High fructose consumption depleted adenosine triphosphate in obese type 2 diabetics
Obese patients with type 2 diabetes who increased their habitual dietary fructose consumption experienced reduced hepatic adenosine triphosphate concentrations compared with those who consumed less, according to data from an observational, cross-sectional study of the NIH-sponsored Look Ahead Fatty Liver Ancillary Study.
“These data support our hypothesis that increased dietary fructose consumption may impair hepatocellular energy homeostasis and thus could be a risk factor for progressive liver injury. Further, hyperuricemia may serve as a surrogate marker of hepatic [adenosine triphosphate] depletion following exposure to fructose in patients with [insulin resistance], and potentially [nonalcoholic fatty liver disease],” the researchers wrote.
Manal F. Abdelmalek, MD, MPH, an associate professor of medicine in the division of gastroenterology at Duke University Medical Center, and colleagues evaluated 244 adults with type 2 diabetes aged 45 to 76 years who were eligible to participate in the study at Johns Hopkins University.
Patients underwent a 130-item food frequency questionnaire to estimate their dietary fructose consumption; researchers also collected uric acid (UA) levels and measured hepatic adenosine triphosphate (ATP) using phosphorus magnetic resonance spectroscopy. A subcategory of patients (n=25) underwent an IV fructose challenge test, the researchers wrote.
Data from the study showed high dietary fructose consumers had “slightly lower baseline hepatic ATP levels and a greater absolute change in hepatic alpha-ATP/Pi ratio (0.08 vs. 0.03, P=.05) and gamma-ATP/Pi ratio, following an intravenous fructose challenge (0.03 vs. 0.06, P=.06). Additionally, patients with high UA levels (≥5.5 mg/dL) showed a lower minimum liver ATP/Pi ratio after the intravenous fructose challenge (4.5 vs. 7, P=.04),” the researchers wrote.
They concluded that impaired hepatic energy homeostasis marks an urgent need for increased public awareness of risks related to high fructose consumption.
Disclosure: Richard J. Johnson, MD, reported publishing a lay book, The Sugar Fix, which 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. All other researchers report no relevant financial disclosures.