TY - JOUR
T1 - Genetic effects on postprandial variations of inflammatory markers in healthy individuals
AU - Cheng, Yu Ching
AU - Kao, Wen Hong L.
AU - Mitchell, Braxton D.
AU - Sharrett, A. Richey
AU - Ryan, Kathleen A.
AU - Vogel, Robert A.
AU - Shuldiner, Alan R.
AU - Pollin, Toni I.
PY - 2010/7
Y1 - 2010/7
N2 - Circulating levels of inflammatory markers predict the risk of cardiovascular disease (CVD), mediated perhaps in part by dietary fat intake, through mechanisms only partially understood. To evaluate post-fat load changes in inflammatory markers and genetic influences on these changes, we administered a standardized high-fat meal to 838 related Amish subjects as part of the Heredity and Phenotype Intervention (HAPI) Heart Study and measured a panel of inflammatory markers, including C-reactive protein (CRP), interleukin-1Β (IL-1Β), matrix metalloproteinase-1 and-9 (MMP-1 and MMP-9), and white blood cell (WBC) count, before and 4h after fat challenge (CRP prechallenge only). Heritabilities (h2 ± s.d.) of basal inflammatory levels ranged from 16 8% for MMP-9 (P = 0.02) to 90 7% for MMP-1 (P <0.0001). Post-fat load, circulating levels of WBC, MMP-1, and MMP-9 increased by 16, 32, and 43% (all P < 0.0001), with no significant changes in IL-1Β. Postprandial changes over the 4-h period were modestly heritable for WBC (age-and sex-adjusted h2 = 14 ± 9%, P = 0.04), but the larger MMP-1 and MMP-9 changes appeared to be independent of additive genetic effects. These results reveal that a high-fat meal induces a considerable inflammatory response. Genetic factors appear to play a significant role influencing basal inflammatory levels but to have minimal influence on post-fat intake inflammatory changes.
AB - Circulating levels of inflammatory markers predict the risk of cardiovascular disease (CVD), mediated perhaps in part by dietary fat intake, through mechanisms only partially understood. To evaluate post-fat load changes in inflammatory markers and genetic influences on these changes, we administered a standardized high-fat meal to 838 related Amish subjects as part of the Heredity and Phenotype Intervention (HAPI) Heart Study and measured a panel of inflammatory markers, including C-reactive protein (CRP), interleukin-1Β (IL-1Β), matrix metalloproteinase-1 and-9 (MMP-1 and MMP-9), and white blood cell (WBC) count, before and 4h after fat challenge (CRP prechallenge only). Heritabilities (h2 ± s.d.) of basal inflammatory levels ranged from 16 8% for MMP-9 (P = 0.02) to 90 7% for MMP-1 (P <0.0001). Post-fat load, circulating levels of WBC, MMP-1, and MMP-9 increased by 16, 32, and 43% (all P < 0.0001), with no significant changes in IL-1Β. Postprandial changes over the 4-h period were modestly heritable for WBC (age-and sex-adjusted h2 = 14 ± 9%, P = 0.04), but the larger MMP-1 and MMP-9 changes appeared to be independent of additive genetic effects. These results reveal that a high-fat meal induces a considerable inflammatory response. Genetic factors appear to play a significant role influencing basal inflammatory levels but to have minimal influence on post-fat intake inflammatory changes.
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U2 - 10.1038/oby.2009.416
DO - 10.1038/oby.2009.416
M3 - Article
C2 - 19910936
AN - SCOPUS:77954145906
SN - 1930-7381
VL - 18
SP - 1417
EP - 1422
JO - Obesity
JF - Obesity
IS - 7
ER -