Print Email Facebook Twitter Hepatic Steatosis: A Mediator of the Metabolic Syndrome. Lessons from Animal Models Title Hepatic Steatosis: A Mediator of the Metabolic Syndrome. Lessons from Animal Models Author den Boer, M. Voshol, P.J. Kuipers, F. Havekes, L.M. Romijn, J.A. TNO Preventie en Gezondheid Publication year 2004 Abstract Epidemiological studies in humans, as well as experimental studies in animal models, have shown an association between visceral obesity and dyslipidemia, insulin resistance, and type 2 diabetes mellitus. Recently, attention has been focused on the excessive accumulation of triglycerides (TG) in the liver as part of this syndrome. In this review, important principles of the pathophysiological involvement of the liver in the metabolic syndrome obtained in rodent models are summarized. We focus on non-alcoholic causes of steatosis, because the animal experiments we refer to did not include alcohol as an experimental condition. In general, there is continuous cycling and redistribution of non-oxidized fatty acids between different organs. The amount of TG in an intrinsically normal liver is not fixed but can readily be increased by nutritional, metabolic, and endocrine interactions involving TG/free fatty acid (FFA) partitioning and TG/FFA metabolism. Several lines of evidence indicate that hepatic TG accumulation is also a causative factor involved in hepatic insulin resistance. Complex interactions between endocrine, metabolic, and transcriptional pathways are involved in TG-induced hepatic insulin resistance. Therefore, the liver participates passively and actively in the metabolic derangements of the metabolic syndrome. We speculate that similar mechanisms may also be involved in human pathophysiology. Chemicals / CAS: alcohol, 64-17-5; Fatty Acids; Glucose, 50-99-7; Triglycerides Subject BiologyBiomedical ResearchFatty acid metabolismGlucose metabolismInsulin resistanceLipoprotein metabolismMouse modelsAlcoholTriacylglycerolAnimal experimentAnimal modelDisease associationDyslipidemiaEndocrine systemGenetic transcriptionGlucose metabolismLnsulin resistanceLipid liver levelMetabolic syndrome XMouseNon insulin dependent diabetes mellitusNonhumanPartition coefficientPathophysiologyRodentShort surveyAdipose TissueAnimalsDiabetes Mellitus, Type 2DogsFatty AcidsFatty LiverGlucoseHomeostasisHumansHyperlipidemiasInsulin ResistanceLiverMetabolic Syndrome XMiceModels, AnimalModels, BiologicalObesityRatsRats, ZuckerTranscription, GeneticTriglycerides To reference this document use: http://resolver.tudelft.nl/uuid:be392251-9609-4963-b31c-e5b79d48e8d8 DOI https://doi.org/10.1161/01.atv.0000116217.57583.6e TNO identifier 237683 ISSN 1079-5642 Source Arteriosclerosis, Thrombosis, and Vascular Biology, 24 (4), 644-649 Document type article Files To receive the publication files, please send an e-mail request to TNO Library.