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  • Perez-Martinez, Pablo (author)

Glucokinase Regulatory Protein Genetic Variant Interacts with Omega-3 PUFA to Influence Insulin Resistance and Inflammation in Metabolic Syndrome

  • Article/chapterEnglish2011

Publisher, publication year, extent ...

  • 2011-06-06
  • Public Library of Science (PLoS),2011
  • printrdacarrier

Numbers

  • LIBRIS-ID:oai:DiVA.org:uu-155218
  • https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-155218URI
  • https://doi.org/10.1371/journal.pone.0020555DOI

Supplementary language notes

  • Language:English
  • Summary in:English

Part of subdatabase

Classification

  • Subject category:ref swepub-contenttype
  • Subject category:art swepub-publicationtype

Notes

  • Glucokinase Regulatory Protein (GCKR) plays a central role regulating both hepatic triglyceride and glucose metabolism. Fatty acids are key metabolic regulators, which interact with genetic factors and influence glucose metabolism and other metabolic traits. Omega-3 polyunsaturated fatty acids (n-3 PUFA) have been of considerable interest, due to their potential to reduce metabolic syndrome (MetS) risk. Objective: To examine whether genetic variability at the GCKR gene locus was associated with the degree of insulin resistance, plasma concentrations of C-reactive protein (CRP) and n-3 PUFA in MetS subjects. Design: Homeostasis model assessment of insulin resistance (HOMA-IR), HOMA-B, plasma concentrations of C-peptide, CRP, fatty acid composition and the GCKR rs1260326-P446L polymorphism, were determined in a cross-sectional analysis of 379 subjects with MetS participating in the LIPGENE dietary cohort. Results: Among subjects with n-3 PUFA levels below the population median, carriers of the common C/C genotype had higher plasma concentrations of fasting insulin (P = 0.019), C-peptide (P = 0.004), HOMA-IR (P = 0.008) and CRP (P = 0.032) as compared with subjects carrying the minor T-allele (Leu446). In contrast, homozygous C/C carriers with n-3 PUFA levels above the median showed lower plasma concentrations of fasting insulin, peptide C, HOMA-IR and CRP, as compared with individuals with the T-allele. Conclusions: We have demonstrated a significant interaction between the GCKR rs1260326-P446L polymorphism and plasma n-3 PUFA levels modulating insulin resistance and inflammatory markers in MetS subjects. Further studies are needed to confirm this gene-diet interaction in the general population and whether targeted dietary recommendations can prevent MetS in genetically susceptible individuals.

Subject headings and genre

  • MEDICINE
  • MEDICIN

Added entries (persons, corporate bodies, meetings, titles ...)

  • Delgado-Lista, Javier (author)
  • Garcia-Rios, Antonio (author)
  • Mc Monagle, Jolene (author)
  • Gulseth, Hanne L. (author)
  • Ordovas, Jose M. (author)
  • Shaw, Danielle I. (author)
  • Karlström, BritaUppsala universitet,Klinisk nutrition och metabolism(Swepub:uu)britkarl (author)
  • Kiec-Wilk, Beata (author)
  • Blaak, Ellen E. (author)
  • Helal, Olfa (author)
  • Malczewska-Malec, Malgorzata (author)
  • Defoort, Catherine (author)
  • Risérus, UlfUppsala universitet,Klinisk nutrition och metabolism(Swepub:uu)ulfriser (author)
  • Saris, Wim H. M. (author)
  • Lovegrove, Julie A. (author)
  • Drevon, Christian A. (author)
  • Roche, Helen M. (author)
  • Lopez-Miranda, Jose (author)
  • Uppsala universitetKlinisk nutrition och metabolism (creator_code:org_t)

Related titles

  • In:PLOS ONE: Public Library of Science (PLoS)6:6, s. e20555-1932-6203

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