ArticleCommunications biology2024
A genetic mouse model of lean-NAFLD unveils sexual dimorphism in the liver-heart axis.
Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 13 citations in OpenAlex.
- Sex-based multiomics analysis uncovers metabolic and molecular mediators linking MASH and atherosclerosis.JHEP reports : innovation in hepatology · 2026Article
- Application of Machine Learning Models in Predicting Non-Alcoholic Fatty Liver Disease Among Inactive Chronic Hepatitis B Patients: A Cross-Sectional Analysis.Journal of clinical medicine · 2025Article
- Mitigating Metabolic Dysfunction-associated Steatotic Liver Disease (MASLD): The Role of Bioactive Phytoconstituents in Indian Culinary Spices.Current nutrition reports · 2025Review
- Long-term outcomes and risk modifiers of metabolic dysfunction-associated steatotic liver disease between lean and non-lean populations.Clinical and molecular hepatology · 2025Review
- Sexual dimorphism in hepatic PPAR alpha and CYP4a12a expression is associated with reduced development of drug-induced non-alcoholic steatohepatitis in female IL-33Frontiers in medicine · 2024Article
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Authors and funding
18 authors at 3 institutions in 1 country.
Funding
Abstract
Lean patients with NAFLD may develop cardiac complications independently of pre-existent metabolic disruptions and comorbidities. To address the underlying mechanisms independent of the development of obesity, we used a murine model of hepatic mitochondrial deficiency. The liver-heart axis was studied as these mice develop microvesicular steatosis without obesity. Our results unveil a sex-dependent phenotypic remodeling beyond liver damage. Males, more than females, show fasting hypoglycemia and increased insulin sensitivity. They exhibit diastolic dysfunction, remodeling of the circulating lipoproteins and cardiac lipidome. Conversely, females do not manifest cardiac dysfunction but exhibit cardiometabolic impairments supported by impaired mitochondrial integrity and β-oxidation, remodeling of circulating lipoproteins and intracardiac accumulation of deleterious triglycerides. This study underscores metabolic defects in the liver resulting in significant sex-dependent cardiac abnormalities independent of obesity. This experimental model may prove useful to better understand the sex-related variability, notably in the heart, involved in the progression of lean-NAFLD.
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