Obesity and nonalcoholic fatty liver disease: biochemical, metabolic, and clinical implications

Fabbrini, Elisa; Sullivan, Shelby; Klein, Samuel

doi:10.1002/hep.23280

Cited by 2,100Liver Disease Diagnosis and TreatmentDiet, Metabolism, and DiseaseDiabetes, Cardiovascular Risks, and Lipoproteins

Obesity and nonalcoholic fatty liver disease: biochemical, metabolic, and clinical implications

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Fabbrini, Elisa, Sullivan, Shelby, Klein, Samuel·2010·Hepatology

DOI 10.1002/hep.23280PMC PMC3575093

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Abstract

Obesity is associated with an increased risk of nonalcoholic fatty liver disease (NAFLD). Steatosis, the hallmark feature of NAFLD, occurs when the rate of hepatic fatty acid uptake from plasma and de novo fatty acid synthesis is greater than the rate of fatty acid oxidation and export (as triglyceride within very low-density lipoprotein). Therefore, an excessive amount of intrahepatic triglyceride (IHTG) represents an imbalance between complex interactions of metabolic events. The presence of steatosis is associated with a constellation of adverse alterations in glucose, fatty acid, and lipoprotein metabolism. It is likely that abnormalities in fatty acid metabolism, in conjunction with adipose tissue, hepatic, and systemic inflammation, are key factors involved in the development of insulin resistance, dyslipidemia, and other cardiometabolic risk factors associated with NAFLD. However, it is not clear whether NAFLD causes metabolic dysfunction or whether metabolic dysfunction is responsible for IHTG accumulation, or possibly both. Understanding the precise factors involved in the pathogenesis and pathophysiology of NAFLD will provide important insights into the mechanisms responsible for the cardiometabolic complications of obesity. (Hepatology 2009.)

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Presence, duration and severity of excess weight are associated with an increased risk of disease progression in MASLD.
“Presence, duration and severity of excess weight are associated with an increased risk of disease progression in MASLD. 223”
From EASL-EASD-EASO Clinical Practice Guidelines on the management of metabolic dysfunction-associated steatotic liver disease (MASLD). (2024) · cites this paper as [223]
The Diagnosis and Prevalence section reports that steatohepatitis is more prevalent at higher BMI, supporting an association between excess-weight severity and more serious liver disease. The Abstract notes that NAFLD can progress to severe liver disease, but the paper does not establish that the presence or duration of excess weight increases the risk of disease progression. (LLM, conf=0.84)
Experimental — accuracy not yet measured
Three participants had liver fat concentration >5% at baseline, consistent with nonalcoholic fatty liver disease (NAFLD); all three were from the palm olein (POo) group.
“Three participants had liver fat concentration > 5%atbaseline, consistent with the presence of nonalcoholic fatty liver disease (NAFLD) (36); all 3 were from the POo group.”
From Eucaloric diets enriched in palm olein, cocoa butter, and soybean oil did not differentially affect liver fat concentration in healthy participants: a 16-week randomized controlled trial. (2021) · cites this paper as [36]
Some factors are also related to obesity comorbidities such as fatty liver diseases and type 2 diabetes.
“Some are also related to obesity comorbidities such as fatty liver diseases [6] and type 2 diabetes [7,8].”
From Identification of factors associated with sarcopenic obesity development: Literature review and expert panel voting (2024) · cites this paper as [6]

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Disruption of LDL receptor gene in transgenic SREBP-1a mice unmasks hyperlipidemia resulting from production of lipid-rich VLDL
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Increased intrahepatic triglyceride is associated with peripheral insulin resistance: in vivo MR imaging and spectroscopy studies
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Roux‐en‐Y Gastric Bypass Improves Liver Histology in Patients with Non‐Alcoholic Fatty Liver Disease
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Fat Accumulation in the Liver Is Associated with Defects in Insulin Suppression of Glucose Production and Serum Free Fatty Acids Independent of Obesity in Normal Men
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Blocking VLDL secretion causes hepatic steatosis but does not affect peripheral lipid stores or insulin sensitivity in mice
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PPAR agonists treatment is effective in a nonalcoholic fatty liver disease animal model by modulating fatty‐acid metabolic enzymes
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Human skeletal muscle ceramide content is not a major factor in muscle insulin sensitivity
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Liver Pathology in Morbidly Obese Patients Undergoing Roux-en-Y Gastric Bypass Surgery
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Hepatic Overexpression of Glycerol-sn-3-phosphate Acyltransferase 1 in Rats Causes Insulin Resistance
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Real-time assessment of postprandial fat storage in liver and skeletal muscle in health and type 2 diabetes
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Liver fat and lipid oxidation in humans
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Increased lipid accumulation and insulin resistance in transgenic mice expressing DGAT2 in glycolytic (type II) muscle
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Effect of weight loss on VLDL-triglyceride and apoB-100 kinetics in women with abdominal obesity
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Metabolic correlates of nonalcoholic fatty liver in women and men
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Hepatic Blood Flow Measurements With Arterial and Portal Blood Flow Mapping in the Human Liver by Means of Xenon CT
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Hepatic fuel selection
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[39]Klein S Jeejeebhoy K Feldman M Freidman L Sleisenger M The malnourished patient: nutritional assessment and management Sleisenger & Fordtran’s Gastrointestinal and Liver Disease 7 Philadelphia W.B. Saunders Co 2002 265 285

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AASLD practice guidance on the clinical assessment and management of nonalcoholic fatty liver disease
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EASL-EASD-EASO Clinical Practice Guidelines on the management of metabolic dysfunction-associated steatotic liver disease (MASLD).
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Why does obesity cause diabetes?
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Dynamic shifts in the composition of resident and recruited macrophages influence tissue remodeling in NASH
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“NASH is common in people with obesity and diabetes and accounts for an increasing number of patients with cirrhosis and liver failure (Fabbrini et al., 2010; Vernon et al., 2011; Wree et al., 2013).”
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Metabolically normal obese people are protected from adverse effects following weight gain
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Selective insulin resistance with differential expressions of IRS-1 and IRS-2 in human NAFLD livers
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Enhancing liver mitochondrial fatty acid oxidation capacity in obese mice improves insulin sensitivity independently of hepatic steatosis
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“The early stages of the disease are characterized by the accumulation of triglycerides (TAG) in over 5% of hepatic cells, resulting in not only ectopic fat accumulation, but the negative repercussion of low-grade chronic inflammation resulting in tissue normally not accustomed to lipid accumulation (Fabbrini et al. 20…”
Background
Circadian- and UPR-dependent control of CPEB4 mediates a translational response to counteract hepatic steatosis under ER stress
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Association of bariatric surgery with cardiovascular outcomes in adults with severe obesity and nonalcoholic fatty liver disease
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Superior reductions in hepatic steatosis and fibrosis with co-administration of a glucagon-like peptide-1 receptor agonist and obeticholic acid in mice
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Intramyocellular ceramides: subcellular concentrations and fractional de novo synthesis in postabsorptive humans
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Authors: Fabbrini, E., Sullivan, S., & Klein, S.
Affiliations: Washington University in St. Louis (US)
Corresponding author: Klein, Samuel
ORCID: Fabbrini, Elisa
Sullivan, Shelby
Klein, Samuel
Venue: Hepatology
Publisher: Ovid Technologies (Wolters Kluwer Health)
Published: 2010-02
Volume: 51
Issue: 2
Pages: 679-689
ISSN: 0270-9139 (ISSN-L)
DOI: 10.1002/hep.23280
PMC: PMC3575093
OpenAlex: W2112291880
Cited by: 2,100
References: 100
Citations by year: 2026: 97 · 2025: 118 · 2024: 169 · 2023: 169 · 2022: 177 · 2021: 162 · 2020: 160 · 2019: 149 · 2018: 138 · 2017: 138 · 2016: 118 · 2015: 109 · 2014: 96 · 2013: 87 · 2012: 79
FWCI: 8.51
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: doi.wiley.com/10.1002/tdm_license_1.1 (tdm, 2038 d)
Locations: Hepatology (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: National Institute of Diabetes and Digestive and Kidney Diseases (DK37948, DK56341, R01DK037948, P30DK056341)
National Center for Research Resources (UL1RR024992)
Topics: Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diet, Metabolism, and Disease
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
Keywords: obesity, non-alcoholic fatty liver disease, hepatic steatosis, fatty acid metabolism, lipoprotein metabolism, insulin resistance, dyslipidemia, cardiometabolic risk, adipose tissue inflammation, liver inflammation, NAFLD pathogenesis
MeSH terms: Fatty Liver, Humans, Liver, Obesity, Lipid Metabolism

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Obesity and nonalcoholic fatty liver disease: biochemical, metabolic, and clinical implications

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