Hepatic ATP reserve and efficiency of replenishing: comparison between obese and nonobese normal individuals.

Although obesity-associated fatty liver disease is emerging as one of the most common diseases in hepatology practice, it is unclear why liver disease prevalence increases with obesity. Because impaired energy homeostasis enhances the susceptibility of hepatocytes to injury, the aim of this study was to determine whether increased body mass index (BMI) is associated with decreased basal hepatic adenosine triphosphate (ATP) stores or impaired recovery from fructose-induced hepatic ATP depletion. Hepatic ATP stores were assessed by nuclear magnetic resonance spectroscopy in 19 healthy subjects with varying BMI. After obtaining the baseline spectra, 0.5 ml/kg of 50% fructose solution was administered to all subjects to deplete the ATP reserve, and follow-up nuclear magnetic resonance spectra was obtained at 5-min intervals for the ensuing hour. AST and ALT were determined at 24 h to assess whether ATP depletion caused any appreciable hepatocyte injury. Among the 19 subjects who participated in the study, five had BMI of < or =25, seven had BMI between 25-30, and seven had BMI of >30. The baseline ATP content was inversely related to BMI (correlation coefficient -0.63, p = 0.02), decreasing steadily with increasing BMI. Fructose injection decreased hepatic ATP stores in all subjects and did not increase transaminases in anyone. Neither the postfructose ATP nadir values nor the extent of ATP recovery correlated with BMI. Reduced hepatic ATP stores are more prevalent in overweight and obese subjects than in lean subjects. However, a cause-effect relationship between these abnormalities was not demonstrated by our study.