Imperial College London
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ProfessorAbbasDehghan

Faculty of Medicine, School of Public Health

Professor in Molecular Epidemiology
 
 
 
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Contact

 

+44 (0)20 7594 3347a.dehghan CV

 
 
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Location

 

Sir Michael Uren HubWhite City Campus

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Summary

 

Publications

Citation

BibTex format

@article{Murphy:2019:10.1002/mnfr.201900226,
author = {Murphy, AM and Smith, CE and Murphy, LM and Follis, JL and Tanaka, T and Richardson, K and Noordam, R and Lemaitre, RN and Kähönen, M and Dupuis, J and Voortman, T and Marouli, E and Mook-Kanamori, DO and Raitakari, OT and Hong, J and Dehghan, A and Dedoussis, G and de, Mutsert R and Lehtimäki, T and Liu, C-T and Rivadeneira, F and Deloukas, P and Mikkilä, V and Meigs, JB and Uitterlinden, A and Ikram, MA and Franco, OH and Hughes, M and O', Gaora P and Ordovás, JM and Roche, HM},
doi = {10.1002/mnfr.201900226},
journal = {Mol Nutr Food Res},
title = {Potential Interplay between Dietary Saturated Fats and Genetic Variants of the NLRP3 Inflammasome to Modulate Insulin Resistance and Diabetes Risk: Insights from a Meta-Analysis of 19 005 Individuals.},
url = {http://dx.doi.org/10.1002/mnfr.201900226},
volume = {63},
year = {2019}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - SCOPE: Insulin resistance (IR) and inflammation are hallmarks of type 2 diabetes (T2D). The nod-like receptor pyrin domain containing-3 (NLRP3) inflammasome is a metabolic sensor activated by saturated fatty acids (SFA) initiating IL-1β inflammation and IR. Interactions between SFA intake and NLRP3-related genetic variants may alter T2D risk factors. METHODS: Meta-analyses of six Cohorts for Heart and Aging Research in Genomic Epidemiology Consortium (n = 19 005) tested interactions between SFA and NLRP3-related single-nucleotide polymorphisms (SNPs) and modulation of fasting insulin, fasting glucose, and homeostasis model assessment of insulin resistance. RESULTS: SFA interacted with rs12143966, wherein each 1% increase in SFA intake increased insulin by 0.0063 IU mL-1 (SE ± 0.002, p = 0.001) per each major (G) allele copy. rs4925663, interacted with SFA (β ± SE = -0.0058 ± 0.002, p = 0.004) to increase insulin by 0.0058 IU mL-1 , per additional copy of the major (C) allele. Both associations are close to the significance threshold (p < 0.0001). rs4925663 causes a missense mutation affecting NLRP3 expression. CONCLUSION: Two NLRP3-related SNPs showed potential interaction with SFA to modulate fasting insulin. Greater dietary SFA intake accentuates T2D risk, which, subject to functional validation, may be further elaborated depending on NLRP3-related genetic variants.
AU  - Murphy,AM
AU  - Smith,CE
AU  - Murphy,LM
AU  - Follis,JL
AU  - Tanaka,T
AU  - Richardson,K
AU  - Noordam,R
AU  - Lemaitre,RN
AU  - Kähönen,M
AU  - Dupuis,J
AU  - Voortman,T
AU  - Marouli,E
AU  - Mook-Kanamori,DO
AU  - Raitakari,OT
AU  - Hong,J
AU  - Dehghan,A
AU  - Dedoussis,G
AU  - de,Mutsert R
AU  - Lehtimäki,T
AU  - Liu,C-T
AU  - Rivadeneira,F
AU  - Deloukas,P
AU  - Mikkilä,V
AU  - Meigs,JB
AU  - Uitterlinden,A
AU  - Ikram,MA
AU  - Franco,OH
AU  - Hughes,M
AU  - O',Gaora P
AU  - Ordovás,JM
AU  - Roche,HM
DO  - 10.1002/mnfr.201900226
PY  - 2019///
TI  - Potential Interplay between Dietary Saturated Fats and Genetic Variants of the NLRP3 Inflammasome to Modulate Insulin Resistance and Diabetes Risk: Insights from a Meta-Analysis of 19 005 Individuals.
T2  - Mol Nutr Food Res
UR  - http://dx.doi.org/10.1002/mnfr.201900226
UR  - https://www.ncbi.nlm.nih.gov/pubmed/31432628
VL  - 63
ER  -
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