ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2010
Insulin- and leptin-regulated fatty acid uptake plays a key causal role in hepatic steatosis in mice with intact leptin signaling but not in ob/ob or db/db mice.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 58 citations in OpenAlex.
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- Mulberry (Nutrition research and practice · 2022Article
- Animal Models of Dysregulated Cardiac Metabolism.Circulation research · 2022Review
- Pathogenesis of Alcohol-Associated Fatty Liver: Lessons From Transgenic Mice.Frontiers in physiology · 2022Review
- LC-N2G: a local consistency approach for nutrigenomics data analysis.BMC bioinformatics · 2020Article
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- Lipidomic Profiling Reveals Disruption of Lipid Metabolism in Valproic Acid-Induced Hepatotoxicity.Frontiers in pharmacology · 2019Article
- Hepatic lesions induced by feeding Western diets to Zucker fatty rats, an insulin-resistant model.Journal of toxicologic pathology · 2018Article
- Dai-Zong-Fang, A Traditional Chinese Herbal Formula, Ameliorates Insulin Resistance inFrontiers in physiology · 2018Article
- Effects of Periconception Cadmium and Mercury Co-Administration to Mice on Indices of Chronic Diseases in Male Offspring at Maturity.Environmental health perspectives · 2017Article
- Alcohol, Adipose Tissue and Lipid Dysregulation.Biomolecules · 2017Article
- Nonalcoholic Fatty Liver Disease: Lipids and Insulin Resistance.Clinics in liver disease · 2016Review
- Isoxazole Alters Metabolites and Gene Expression, Decreasing Proliferation and Promoting a Neuroendocrine Phenotype in β-Cells.ACS chemical biology · 2016Article
- Facilitated long chain fatty acid uptake by adipocytes remains upregulated relative to BMI for more than a year after major bariatric surgical weight loss.Obesity (Silver Spring, Md.) · 2016Article
- Nuclear Receptors as Therapeutic Targets in Liver Disease: Are We There Yet?Annual review of pharmacology and toxicology · 2016Review
- Female spontaneously diabetic Torii fatty rats develop nonalcoholic steatohepatitis-like hepatic lesions.World journal of gastroenterology · 2015Article
- Strategies, models and biomarkers in experimental non-alcoholic fatty liver disease research.Progress in lipid research · 2015Review
- The anti-TNF-α antibody infliximab inhibits the expression of fat-transporter-protein FAT/CD36 in a selective hepatic-radiation mouse model.International journal of molecular sciences · 2015Article
- Approach to assessing determinants of glucose homeostasis in the conscious mouse.Mammalian genome : official journal of the International Mammalian Genome Society · 2014Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Hepatic steatosis results from several processes. To assess their relative roles, hepatocellular long-chain fatty acid (LCFA) uptake was assayed in hepatocytes from C57BL/6J control mice, mice with steatosis from a high-fat diet (HFD) or 10%, 14%, or 18% ethanol (EtOH) in drinking water [functioning leptin-signaling groups (FLSGs)], and ob/ob and db/db mice. V(max) for uptake was increased vs. controls (P < 0.001) and correlated significantly with liver weight and triglycerides (TGs) in all FLSG mice but was minimally or not increased in ob/ob and db/db mice, in which liver weights and TGs greatly exceeded projections from regressions in FLSG animals. Coefficients of determination (R(2)) for these FLSG regressions suggest that increased LCFA uptake accounts for ∼80% of the increase in hepatic TGs within these groups, but increased lipogenic gene expression data suggest that enhanced LCFA synthesis is the major contributor in ob/ob and db/db. Got2, Cd36, Slc27a2, and Slc27a5 gene expression ratios were significantly upregulated in the EtOH groups, correlating with sterol regulatory element binding protein 1c (SREBP1c) and V(max), but only Cd36 expression was increased in HFD, ob/ob, and db/db mice. Comparison of V(max) with serum insulin and leptin suggests that both hormones contribute to upregulation of uptake in the FLSG animals. Thus, increased LCFA uptake, reflecting SREBP1c-mediated upregulation of four distinct transporters, is the dominant cause of steatosis in EtOH-fed mice. In ob/ob and db/db mice, increased LCFA synthesis appears more important. In FLSG animals, insulin upregulates hepatocellular LCFA uptake. Leptin appears to upregulate LCFA uptake or to be essential for full expression of upregulation by insulin.
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