Journal article
Higher dietary fructose is associated with impaired hepatic adenosine triphosphate homeostasis in obese individuals with type 2 diabetes
Hepatology (Baltimore, Md.), v 56(3), pp 952-960
Sep 2012
PMID: 22467259
Abstract
Fructose consumption predicts increased hepatic fibrosis in those with nonalcoholic fatty liver disease (NAFLD). Because of its ability to lower hepatic adenosine triphosphate (ATP) levels, habitual fructose consumption could result in more hepatic ATP depletion and impaired ATP recovery. The degree of ATP depletion after an intravenous (IV) fructose challenge test in low- versus high-fructose consumers was assessed. We evaluated diabetic adults enrolled in the Action for Health in Diabetes Fatty Liver Ancillary Study (n = 244) for whom dietary fructose consumption estimated by a 130-item food frequency questionnaire and hepatic ATP measured by phosphorus magnetic resonance spectroscopy and uric acid (UA) levels were performed (n = 105). In a subset of participants (n = 25), an IV fructose challenge was utilized to assess change in hepatic ATP content. The relationships between dietary fructose, UA, and hepatic ATP depletion at baseline and after IV fructose challenge were evaluated in low- (<15 g/day) versus high-fructose (=15 g/day) consumers. High dietary fructose consumers had slightly lower baseline hepatic ATP levels and a greater absolute change in hepatic a-ATP/ inorganic phosphate (Pi) ratio (0.08 versus 0.03; P = 0.05) and ?-ATP /Pi ratio after an IV fructose challenge (0.03 versus 0.06; P = 0.06). Patients with high UA (=5.5 mg/dL) showed a lower minimum liver ATP/Pi ratio postfructose challenge (4.5 versus 7.0; P = 0.04). Conclusions: 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. Both high dietary fructose intake and elevated UA level may predict more severe hepatic ATP depletion in response to fructose and hence may be risk factors for the development and progression of NAFLD. (HEPATOLOGY 2012;56:952960)
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- Title
- Higher dietary fructose is associated with impaired hepatic adenosine triphosphate homeostasis in obese individuals with type 2 diabetes
- Creators
- Manal F. Abdelmalek - Duke UniversityMariana Lazo - Johns Hopkins UniversityAlena Horska - Johns Hopkins UniversitySusanne Bonekamp - Johns Hopkins UniversityEdward W. Lipkin - University of WashingtonAshok Balasubramanyam - Baylor College of MedicineJohn P. Bantle - University of MinnesotaRichard J. Johnson - University of Colorado DenverAnna Mae Diehl - Duke UniversityJeanne M. Clark - Johns Hopkins UniversityLook AHEAD Res Grp
- Publication Details
- Hepatology (Baltimore, Md.), v 56(3), pp 952-960
- Publisher
- Wiley
- Number of pages
- 9
- Grant note
- M01RR000052 / NATIONAL CENTER FOR RESEARCH RESOURCES; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Center for Research Resources (NCRR) R01DK060427 / NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Institute of Diabetes & Digestive & Kidney Diseases (NIDDK) R01HL068607 / NATIONAL HEART, LUNG, AND BLOOD INSTITUTE; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Heart Lung & Blood Institute (NHLBI) M01-RR00052 / John Hopkins University School of Medicine General Clinical Research Center RO1-DK060427; UO1-DK57149; K23-DK062116 / National Institutes of Health/National Institute of Diabetes and Digestive and Kidney Disorders (NIH/NIDDK)
- Resource Type
- Journal article
- Language
- English
- Academic Unit
- Urban Health Collaborative; Community Health and Prevention
- Web of Science ID
- WOS:000308046700019
- Scopus ID
- 2-s2.0-84865552258
- Other Identifier
- 991022171246504721