ArticleThe Journal of clinical investigation2019
Brown fat activation mitigates alcohol-induced liver steatosis and injury in mice.
Article in The Journal of clinical investigation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
35 citing papers in PubMed, 56 citations in OpenAlex.
- Article
- Gut microbiota, brown adipose tissue whitening, and obesity: nutritional modulators and metabolic crosstalk.Nutrition & metabolism · 2026Review
- The versatile interplay between steatotic liver disease and liver cancer.Nature reviews. Cancer · 2026Review
- Brown adipose tissue inactivation exacerbates alcohol-induced liver steatosis, inflammation, and fibrosis.American journal of physiology. Gastrointestinal and liver physiology · 2026Article
- Deciphering Uncoupling Proteins in Cellular Homeostasis and Metabolic Health.International journal of biological sciences · 2026Review
- Biliary NF-κB-Inducing Kinase Promotes Ductular Reaction, Inflammation, and Fibrosis and Impedes Liver Disease Resolution.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Endocrine regulation of metabolic crosstalk between liver and brown adipose tissue by natural active ingredients.International journal of obesity (2005) · 2025Review
- Bridging systemic metabolic dysfunction and Alzheimer's disease: the liver interface.Molecular neurodegeneration · 2025Review
- The Role of Solute Carrier Family Transporters in Hepatic Steatosis and Hepatic Fibrosis.Journal of clinical and translational hepatology · 2025Review
- PRDM16 in thermogenic adipocytes mediates an inter-organ protective signaling against alcohol-associated liver disease.Molecular and cellular endocrinology · 2025Article
- Steatotic liver disease and cancer: from pathogenesis to therapeutic targets.eGastroenterology · 2025Review
- Immunological mechanisms in steatotic liver diseases: An overview and clinical perspectives.Clinical and molecular hepatology · 2024Review
- Hepatic Snai1 and Snai2 promote liver regeneration and suppress liver fibrosis in mice.Cell reports · 2024Article
- Neuregulin 4 mediates the metabolic benefits of mild cold exposure by promoting beige fat thermogenesis.JCI insight · 2024Article
- Enhanced CaNature communications · 2023Article
- Molecular and cellular regulation of thermogenic fat.Frontiers in endocrinology · 2023Review
- Effects of multi-organ crosstalk on the physiology and pathology of adipose tissue.Frontiers in endocrinology · 2023Review
- The evolving view of thermogenic fat and its implications in cancer and metabolic diseases.Signal transduction and targeted therapy · 2022Review
- Reprogramming of Hepatic Metabolism and Microenvironment in Nonalcoholic Steatohepatitis.Annual review of nutrition · 2022Review
- Modulation of the Bile Acid Enterohepatic Cycle by Intestinal Microbiota Alleviates Alcohol Liver Disease.Cells · 2022Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Chronic alcohol consumption causes liver injury, inflammation and fibrosis, thereby increasing morbidity and mortality. Paradoxically, modest drinking is believed to confer metabolic improvement, but the underlying mechanism remains elusive. Here, we have identified a novel hepatoprotective brain/brown adipose tissue (BAT)/liver axis. Alcohol consumption or direct alcohol administration into the brain stimulated hypothalamic neural circuits and sympathetic nerves innervating BAT, and dramatically increased BAT uncoupling protein 1 (Ucp1) expression and activity in a BAT sympathetic nerve-dependent manner. BAT and beige fat oxidized fatty acids to fuel Ucp1-mediated thermogenesis, thereby inhibiting lipid trafficking into the liver. BAT also secreted several adipokines, including adiponectin that suppressed hepatocyte injury and death. Genetic deletion of Ucp1 profoundly augmented alcohol-induced liver steatosis, injury, inflammation and fibrosis in male and female mice. Conversely, activation of BAT and beige fat through cold exposure suppressed alcoholic liver disease development. Our results unravel an unrecognized brain alcohol-sensing/sympathetic nerve/BAT/liver axis that counteracts liver steatosis and injury.
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