Fructose and uric acid: is there a role in endothelial function?
Population level data support that consumption of fructose and fructose-based sweeteners has dramatically increased and suggest that high dietary intake of fructose is an important factor in the development of the cardiorenal metabolic syndrome (CRS). The CRS is a constellation of cardiac, kidney and metabolic disorders including insulin resistance, obesity, metabolic dyslipidemia, high blood pressure, and evidence of early cardiac and kidney disease. The consequences of fructose metabolism may result in intracellular ATP depletion, increased uric acid production, oxidative stress, inflammation, and increased lipogenesis, which are associated with endothelial dysfunction. Endothelial dysfunction is an early manifestation of vascular disease and a driver for the development of CRS. A better understanding of fructose overconsumption in the development of CRS may provide new insights into pathogenesis and future therapeutic strategies.
Division of Endocrinology and Metabolism, Department of Medicine, University of Missouri School of Medicine, Columbia, MO, USA.
Guanghong
G
Jia
Annayya R
AR
Aroor
Adam T
AT
Whaley-Connell
James R
JR
Sowers
D059347:Cardio-Renal Syndrome / Q000209:etiology* / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000378:metabolism / Q000503:physiopathology*; D005260:Female; D005632:Fructose / Q000009:adverse effects / Q000378:metabolism*; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology; D008297:Male; D024821:Metabolic Syndrome / Q000209:etiology* / Q000503:physiopathology; D018570:Risk Assessment; D012680:Sensitivity and Specificity; D013549:Sweetening Agents / Q000009:adverse effects; D014527:Uric Acid / Q000009:adverse effects / Q000378:metabolism*
D013549:Sweetening Agents; D014527:Uric Acid; D005632:Fructose