The Jones Lab

Bioinformatics | Microbiome | Health Disparities | Nutrition

PNPLA3 Genotype, Arachidonic Acid Intake, and Unsaturated Fat Intake Influences Liver Fibrosis in Hispanic Youth with Obesity


Journal article


Roshonda B Jones, Lide Arenaza, C. Rios, J. Plows, Paige K. Berger, Tanya L. Alderete, Jennifer L. Fogel, K. Nayak, Passant Mohamed, D. Hwang, S. Palmer, F. Sinatra, H. Allayee, Rohit Kohli, M. Goran
Nutrients, 2021

Semantic Scholar DOI PubMedCentral PubMed
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APA   Click to copy
Jones, R. B., Arenaza, L., Rios, C., Plows, J., Berger, P. K., Alderete, T. L., … Goran, M. (2021). PNPLA3 Genotype, Arachidonic Acid Intake, and Unsaturated Fat Intake Influences Liver Fibrosis in Hispanic Youth with Obesity. Nutrients.


Chicago/Turabian   Click to copy
Jones, Roshonda B, Lide Arenaza, C. Rios, J. Plows, Paige K. Berger, Tanya L. Alderete, Jennifer L. Fogel, et al. “PNPLA3 Genotype, Arachidonic Acid Intake, and Unsaturated Fat Intake Influences Liver Fibrosis in Hispanic Youth with Obesity.” Nutrients (2021).


MLA   Click to copy
Jones, Roshonda B., et al. “PNPLA3 Genotype, Arachidonic Acid Intake, and Unsaturated Fat Intake Influences Liver Fibrosis in Hispanic Youth with Obesity.” Nutrients, 2021.


BibTeX   Click to copy

@article{roshonda2021a,
  title = {PNPLA3 Genotype, Arachidonic Acid Intake, and Unsaturated Fat Intake Influences Liver Fibrosis in Hispanic Youth with Obesity},
  year = {2021},
  journal = {Nutrients},
  author = {Jones, Roshonda B and Arenaza, Lide and Rios, C. and Plows, J. and Berger, Paige K. and Alderete, Tanya L. and Fogel, Jennifer L. and Nayak, K. and Mohamed, Passant and Hwang, D. and Palmer, S. and Sinatra, F. and Allayee, H. and Kohli, Rohit and Goran, M.}
}

Abstract

Non-alcoholic fatty liver disease impacts 15.2% of Hispanic adolescents and can progress to a build-up of scared tissue called liver fibrosis. If diagnosed early, liver fibrosis may be reversible, so it is necessary to understand risk factors. The aims of this study in 59 Hispanic adolescents with obesity were to: (1) identify potential biological predictors of liver fibrosis and dietary components that influence liver fibrosis, and (2) determine if the association between dietary components and liver fibrosis differs by PNPLA3 genotype, which is highly prevalent in Hispanic adolescents and associated with elevated liver fat. We examined liver fat and fibrosis, genotyped for PNPLA3 gene, and assessed diet via 24-h diet recalls. The prevalence of increased fibrosis was 20.9% greater in males, whereas participants with the GG genotype showed 23.7% greater prevalence. Arachidonic acid was associated with liver fibrosis after accounting for sex, genotype, and liver fat (β = 0.072, p = 0.033). Intakes of several dietary types of unsaturated fat have different associations with liver fibrosis by PNPLA3 genotype after accounting for sex, caloric intake, and liver fat. These included monounsaturated fat (βCC/CG = −0.0007, βGG = 0.03, p-value = 0.004), polyunsaturated fat (βCC/CG = −0.01, βGG = 0.02, p-value = 0.01), and omega-6 (βCC/CG = −0.0102, βGG = 0.028, p-value = 0.01). Results from this study suggest that reduction of arachidonic acid and polyunsaturated fatty acid intake might be important for the prevention of non-alcoholic fatty liver disease progression, especially among those with PNPLA3 risk alleles.