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dc.contributor.author Csala, Miklós
dc.date.accessioned 2018-10-01T08:52:49Z
dc.date.available 2018-10-01T08:52:49Z
dc.date.issued 2016
dc.identifier 84967205168
dc.identifier.citation pagination=733-739; journalVolume=157; journalIssueNumber=19; journalTitle=ORVOSI HETILAP;
dc.identifier.uri http://repo.lib.semmelweis.hu//handle/123456789/5856
dc.identifier.uri doi:10.1556/650.2016.30439
dc.description.abstract The increasing prevalence of type 2 diabetes correlates with the rapid spread of obesity worldwide. Adipocytes are strained by the demand of excessive storage, and the local inflammation accelerates triglyceride turnover, which elevates the plasma levels of free fatty acids. Sustained hyper-free fatty acidemia leads to disturbances in cellular functions (lipotoxicity) or even to programmed cell death. Activated stress kinases interfere with insulin signaling, and often facilitate apoptosis. Hyper-free fatty acidemia, therefore, links obesity to diabetes through insulin resistance and beta-cell damage. Lipotoxicity research - including the comparison of the effects exerted by saturated, unsaturated and trans fatty acids - provides explanations for long-known phenomena. Our widening knowledge in the field offers new strategies for prevention and treatment of the metabolic syndrome and diabetes. Orv. Hetil., 2016, 157(19), 733-739.
dc.relation.ispartof urn:issn:0030-6002
dc.title Zsírsavtúltengés - inzulinrezisztencia és béta-sejt-halál [Hyper-free fatty acidemia - insulin resistance and β-cell death]
dc.type Journal Article
dc.date.updated 2018-07-16T13:20:37Z
dc.language.rfc3066 hu
dc.identifier.mtmt 3059872
dc.identifier.wos 000375231200003
dc.identifier.pubmed 27133272


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