serum C-reactive protein (CRP), apolipoprotein-B (apoB), insulin resistance markers, 2-h blood glucose (2hG) and triglyceride, and fasting blood glucose (FBG) (TyG) index (all p < .001), while none of the potential mediators (BMI, apVAT, WC) had an impact on the link between FBG and glycated hemoglobin with SUA (all p > 0.05). We have found that all of our mediators partially mediated the link between inflammation and glucose/insulin homeostasis parameters and SUA. Of note, apVAT fully mediated the association between SUA and 2hG. CONCLUSIONS: By applying advanced statistical techniques, we shed light on the complex link of SUA with inflammation and glucose/insulin homeostasis and quantify the role of adiposity factors in that link.
Authors: Alessandro Volpe; Chang Ye; Anthony J Hanley; Philip W Connelly; Bernard Zinman; Ravi Retnakaran Journal: J Clin Endocrinol Metab Date: 2020-03-01 Impact factor: 5.958