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- An, Ping1
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- Srinivasasainagendra, Vinodh1
JLR Patient-Oriented and Epidemiological Research
2 Results
- Patient-Oriented and Epidemiological ResearchOpen Access
Does pregnancy alter life-course lipid trajectories? Evidence from the HUNT Study in Norway
Journal of Lipid ResearchVol. 59Issue 12p2403–2412Published online: October 12, 2018- Amanda R. Markovitz
- Eirin B. Haug
- Julie Horn
- Abigail Fraser
- Corrie Macdonald-Wallis
- Kate Tilling
- and others
Cited in Scopus: 11We examined the association between pregnancy and life-course lipid trajectories. Linked data from the Nord-Trøndelag Health Study and the Medical Birth Registry of Norway yielded 19,987 parous and 1,625 nulliparous women. Using mixed-effects spline models, we estimated differences in nonfasting lipid levels from before to after first birth in parous women and between parous and nulliparous women. HDL cholesterol (HDL-C) dropped by −4.2 mg/dl (95% CI: −5.0, −3.3) from before to after first birth in adjusted models, a 7% change, and the total cholesterol (TC) to HDL-C ratio increased by 0.18 (95% CI: 0.11, 0.25), with no change in non-HDL-C or triglycerides. - Patient-Oriented and Epidemiological ResearchOpen Access
An exome-wide sequencing study of lipid response to high-fat meal and fenofibrate in Caucasians from the GOLDN cohort
Journal of Lipid ResearchVol. 59Issue 4p722–729Published online: January 20, 2018- Xin Geng
- Marguerite R. Irvin
- Bertha Hidalgo
- Stella Aslibekyan
- Vinodh Srinivasasainagendra
- Ping An
- and others
Cited in Scopus: 5Our understanding of genetic influences on the response of lipids to specific interventions is limited. In this study, we sought to elucidate effects of rare genetic variants on lipid response to a high-fat meal challenge and fenofibrate (FFB) therapy in the Genetics of Lipid Lowering Drugs and Diet Network (GOLDN) cohort using an exome-wide sequencing-based association study. Our results showed that the rare coding variants in ITGA7, SIPA1L2, and CEP72 are significantly associated with fasting LDL cholesterol response to FFB (P = 1.24E-07), triglyceride postprandial area under the increase (AUI) (P = 2.31E-06), and triglyceride postprandial AUI response to FFB (P = 1.88E-06), respectively.