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Increased De Novo Lipogenesis Is a Distinct Characteristic of Individuals With Nonalcoholic Fatty Liver Disease
Open accessAbstract
Background & aims There have been few studies of the role of de novo lipogenesis in the development of nonalcoholic fatty liver disease (NAFLD). We used isotope analyses to compare de novo lipogenesis and fatty acid flux between subjects with NAFLD and those without, matched for metabolic factors (controls).Methods We studied subjects with metabolic syndrome and/or levels of alanine aminotransferase and aspartate aminotransferase >30 mU/L, using magnetic resonance spectroscopy to identify those with high levels (HighLF, n = 13) or low levels (LowLF, n = 11) of liver fat. Clinical and demographic information was collected from all participants, and insulin sensitivity was measured using the insulin-modified intravenous glucose tolerance test. Stable isotopes were administered and gas chromatography with mass spectrometry was used to analyze free (nonesterified) fatty acid (FFA) and triacylglycerol flux and lipogenesis.Results Subjects with HighLF (18.4% ± 3.6%) had higher plasma levels of FFAs during the nighttime and higher concentrations of insulin than subjects with LowLF (3.1% ± 2.7%; P = .04 and P < .001, respectively). No differences were observed between groups in adipose flux of FFAs (414 ± 195 μmol/min for HighLF vs 358 ± 105 μmol/min for LowLF; P = .41) or production of very-low-density lipoprotein triacylglycerol from FFAs (4.06 ± 2.57 μmol/min vs 4.34 ± 1.82 μmol/min; P = .77). In contrast, subjects with HighLF had more than 3-fold higher rates of de novo fatty acid synthesis than subjects with LowLF (2.57 ± 1.53 μmol/min vs 0.78 ± 0.42 μmol/min; P = .001). As a percentage of triacylglycerol palmitate, de novo lipogenesis was 2-fold higher in subjects with HighLF (23.2% ± 7.9% vs 10.1% ± 6.7%; P < .001); this level was independently associated with the level of intrahepatic triacylglycerol (r = 0.53; P = .007).Conclusions By administering isotopes to subjects with NAFLD and control subjects, we confirmed that those with NAFLD have increased synthesis of fatty acids. Subjects with NAFLD also had higher nocturnal plasma levels of FFAs and did not suppress the contribution from de novo lipogenesis on fasting. These findings indicate that lipogenesis might be a therapeutic target for NAFLD.
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“Fasting DNL correlated with plasma TAG concentrations48 and was higher in individuals with MASLD.49”
From Lipid metabolism in MASLD and MASH: From mechanism to the clinic (2024) · cites this paper as [49]
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“Postprandial DNL contributes to 15-26% of liver TAGs in individuals with MASLD49,56 vs. 1-6% in the fasting state in healthy individuals.48”
From Lipid metabolism in MASLD and MASH: From mechanism to the clinic (2024) · cites this paper as [49]
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“The latter is key to increase TG deposit due to accelerated de novo lipogenesis (DNL) (Donnelly et al., 2005; Fon Tacer and Rozman, 2011; Lambert et al., 2014) and uptake of non-esterified fatty acids (NEFAs) (Sunny et al., 2011).”
BackgroundContribution of de novo lipogenesis to the progression of nonalcoholic fatty liver disease
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Non-Alcoholic Fatty Liver Disease and Steatohepatitis
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Global molecular landscape of early MASLD progression in human obesityPreprint
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“Hepatic steatosis is often accompanied by increased glucose production ( Scoditti et al., 2024 ), elevated de novo lipogenesis ( Lambert et al., 2014 ), and disrupted cholesterol homeostasis ( Sakuma et al., 2025 ).”
Półkośnik, K., Łebkowska, A., Kowalska, I., & Lebensztejn, D. M. (2023) · Medical Science Monitor · doi:10.12659/msm.940398 · Cited by 2
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“…between glucose variability and plasma lactate shown here are also consistent with the high rates of DNL observed in individuals with MASLD [26] and further corroborate the hypothesis that these pathways (i.e., glycolysis and DNL), in the context of insulin resistance, may be enhanced due…”
Li, N., Liu, C., Lu, Z., Wu, W., Zhang, F., Qiu, L., Shen, C., Sheng, D., & Liu, Z. (2025) · BMC Gastroenterology · doi:10.1186/s12876-025-03598-4 · Cited by 2
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“Furthermore, PPAR-α regulates the expression of CPT1A, which plays an essential role in fatty acid β -oxidation (31, 32).”
An Overview of Non-alcoholic Fatty Liver Diseases (NAFLD)
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MicroRNA-18a-5p regulates hepatic lipid accumulation in response to high-fat diet
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Self-citationE-cigarette vaping is associated with pro-fibrotic gene expression in kidney and liver tissues
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“Conversely, the downregulation of Sterol Regulatory Element-Binding Transcription Factor 1 ( Srebf1 ), which regulates lipid homeostasis, reflects impaired lipid produc - tion, potentially contributing to metabolic disorders such as non-alcoholic fatty liver disease (NAFLD) [51, 52 ].”
Human Cyclophilins—An Emerging Class of Drug Targets
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“The multifactorial mechanism of NAFLD includes fat accumulation [218], triglyceride de novo lipogenesis [218, 219], and mitochondrial dysfunction represented by impaired hepatic lipid homeostasis and decreased energy transducing capacity [220, 221].”
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“(16) In addition, AST and ALT are common indicators of hepatic metabolism and transport function.”
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“Fructose is particularly damaging as it bypasses normal metabolic checks to drive triglyceride production [13, 14, 16].”
InfluentialMetabolic Liver Disease Beyond the Liver
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DDR2 ameliorates nonalcoholic hepatic steatosis by activating the AMPK/ACC pathway
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“However, in MASLD, hepatic DNL is significantly upregulated, with more than 25% of VLDL triglycerides potentially originating from this pathway 11,16 .”
Bilirubin Ameliorates Oleic and Palmitic Acid Accumulation in an In Vitro Model of MASLD
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“DNL is a major contributor to the hepatic free fatty acid pool with patients suffering from MAFLD showing a significant increase in DNL [37].”
Patients with MASLD exhibit in vivo changes in hepatic response to oral fructose consumption
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Current management of MASLD in type 2 diabetes
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Exercise as a Metabolic Therapy for MASLD: Beyond Weight Loss Toward Sustainable Exercise Strategies
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“Concurrently, fatty acid oxidation is impaired due to reduced peroxisome proliferator-activated receptor-α (PPAR α ) signaling and mitochondrial dysfunction, further exacerbating lipid accumulation within hepatocytes [26–29].”
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“This activates Sterol Regulatory Element-Binding Protein 1c (SREBP-1c) and Carbohydrate-Responsive Element-Binding Protein (ChREBP), inducing de novo lipogenesis (DNL) via Acetyl-CoA Carboxylase (ACC), Fatty Acid Synthase (FASN), and Stearoyl-CoA Desaturase 1 (SCD1) [15,16].”
Hepatic Lipoprotein Production, Cardiometabolic Phenotypes, and Subtypes of Steatotic Liver Disease
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“…more closely emulate concurrent metabolic dysfunction, defined stimuli enhance standardization and still align with physiological sources of hepatic lipid load, as peripheral lipolysis and dietary fatty acids represent the main contributors to hepatic lipid influx in MASLD (Lambert et al., 2014).”
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“For example, DNL is increased 3-fold in individuals with a fatty liver compared to age- and BMI-matched controls [12].”
BackgroundHepatobiliary continuum: non-alcoholic fatty liver disease, cholelithiasis ... what else?
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“Previous studies have reported that liver fat accumulation was linked to DNL (23).”
BackgroundInfluentialLiver Cancer - Genesis, Progression and Metastasis
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Metadata
- Authors
- Lambert, J. E., Ramos–Roman, M. A., Browning, J. D., & Parks, E. J.
- Affiliations
- The University of Texas Southwestern Medical Center (US)
- Corresponding author
- Parks, Elizabeth J.
- ORCID
- Parks, Elizabeth J.
- Venue
- Gastroenterology
- Publisher
- Elsevier BV
- Published
- 2014-03
- Volume
- 146
- Issue
- 3
- Pages
- 726-735
- ISSN
- 0016-5085 (ISSN-L)
- PMC
- PMC6276362
- OpenAlex
- W2139351004
- Cited by
- 1,069
- References
- 58
- Citations by year
- 2026: 67 · 2025: 111 · 2024: 110 · 2023: 108 · 2022: 124 · 2021: 111 · 2020: 106 · 2019: 92 · 2018: 75 · 2017: 47 · 2016: 49 · 2015: 45 · 2014: 23
- FWCI
- 28.42
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Gastroenterology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (RL1DK081187, UL1DE019584, UL1-RR024982)
- National Center for Advancing Translational Sciences (RL1DK081187, UL1DE019584, UL1-RR024982)
- Topics
- Health Sciences › Medicine › Hepatology › Liver Disease Diagnosis and Treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
- Keywords
- de novo lipogenesis, non-alcoholic fatty liver disease, fatty acid synthesis, triglyceride synthesis, liver fat, metabolic syndrome, insulin sensitivity, stable isotope tracer studies, hepatic lipid metabolism, insulin
- MeSH terms
- Fatty Acids, Nonesterified, Fatty Liver, Female, Humans, Hyperlipidemias, Liver, Magnetic Resonance Imaging, Male, Comorbidity, Case-Control Studies, Metabolic Syndrome, Lipogenesis, Non-alcoholic Fatty Liver Disease
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