Diabetic and dyslipidaemic morbidly obese exhibit more liver alterations compared with healthy morbidly obese

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dc.contributor.authorPardina, Eva
dc.contributor.authorFerrer, Roser
dc.contributor.authorRossell, Joana
dc.contributor.authorBaena-Fustegueras, Juan A
dc.contributor.authorLecube Torelló, Albert
dc.contributor.authorFort, José Manuel
dc.contributor.authorCaubet, Enric
dc.contributor.authorGonzález, Óscar
dc.contributor.authorVilallonga, Ramón
dc.contributor.authorVargas, Víctor
dc.contributor.authorBalibrea, José María
dc.contributor.authorPeinado-Onsurbe, Julia
dc.date.accessioned2021-04-12T12:39:37Z
dc.date.available2021-04-12T12:39:37Z
dc.date.issued2016
dc.description.abstractBackground & aims: To study the origin of fat excess in the livers of morbidly obese (MO) individuals, we analysed lipids and lipases in both plasma and liver and genes involved in lipid transport, or related with, in that organ. Methods: Thirty-two MO patients were grouped according to the absence (healthy: DM−DL−) or presence of comorbidities (dyslipidemic: DM−DL+; or dyslipidemic with type 2 diabetes: DM+DL+) before and one year after gastric bypass. Results: The livers of healthy, DL and DM patients contained more lipids (9.8, 9.5 and 13.7 times, respectively) than those of control subjects. The genes implicated in liver lipid uptake, including HL, LPL, VLDLr, and FAT/CD36, showed increased expression compared with the controls. The expression of genes involved in lipid-related processes outside of the liver, such as apoB, PPARα and PGC1α, CYP7a1 and HMGCR, was reduced in these patients compared with the controls. PAI1 and TNFα gene expression in the diabetic livers was increased compared with the other obese groups and control group. Increased steatosis and fibrosis were also noted in the MO individuals. Conclusions: Hepatic lipid parameters in MO patients change based on their comorbidities. The gene expression and lipid levels after bariatric surgery were less prominent in the diabetic patients. Lipid receptor overexpression could enable the liver to capture circulating lipids, thus favouring the steatosis typically observed in diabetic and dyslipidaemic MO individuals.ca_ES
dc.description.sponsorshipThis research has received funding from the Fondo de Investigación Sanitaria del Instituto de Salud Carlos III of the Spanish Ministry for Health and Consumer Affairs (PI030024, PI030042, PI070079 and PI11/01159)ca_ES
dc.identifier.doihttps://doi.org/10.1016/j.bbacli.2015.12.002
dc.identifier.idgrec026120
dc.identifier.issn2214-6474
dc.identifier.urihttp://hdl.handle.net/10459.1/71003
dc.language.isoengca_ES
dc.publisherElsevierca_ES
dc.relation.isformatofReproducció del document publicat a https://doi.org/10.1016/j.bbacli.2015.12.002ca_ES
dc.relation.ispartofBBA Clinical, 2016, vol. 5, p. 54-65ca_ES
dc.rightscc-by-nc-nd (c) Pardina, et al., 2016ca_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccessca_ES
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectSteatosisca_ES
dc.subjectNAFLDca_ES
dc.subjectLiverca_ES
dc.subjectLipasesca_ES
dc.subjectDiabetesca_ES
dc.subjectLipidsca_ES
dc.titleDiabetic and dyslipidaemic morbidly obese exhibit more liver alterations compared with healthy morbidly obeseca_ES
dc.typeinfo:eu-repo/semantics/articleca_ES
dc.type.versioninfo:eu-repo/semantics/publishedVersionca_ES
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