Dietary Sugars Alter Hepatic Fatty Acid Oxidation via Transcriptional and Post-translational Modifications of Mitochondrial Proteins
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Dietary sugars, fructose and glucose, promote hepatic de novo lipogenesis and modify the effects of a high-fat diet (HFD) on the development of insulin resistance. Here, we show that fructose and glucose supplementation of an HFD exert divergent effects on hepatic mitochondrial function and fatty acid oxidation. This is mediated via three different nodes of regulation, including differential effects on malonyl-CoA levels, effects on mitochondrial size/protein abundance, and acetylation of mitochondrial proteins. HFD- and HFD plus fructose-fed mice have decreased CTP1a activity, the rate-limiting enzyme of fatty acid oxidation, whereas knockdown of fructose metabolism increases CPT1a and its acylcarnitine products. Furthermore, fructose-supplemented HFD leads to increased acetylation of ACADL and CPT1a, which is associated with decreased fat metabolism. In summary, dietary fructose, but not glucose, supplementation of HFD impairs mitochondrial size, function, and protein acetylation, resulting in decreased fatty acid oxidation and development of metabolic dysregulation.
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Dietary fructose may inhibit fatty acid oxidation in the liver by impairing mitochondrial size and function and acetylation of the rate limiting enzyme.
“Dietary fructose may also inhibit fatty acid oxidation in the liver by impairing mitochondrial size and function and acetylation of the rate limiting enzyme.100”
From Dietary sugar consumption and health: umbrella review (2023) · cites this paper as [100]
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Dietary sugar consumption and health: umbrella review
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- Authors
- Softic, S., Meyer, J. G., Wang, G.-X., Gupta, M. K., Batista, T. M., Lauritzen, H. P. M. M., Fujisaka, S., Serra, D., Herrero, L., Willoughby, J., Fitzgerald, K., Ilkayeva, O., Newgard, C. B., Gibson, B. W., Schilling, B., Cohen, D. E., & Kahn, C. R.
- Affiliations
- University of Kentucky HealthCare (US)
- Buck Institute for Research on Aging (US)
- Joslin Diabetes Center (US)
- Instituto de Salud Carlos III (ES)
- Alnylam Pharmaceuticals (United States) (US)
- Duke University (US)
- Weill Cornell Medicine (US)
- Corresponding author
- Softic, Samir
- Kahn, C. Ronald
- ORCID
- Venue
- Cell Metabolism
- Publisher
- Elsevier BV
- Published
- 2019-10
- Volume
- 30
- Issue
- 4
- Pages
- 735-753.e4
- ISSN
- 1550-4131 (ISSN-L)
- PMC
- PMC7816129
- OpenAlex
- W2977959633
- Cited by
- 227
- References
- 66
- Citations by year
- 2026: 21 · 2025: 29 · 2024: 38 · 2023: 40 · 2022: 33 · 2021: 37 · 2020: 25 · 2019: 3
- FWCI
- 19.88
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Dipòsit Digital de la Universitat de Barcelona (Universitat de Barcelona) (submittedVersion, cc-by-nc-nd)
- Funders
- National Institutes of Health (K12 HD000850, P30 DK40561, R01 DK031036, R01 DK033201, R01 DK056626, R01 DK103046, R24 DK085610, R37 DK048873)
- Alnylam Pharmaceuticals
- Diabetes Research Center (P30DK034834)
- Fundació la Marató de TV3
- Generalitat de Catalunya (1S10 OD016281, 2014SGR465, T32 AG000266)
- European Regional Development Fund
- Centro de Investigación Biomédica en Red-Fisiopatología de la Obesidad y Nutrición (CB06/03/0001)
- Juvenile Diabetes Research Foundation United States of America
- North American Society for Pediatric Gastroenterology, Hepatology and Nutrition
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diet, Metabolism, and Disease
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
- Keywords
- dietary fructose, dietary glucose, high-fat diet, hepatic fatty acid oxidation, mitochondrial protein acetylation, CPT1A, ACADL, malonyl-CoA, mitochondrial size, acylcarnitines, insulin resistance, de novo lipogenesis
- MeSH terms
- Dietary Sugars, Animals, Cell Line, Fatty Acids, Fructose, Glucose, Liver, Male, Mice, Inbred C57BL, Mitochondria, Obesity, Protein Processing, Post-Translational, Transcription, Genetic, Mitochondrial Proteins, Lipogenesis, Mice, Diet, High-Fat
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