Characteristic Gene Alterations During Fatty Acid Metabolism in the Goose Liver
Anna Koseniuk

TL;DR
This paper explores how specific genes regulate fatty acid metabolism in geese, making them a useful model for studying human fatty liver disease.
Contribution
The study identifies and summarizes key genes involved in hepatic steatosis in geese, offering insights into non-alcoholic fatty liver disease.
Findings
Genes like ME1, SCD1, ACSL1, and ELOVL6 are key in lipid metabolism during goose liver steatosis.
Goose hepatic steatosis is reversible and non-inflammatory, similar to human NAFLD.
Diet-induced lipid accumulation in geese mirrors human metabolic conditions.
Abstract
The development of hepatic steatosis in geese is a complex, multistage process involving genes related to lipid synthesis, transport, storage, and metabolism. Key genes activated during this process include ME1 (malic enzyme 1), SCD1 (stearoyl-CoA desaturase), ACSL1 (acyl-CoA synthetase long-chain family member 1), and ELOVL6 (elongation of very-long-chain fatty acids protein 6). The expression of these genes varies depending on the tissue, breed, and metabolic context. Geese possess a unique ability to develop hepatic steatosis (fatty liver) without accompanying inflammation or liver damage. This condition typically arises from overfeeding, either through carbohydrates or fats, leading to significant triglyceride accumulation in hepatocytes. Importantly, this state remains reversible and is considered non-pathological. The physiological and molecular changes observed in overfed geese,…
Genes, proteins, chemicals, diseases, species, mutations and cell lines named across the full text — each resolved to its canonical identifier and authoritative record.
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Taxonomy
TopicsFatty Acid Research and Health · Lipid metabolism and biosynthesis · Adipose Tissue and Metabolism
