Sugar, Uric Acid, and the Etiology of Diabetes and Obesity

Richard J. Johnson; Takahiko Nakagawa; L. Gabriela Sanchez-Lozada; Mohamed Shafiu; Shikha Sundaram; Myphuong Le; Takuji Ishimoto; Yuri Y. Sautin; Miguel A. Lanaspa

Disclosures

Diabetes. 2013;62(10):3307-3315. 

In This Article

Conclusions

Searching for the cause of type 2 diabetes has been a prime area of research since Etienne Lancereaux described fat diabetes (diabetes gras) in 1880. Though more studies are needed, the evidence that fructose-induced hyperuricemia may have a contributory role is gaining ground. While it still remains a hypothesis,[103] increasing evidence suggests uric acid may have a fundamental role in the manifestations of metabolic syndrome (Fig. 3). Given that hyperuricemia is a remediable risk factor, we recommend both basic and clinical studies to address this important possibility.

Figure 3.

Uric acid: potential mechanisms for insulin resistance and diabetes. Uric acid may contribute to insulin resistance in the liver by inducing mitochondrial oxidative stress and steatosis.[28] Uric acid also blocks the ability of insulin to stimulate vasodilation of blood vessels, which is important for the delivery of glucose to the skeletal muscle.[4,32] Uric acid also induces local inflammation in the adipose tissue with a reduction in the production of adiponectin.[44] Finally, uric acid may also have direct effects on the islet cells leading to local oxidative stress and islet dysfunction.[5] Mt, mitochondria; PO4, phosphate.

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