Liver fattening during feast and famine: an evolutionary paradox.
Liver disease is one of the features of metabolic syndrome, one of the most occurring diseases of the twenty-first century. During food deprivation and starvation, adipose tissue elsewhere in the body delivers lipid components to the liver where they are stored as triacylglycerols (TG). Continuous and excessive food intake, on the other hand, leads to liver fattening (hepatic steatosis). In the long term this reaction is pathogenic mainly by inflammation reactions. We postulate the hypothesis in the evolutionary context that individuals with genes promoting the efficient deposition of fat during periods between famines (thrifty genes) in combination with a proinflammatory genotype would be favored and be selected during the course of evolution. Furthermore we postulate the hypothesis that the majority of man, living in a world were famine never comes, are physiologically not adapted to modern social behavior with abundance of food.
Department of Anatomy and Embryology, Leiden University Medical Center, P.O. Box 9600, 2300 RC, Leiden, The Netherlands. V.J.T.va.Ginneken@biology.leidenuniv.nl
Vincent J T
VJ
van Ginneken
D000273:Adipose Tissue; D005075:Biological Evolution; D001823:Body Composition; D004435:Eating; D004734:Energy Metabolism; D005234:Fatty Liver / Q000473:pathology; D005508:Food Deprivation; D005838:Genotype; D006801:Humans; D007249:Inflammation; D008110:Liver Extracts / Q000378:metabolism*; D008264:Macrophages / Q000378:metabolism; D008954:Models, Biological; D014280:Triglycerides / Q000378:metabolism*
D008110:Liver Extracts; D014280:Triglycerides