Four-Week Omega-3 Supplementation in Carriers of the Prosteatotic PNPLA3 p.I148M Genetic Variant: An Open-Label Study.


Journal

Lifestyle genomics
ISSN: 2504-3188
Titre abrégé: Lifestyle Genom
Pays: Switzerland
ID NLM: 101716139

Informations de publication

Date de publication:
2019
Historique:
received: 21 05 2019
accepted: 08 07 2019
pubmed: 28 8 2019
medline: 26 8 2020
entrez: 28 8 2019
Statut: ppublish

Résumé

The PNPLA3 loss-of-function variant p.I148M is a strong genetic determinant of nonalcoholic fatty liver disease. The PNPLA3 protein functions as an intracellular lipase in the liver, with a greater activity on unsaturated fatty acids. This study aimed to determine whether short-term supplementation with omega-3 fatty acids impacts hepatic steatosis differently in PNPLA3 p.148I wild-type individuals as compared to homozygous carriers of the PNPLA3 p.148M variant. Twenty subjects with hepatic steatosis (50% women, age 18-77 years) were included. Ten subjects homozygous for the PNPLA3 148M variant were matched to 10 wild-type individuals. The subjects received 4 g omega-3 fatty acids (1,840 mg eicosapentaenoic acid and 1,520 mg docosahexaenoic acid) a day for 4 weeks. Transient elastography with a controlled attenuation parameter (CAP) was used to quantify liver fat before and after the intervention. Body composition, fibrosis, liver function tests, serum free fatty acids (FFA) and glucose markers were compared. Patients homozygous for the PNPLA3 p.148M variant (risk group) demonstrated no significant changes in CAP compared to baseline (284 ± 55 vs. 287 ± 65 dB/m) as did the control group (256 ± 56 vs. 262 ± 55 dB/m). While serum liver enzyme activities remained unchanged in both groups, the risk group displayed significantly (p = 0.02) lower baseline FFA concentrations (334.5 [range 281.0-431.0] vs. 564.5 [range 509.0-682.0] μmol/L), which markedly increased by 9.1% after the intervention. In contrast, FFA concentrations decreased significantly (p = 0.01) by 28.3% in the wild-type group. Short-term omega-3 fatty acid supplementation did not significantly alter hepatic steatosis. The nutrigenomic and metabolic effects of omega-3 fatty acids should be investigated further in carriers of the PNPLA3 148M risk variant.

Sections du résumé

BACKGROUND/AIMS
The PNPLA3 loss-of-function variant p.I148M is a strong genetic determinant of nonalcoholic fatty liver disease. The PNPLA3 protein functions as an intracellular lipase in the liver, with a greater activity on unsaturated fatty acids. This study aimed to determine whether short-term supplementation with omega-3 fatty acids impacts hepatic steatosis differently in PNPLA3 p.148I wild-type individuals as compared to homozygous carriers of the PNPLA3 p.148M variant.
METHODS
Twenty subjects with hepatic steatosis (50% women, age 18-77 years) were included. Ten subjects homozygous for the PNPLA3 148M variant were matched to 10 wild-type individuals. The subjects received 4 g omega-3 fatty acids (1,840 mg eicosapentaenoic acid and 1,520 mg docosahexaenoic acid) a day for 4 weeks. Transient elastography with a controlled attenuation parameter (CAP) was used to quantify liver fat before and after the intervention. Body composition, fibrosis, liver function tests, serum free fatty acids (FFA) and glucose markers were compared.
RESULTS
Patients homozygous for the PNPLA3 p.148M variant (risk group) demonstrated no significant changes in CAP compared to baseline (284 ± 55 vs. 287 ± 65 dB/m) as did the control group (256 ± 56 vs. 262 ± 55 dB/m). While serum liver enzyme activities remained unchanged in both groups, the risk group displayed significantly (p = 0.02) lower baseline FFA concentrations (334.5 [range 281.0-431.0] vs. 564.5 [range 509.0-682.0] μmol/L), which markedly increased by 9.1% after the intervention. In contrast, FFA concentrations decreased significantly (p = 0.01) by 28.3% in the wild-type group.
CONCLUSIONS
Short-term omega-3 fatty acid supplementation did not significantly alter hepatic steatosis. The nutrigenomic and metabolic effects of omega-3 fatty acids should be investigated further in carriers of the PNPLA3 148M risk variant.

Identifiants

pubmed: 31454802
pii: 000502008
doi: 10.1159/000502008
doi:

Substances chimiques

Fatty Acids, Omega-3 0
Membrane Proteins 0
Isoleucine 04Y7590D77
Methionine AE28F7PNPL
Lipase EC 3.1.1.3
adiponutrin, human EC 3.1.1.3

Types de publication

Controlled Clinical Trial Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

10-17

Informations de copyright

© 2019 S. Karger AG, Basel.

Auteurs

Clara-Sophie Kuttner (CS)

Department of Medicine II, Saarland University Medical Center, Saarland University, Homburg, Germany.

Rosellina Mancina (R)

Department of Molecular and Clinical Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.

Gudrun Wagenpfeil (G)

Institute of Medical Biometry, Epidemiology and Medical Informatics, Saarland University, Homburg, Germany.

Frank Lammert (F)

Department of Medicine II, Saarland University Medical Center, Saarland University, Homburg, Germany, frank.lammert@uks.eu.

Caroline S Stokes (CS)

Department of Medicine II, Saarland University Medical Center, Saarland University, Homburg, Germany.

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Classifications MeSH