title: Hypothesis: could excessive fructose intake and uric acid cause type 2 diabetes?
abstract: 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.
authors.affiliation: Division of Nephrology, Hypertension and Transplantation, University of Florida, P.O. Box 100224, Gainesville, Florida 32620-0224, USA. johnsrj@medicine.ufl.edu
authors.forename: Richard J
authors.initials: RJ
authors.lastname: Johnson
authors.forename: Santos E
authors.initials: SE
authors.lastname: Perez-Pozo
authors.forename: Yuri Y
authors.initials: YY
authors.lastname: Sautin
authors.forename: Jacek
authors.initials: J
authors.lastname: Manitius
authors.forename: Laura Gabriela
authors.initials: LG
authors.lastname: Sanchez-Lozada
authors.forename: Daniel I
authors.initials: DI
authors.lastname: Feig
authors.forename: Mohamed
authors.initials: M
authors.lastname: Shafiu
authors.forename: Mark
authors.initials: M
authors.lastname: Segal
authors.forename: Richard J
authors.initials: RJ
authors.lastname: Glassock
authors.forename: Michiko
authors.initials: M
authors.lastname: Shimada
authors.forename: Carlos
authors.initials: C
authors.lastname: Roncal
authors.forename: Takahiko
authors.initials: T
authors.lastname: Nakagawa
mesh_terms: D000818:Animals; D003924:Diabetes Mellitus, Type 2 / Q000139:chemically induced* / Q000453:epidemiology / Q000378:metabolism; D019422:Dietary Sucrose / Q000009:adverse effects; D005632:Fructose / Q000009:adverse effects* / Q000378:metabolism; D006801:Humans; D024821:Metabolic Syndrome / Q000139:chemically induced* / Q000235:genetics / Q000378:metabolism; D013549:Sweetening Agents / Q000009:adverse effects* / Q000378:metabolism; D014527:Uric Acid / Q000378:metabolism*
chemical_list: D019422:Dietary Sucrose; D013549:Sweetening Agents; D014527:Uric Acid; D005632:Fructose