Fructose stimulated de novo lipogenesis is promoted by inflammation
Open accessAbstract
Benign hepatosteatosis, affected by lipid uptake, de novo lipogenesis and fatty acid (FA) oxidation, progresses to non-alcoholic steatohepatitis (NASH) on stress and inflammation. A key macronutrient proposed to increase hepatosteatosis and NASH risk is fructose. Excessive intake of fructose causes intestinal-barrier deterioration and endotoxaemia. However, how fructose triggers these alterations and their roles in hepatosteatosis and NASH pathogenesis remain unknown. Here we show, using mice, that microbiota-derived Toll-like receptor (TLR) agonists promote hepatosteatosis without affecting fructose-1-phosphate (F1P) and cytosolic acetyl-CoA. Activation of mucosal-regenerative gp130 signalling, administration of the YAP-induced matricellular protein CCN1 or expression of the antimicrobial peptide Reg3b (beta) peptide counteract fructose-induced barrier deterioration, which depends on endoplasmic-reticulum stress and subsequent endotoxaemia. Endotoxin engages TLR4 to trigger TNF production by liver macrophages, thereby inducing lipogenic enzymes that convert F1P and acetyl-CoA to FA in both mouse and human hepatocytes.
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Progression from simple steatosis to MASH may depend on secondary hits, including ER stress and inflammation.
“Progression from simple steatosis to MASH may depend on secondary hits, including ER stress and inflammation [89,90].”
From Hepatic Insulin Resistance and Steatosis in Metabolic Dysfunction-Associated Steatotic Liver Disease: New Insights into Mechanisms and Clinical Implications (2025) · cites this paper as [90]
Excessive fructose consumption might lead to intestinal flora disturbance and intestinal barrier deterioration, which promote the development of metabolic endotoxaemia, inflammation, and lipid accumulation, finally leading to colorectal carcinogenesis.
“excessive fructose consumption might lead to intestinal flora disturbance and intestinal barrier deterioration, which promote the development of metabolic endotoxaemia, inflammation, and lipid accumulation, finally leading to colorectal carcinogenesis.20 122 123”
From Dietary sugar consumption and health: umbrella review (2023) · cites this paper as [122]
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- [37]Fukui H Increased Intestinal Permeability and Decreased Barrier Function: Does It Really Influence the Risk of Inflammation? Inflamm. Intest. Dis 1, 135– 145 (2016). 29922669 PMC5988153
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- Authors
- Todoric, J., Di Caro, G., Reibe, S., Henstridge, D. C., Green, C. R., Vrbanac, A., Ceteci, F., Conche, C., McNulty, R., Shalapour, S., Taniguchi, K., Meikle, P. J., Watrous, J. D., Moranchel, R., Najhawan, M., Jain, M., Liu, X., Kisseleva, T., Diaz-Meco, M. T., Moscat, J., Knight, R., Greten, F. R., Lau, L. F., Metallo, C. M., Febbraio, M. A., & Karin, M.
- Affiliations
- University of California San Diego (US)
- Garvan Institute of Medical Research (AU)
- Baker Heart and Diabetes Institute (AU)
- Goethe University Frankfurt (DE)
- University of California, Irvine (US)
- Keio University (JP)
- Sanford Burnham Prebys Medical Discovery Institute (US)
- University of Illinois Chicago (US)
- Monash University (AU)
- Corresponding author
- Karin, Michael
- ORCID
- Todoric, Jelena
- Reibe, Saskia
- Henstridge, Darren C.
- Green, Courtney R.
- Vrbanac, Alison
- Conche, Claire
- McNulty, Reginald
- Shalapour, Shabnam
- Taniguchi, Koji
- Meikle, Peter J.
- Watrous, Jeramie D.
- Najhawan, Mahan
- Jain, Mohit
- Liu, Xiao
- Kisseleva, Tatiana
- Diaz-Meco, Maria T.
- Moscat, Jorge
- Knight, Rob
- Greten, Florian R.
- Lau, Lester F.
- Metallo, Christian M.
- Febbraio, Mark A.
- Karin, Michael
- Venue
- Nature Metabolism
- Published
- 2020-08-24
- Volume
- 2
- Issue
- 10
- Pages
- 1034-1045
- ISSN
- 2522-5812 (ISSN-L)
- PMC
- PMC8018782
- OpenAlex
- W3081134500
- Cited by
- 328
- References
- 54
- Citations by year
- 2026: 35 · 2025: 59 · 2024: 58 · 2023: 56 · 2022: 62 · 2021: 45 · 2020: 13
- FWCI
- 31.51
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Licence
- Locations
- Nature Metabolism (publishedVersion)
- PubMed (publishedVersion)
- UTAS Research Repository (acceptedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Figshare (submittedVersion, cc-by)
- Minerva Access (University of Melbourne) (submittedVersion)
- Funders
- National Institutes of Health (1s10od020025-01)
- Japan Society for the Promotion of Science (15K21775)
- National Institute on Alcohol Abuse and Alcoholism (U01AA027681)
- National Cancer Institute (R01CA234128, R01CA192642, R03CA223717, R01CA198103, R01CA188652, R01CA207177, R01CA218254, R01CA211794)
- National Institute of Allergy and Infectious Diseases (T32AI007469, R01AI043477, K22AI139444)
- National Institute of Diabetes and Digestive and Kidney Diseases (K01DK116917, R01DK108743, R01DK120714, P30DK063491)
- National Institute of Environmental Health Sciences (P42ES010337, R01ES027595)
- Topics
- Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diet, Metabolism, and Disease
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Keywords
- fructose, de novo lipogenesis, hepatic steatosis, nonalcoholic steatohepatitis, intestinal barrier dysfunction, endotoxemia, TLR4, hepatic macrophages, gut microbiota, YAP, CYR61, Reg3b, endoplasmic reticulum stress, fructose-1-phosphate, acetyl-CoA, TNF-α, hepatic lipid metabolism
- MeSH terms
- Gastrointestinal Microbiome, Lipidomics, Acetyl Coenzyme A, Animals, Female, Fructose, Fructosephosphates, Humans, Inflammation, Intestines, Macrophages, Mice, Inbred C57BL, Regeneration, Endotoxemia, Hepatocytes, Lipogenesis, Toll-Like Receptors, Mice, Non-alcoholic Fatty Liver Disease
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