WEDNESDAY, Sept. 19 (HealthDay News) -- Increased dietary fructose consumption may impair hepatocellular energy homeostasis, as seen with reduced levels of liver adenosine triphosphate (ATP), with lower levels seen in those with high uric acid (UA) levels, according to a study published in the September issue of Hepatology.
Manal F. Abdelmalek, M.D., M.P.H., from Duke University in Durham, N.C., and colleagues examined the correlation between dietary fructose, UA, and hepatic ATP depletion in low- versus high-consumers of fructose. Data were obtained from 244 adults with diabetes enrolled in the Action for Health in Diabetes Fatty Liver Ancillary Study. Dietary fructose consumption was estimated using a 130-item food frequency questionnaire. Phosphorus magnetic resonance spectroscopy was used to measure hepatic ATP, and UA levels were measured (105 participants). In 25 patients an intravenous (IV) fructose challenge was performed.
The researchers observed slightly lower baseline hepatic ATP levels for high dietary fructose consumers. In addition, they had a greater absolute change in hepatic α-ATP/inorganic phosphate (Pi) ratio (0.08 versus 0.03; P = 0.05) and γ-ATP/Pi ratio after an IV fructose challenge (0.03 versus 0.06; P = 0.06). Post-fructose challenge, the minimum liver ATP/Pi ratio was lower (4.5 versus 7.0; P = 0.04) in patients with high UA (≥5.5 mg/dL).
"High-fructose consumption depletes hepatic ATP and impairs recovery from ATP depletion after an IV fructose challenge. Subjects with high UA show a greater nadir in hepatic ATP in response to fructose," the authors write. "Impaired hepatic energy homeostasis attributable to increased dietary fructose consumption underscores the urgent, dire need for increased public awareness of the risks associated with high-fructose consumption."
One author has published a lay book (The Sugar Fix) that discusses the potential role of fructose in obesity and fatty liver and has a patent application on lowering uric acid to reduce fatty liver disease.
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