Changgui Li1, Ming-Chia Hsieh, Shun-Jen Chang. 1. Shandong Provincial Key Laboratory of Metabolic Diseases, Qingdao Key Laboratory of Common Diseases Gout Laboratory, the Affiliated Hospital of Medical College, Qingdao University, China.
Abstract
PURPOSE OF REVIEW: To explore the causal relationship between metabolic syndrome, type 2 diabetes and hyperuricemia. RECENT FINDINGS: The prevalence of hyperuricemia in male adults with metabolic syndrome was increased and a large difference in prevalence of metabolic syndrome also existed in those with hyperuricemia compared with normouricemia. Even in those with normouricemia, higher serum uric acid levels were associated with metabolic syndrome. Serum uric acid was an independent risk factor for incident diabetes, and evidence showed that the patients with both gout and type 2 diabetes exhibited a mutual inter-dependent effect on higher incidences. Furthermore, obese patients often demonstrated insulin resistance and adipose tissue macrophage with low-grade inflammation, which is suggested to be the major contributor. Although alcohol intake is considered a risk for developing hyperuricemia, moderate alcohol intake showed a lower risk for developing type 2 diabetes and insulin resistance. Hyperinsulinemia reduces renal excretion of uric acid on the proximal tubular of the kidney leading to hyperuricemia, which has deleterious effects on endothelial function and on nitric oxide bioavailability, thus causing hyperinsulinemia. SUMMARY: We found evidence to suggest that insulin resistance plays a potentially key role in the causal relationship between metabolic syndrome, type 2 diabetes and hyperuricemia. Furthermore, it is likely that hyperuricemia and insulin resistance share a bidirectional causal effect.
PURPOSE OF REVIEW: To explore the causal relationship between metabolic syndrome, type 2 diabetes and hyperuricemia. RECENT FINDINGS: The prevalence of hyperuricemia in male adults with metabolic syndrome was increased and a large difference in prevalence of metabolic syndrome also existed in those with hyperuricemia compared with normouricemia. Even in those with normouricemia, higher serum uric acid levels were associated with metabolic syndrome. Serum uric acid was an independent risk factor for incident diabetes, and evidence showed that the patients with both gout and type 2 diabetes exhibited a mutual inter-dependent effect on higher incidences. Furthermore, obesepatients often demonstrated insulin resistance and adipose tissue macrophage with low-grade inflammation, which is suggested to be the major contributor. Although alcohol intake is considered a risk for developing hyperuricemia, moderate alcohol intake showed a lower risk for developing type 2 diabetes and insulin resistance. Hyperinsulinemia reduces renal excretion of uric acid on the proximal tubular of the kidney leading to hyperuricemia, which has deleterious effects on endothelial function and on nitric oxide bioavailability, thus causing hyperinsulinemia. SUMMARY: We found evidence to suggest that insulin resistance plays a potentially key role in the causal relationship between metabolic syndrome, type 2 diabetes and hyperuricemia. Furthermore, it is likely that hyperuricemia and insulin resistance share a bidirectional causal effect.
Authors: Emily L Goldberg; Jennifer L Asher; Ryan D Molony; Albert C Shaw; Caroline J Zeiss; Chao Wang; Ludmilla A Morozova-Roche; Raimund I Herzog; Akiko Iwasaki; Vishwa Deep Dixit Journal: Cell Rep Date: 2017-02-28 Impact factor: 9.423
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