Hypothesis: could excessive fructose intake and uric acid cause type 2 diabetes?

Endocr Rev. 2009 Feb;30(1):96-116. doi: 10.1210/er.2008-0033. Epub 2009 Jan 16.


We propose that excessive fructose intake (>50 g/d) may be one of the underlying etiologies of metabolic syndrome and type 2 diabetes. The primary sources of fructose are sugar (sucrose) and high fructose corn syrup. First, fructose intake correlates closely with the rate of diabetes worldwide. Second, unlike other sugars, the ingestion of excessive fructose induces features of metabolic syndrome in both laboratory animals and humans. Third, fructose appears to mediate the metabolic syndrome in part by raising uric acid, and there are now extensive experimental and clinical data supporting uric acid in the pathogenesis of metabolic syndrome. Fourth, environmental and genetic considerations provide a potential explanation of why certain groups might be more susceptible to developing diabetes. Finally, we discuss the counterarguments associated with the hypothesis and a potential explanation for these findings. If diabetes might result from excessive intake of fructose, then simple public health measures could have a major impact on improving the overall health of our populace.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Diabetes Mellitus, Type 2 / chemically induced*
  • Diabetes Mellitus, Type 2 / epidemiology
  • Diabetes Mellitus, Type 2 / metabolism
  • Dietary Sucrose / adverse effects
  • Fructose / adverse effects*
  • Fructose / metabolism
  • Humans
  • Metabolic Syndrome / chemically induced*
  • Metabolic Syndrome / genetics
  • Metabolic Syndrome / metabolism
  • Sweetening Agents / adverse effects*
  • Sweetening Agents / metabolism
  • Uric Acid / metabolism*


  • Dietary Sucrose
  • Sweetening Agents
  • Uric Acid
  • Fructose