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dc.contributor.authorPetäistö, Tiina
dc.contributor.authorVicente, David
dc.contributor.authorMäkelä, Kari A
dc.contributor.authorFinnilä, Mikko A
dc.contributor.authorMiinalainen, Ilkka
dc.contributor.authorKoivunen, Jarkko
dc.contributor.authorIzzi, Valerio
dc.contributor.authorAikio, Mari
dc.contributor.authorKarppinen, Sanna-Maria
dc.contributor.authorDavarajan, Raman
dc.contributor.authorThevenot, Jerome
dc.contributor.authorHerzig, Karl-Heinz
dc.contributor.authorHeljasvaara, Ritva Leena
dc.contributor.authorPihlajaniemi, Taina
dc.date.accessioned2021-08-02T11:17:10Z
dc.date.available2021-08-02T11:17:10Z
dc.date.created2021-02-15T14:47:19Z
dc.date.issued2020
dc.identifier.issn0022-3751
dc.identifier.urihttps://hdl.handle.net/11250/2765833
dc.description.abstractLiver and adipose tissues play important roles in the regulation of systemic glucose and lipid metabolism. Extracellular matrix synthesis and remodelling are significantly altered in these tissues in obesity and type 2 diabetes. Collagen XVIII is a ubiquitous extracellular matrix component, and it occurs in three isoforms which differ in terms of molecular size, domain structure and tissue distribution. We recently showed that, in mice, the lack of collagen XVIII, and especially its medium and long isoforms, leads to reduced adiposity and dyslipidaemia. To address the metabolic consequences of these intriguing observations, we assessed whole-body glucose homeostasis in mice challenged with a high-fat diet and in normal physiological conditions. We observed that, in the high caloric diet, the overall adiposity was decreased by 30%, serum triglyceride values were threefold higher and the steatotic area in liver was twofold larger in collagen XVIII knockout mice compared with controls. We demonstrated that mice lacking either all three collagen XVIII isoforms, or specifically, the medium and long isoforms develop insulin resistance and glucose intolerance. Furthermore, we found that ablation of collagen XVIII leads to increased heat production in low temperatures and to reduction of the high blood triglyceride levels of the knockout mice to the level of wild-type mice. Our data indicate that collagen XVIII plays a role in the regulation of glucose tolerance, insulin sensitivity and lipid homeostasis, principally through its ability to regulate the expansion of the adipose tissue. These findings advance the understanding of metabolic disorders.en_US
dc.language.isoengen_US
dc.publisherWileyen_US
dc.rightsNavngivelse-Ikkekommersiell 4.0 Internasjonal*
dc.rights.urihttp://creativecommons.org/licenses/by-nc/4.0/deed.no*
dc.titleLack of collagen XVIII leads to lipodystrophy and perturbs hepatic glucose and lipid homeostasisen_US
dc.typeJournal articleen_US
dc.typePeer revieweden_US
dc.description.versionpublishedVersionen_US
dc.rights.holderCopyright 2020 The Authorsen_US
cristin.ispublishedtrue
cristin.fulltextoriginal
cristin.qualitycode2
dc.identifier.doi10.1113/JP279559
dc.identifier.cristin1889983
dc.source.journalJournal of Physiologyen_US
dc.source.pagenumber3373-3393en_US
dc.identifier.citationJournal of Physiology. 2020, 598(16), 3373-3393en_US
dc.source.volume598en_US
dc.source.issue16en_US


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Navngivelse-Ikkekommersiell 4.0 Internasjonal
Except where otherwise noted, this item's license is described as Navngivelse-Ikkekommersiell 4.0 Internasjonal