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Glucokinase Regulat...
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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 ...
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2011-06-06
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Public Library of Science (PLoS),2011
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printrdacarrier
Numbers
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LIBRIS-ID:oai:DiVA.org:uu-155218
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https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-155218URI
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https://doi.org/10.1371/journal.pone.0020555DOI
Supplementary language notes
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Language:English
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Summary in:English
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Subject category:ref swepub-contenttype
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Subject category:art swepub-publicationtype
Notes
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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.
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Delgado-Lista, Javier
(author)
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Garcia-Rios, Antonio
(author)
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Mc Monagle, Jolene
(author)
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Gulseth, Hanne L.
(author)
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Ordovas, Jose M.
(author)
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Shaw, Danielle I.
(author)
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Karlström, BritaUppsala universitet,Klinisk nutrition och metabolism(Swepub:uu)britkarl
(author)
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Kiec-Wilk, Beata
(author)
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Blaak, Ellen E.
(author)
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Helal, Olfa
(author)
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Malczewska-Malec, Malgorzata
(author)
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Defoort, Catherine
(author)
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Risérus, UlfUppsala universitet,Klinisk nutrition och metabolism(Swepub:uu)ulfriser
(author)
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Saris, Wim H. M.
(author)
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Lovegrove, Julie A.
(author)
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Drevon, Christian A.
(author)
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Roche, Helen M.
(author)
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Lopez-Miranda, Jose
(author)
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Uppsala universitetKlinisk nutrition och metabolism
(creator_code:org_t)
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In:PLOS ONE: Public Library of Science (PLoS)6:6, s. e20555-1932-6203
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Karlström, Brita
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Malczewska-Malec ...
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Defoort, Catheri ...
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Risérus, Ulf
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