ArticleClinical epigenetics2014
Leucine alters hepatic glucose/lipid homeostasis via the myostatin-AMP-activated protein kinase pathway - potential implications for nonalcoholic fatty liver disease.
Article in Clinical epigenetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 29 citations in OpenAlex.
- Sarcopenia and Skeletal Muscle Dysfunction in Liver Cirrhosis: Clinical Perspectives of Myostatin Inhibition.Biomedicines · 2026Review
- Skeletal Muscle as Endocrine Organ.Advances in experimental medicine and biology · 2025Review
- Metabolic Derangement in Non-Alcoholic Fatty Liver Disease: Opportunities for Early Diagnostic and Prognostic Markers.Current molecular medicine · 2025Review
- Myokines: metabolic regulation in obesity and type 2 diabetes.Life metabolism · 2024Review
- New insight of obesity-associated NAFLD: Dysregulated "crosstalk" between multi-organ and the liver?Genes & diseases · 2023Review
- A Transcriptomic Regulatory Network among miRNAs, lncRNAs, circRNAs, and mRNAs Associated with L-leucine-induced Proliferation of Equine Satellite Cells.Animals : an open access journal from MDPI · 2023Article
- Impact of Exercise and Aging on Mitochondrial Homeostasis in Skeletal Muscle: Roles of ROS and Epigenetics.Cells · 2022Review
- Different Effects of Leucine Supplementation and/or Exercise on Systemic Insulin Sensitivity in Mice.Frontiers in endocrinology · 2021Article
- Abnormal metabolic processes involved in the pathogenesis of non-alcoholic fatty liver disease (Review).Experimental and therapeutic medicine · 2020Review
- Blood multiomics reveal insights into population clusters with low prevalence of diabetes, dyslipidemia and hypertension.PloS one · 2020Article
- Dietary Leucine Supplementation Restores Serum Glucose Levels, and Modifying Hepatic Gene Expression Related to the Insulin Signal Pathway in IUGR Piglets.Animals : an open access journal from MDPI · 2019Article
- The Fatty Acid β-Oxidation Pathway is Activated by Leucine Deprivation in HepG2 Cells: A Comparative Proteomics Study.Scientific reports · 2017Article
- MicroRNA Expression Relating to Dietary-Induced Liver Steatosis and NASH.Journal of clinical medicine · 2015Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundElevated plasma levels of the branched-chain amino acid (BCAA) leucine are associated with obesity and insulin resistance (IR), and thus the propensity for type 2 diabetes mellitus development. However, other clinical studies suggest the contradictory view that leucine may in fact offer a degree of protection against metabolic syndrome. Aiming to resolve this apparent paradox, we assessed the effect of leucine supplementation on the metabolism of human hepatic HepG2 cells.
resultsWe demonstrate that pathophysiological leucine appears to be antagonistic to insulin, promotes glucose uptake (and not glycogen synthesis), but results in hepatic cell triglyceride (TG) accumulation. Further, we provide evidence that myostatin (MSTN) regulation of AMP-activated protein kinase (AMPK) is a key pathway in the metabolic effects elicited by excess leucine. Finally, we report associated changes in miRNA expression (some species previously linked to metabolic disease etiology), suggesting that epigenetic processes may contribute to these effects.
conclusionsCollectively, our observations suggest leucine may be both 'friend' and 'foe' in the context of metabolic syndrome, promoting glucose sequestration and driving lipid accumulation in liver cells. These observations provide insight into the clinical consequences of excess plasma leucine, particularly for hyperglycemia, IR and nonalcoholic fatty liver disease (NAFLD).
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.