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Circulating triacylglycerol signatures in nonalcoholic fatty liver disease associated with the I148M variant in PNPLA3 and with obesity
Department of Medicine, University of Helsinki, Helsinki, Finland; Minerva Foundation Institute for Medical Research, Helsinki, Finland.
VTT Technical Research Centre of Finland, Espoo, Finland.
Minerva Foundation Institute for Medical Research, Helsinki, Finland.
Örebro University, School of Science and Technology. VTT Technical Research Centre of Finland, Espoo, Finland.
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2014 (English)In: Diabetes, ISSN 0012-1797, E-ISSN 1939-327X, Vol. 63, no 1, p. 312-322Article in journal (Refereed) Published
Abstract [en]

We examined whether relative concentrations of circulating triacylglycerols (TAGs) between carriers compared with noncarriers of PNPLA3(I148M) gene variant display deficiency of TAGs, which accumulate in the liver because of defective lipase activity. We also analyzed the effects of obesity-associated nonalcoholic fatty liver disease (NAFLD) independent of genotype, and of NAFLD due to either PNPLA3(I148M) gene variant or obesity on circulating TAGs. A total of 372 subjects were divided into groups based on PNPLA3 genotype or obesity. Absolute and relative deficiency of distinct circulating TAGs was observed in the PNPLA3(148MM/148MI) compared with the PNPLA3(148II) group. Obese and 'nonobese' groups had similar PNPLA3 genotypes, but the obese subjects were insulin-resistant. Liver fat was similarly increased in obese and PNPLA3(148MM/148MI) groups. Relative concentrations of TAGs in the obese subjects versus nonobese displayed multiple changes. These closely resembled those between obese subjects with NAFLD but without PNPLA3(I148M) versus those with the I148M variant and NAFLD. The etiology of NAFLD influences circulating TAG profiles. 'PNPLA3 NAFLD' is associated with a relative deficiency of TAGs, supporting the idea that the I148M variant impedes intrahepatocellular lipolysis rather than stimulates TAG synthesis. 'Obese NAFLD' is associated with multiple changes in TAGs, which can be attributed to obesity/insulin resistance rather than increased liver fat content per se.

Place, publisher, year, edition, pages
American Diabetes Association , 2014. Vol. 63, no 1, p. 312-322
National Category
Analytical Chemistry Endocrinology and Diabetes
Identifiers
URN: urn:nbn:se:oru:diva-63689DOI: 10.2337/db13-0774ISI: 000328680400037PubMedID: 24009255Scopus ID: 2-s2.0-84891810442OAI: oai:DiVA.org:oru-63689DiVA, id: diva2:1169254
Funder
Academy of FinlandNovo Nordisk
Note

Funding agencies:

Sigrid Juselius Foundation

Finnish Diabetes Research Foundation

Emil Aaltonen Foundation

Finnish Medical Foundation

Academy of Finland Centre of Excellence in Molecular Systems Immunology and Physiology Research 250114

European Commission LSHM-CT-2005-018734

European Union/European Federation of Pharmaceutical Industries and Associations Innovative Medicines Initiative Joint Undertaking

Available from: 2017-12-22 Created: 2017-12-22 Last updated: 2018-01-30Bibliographically approved

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Hyötyläinen, TuuliaOresic, Matej

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