Comprehensive Analysis of Established Dyslipidemia-Associated Loci in the Diabetes Prevention Program

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Comprehensive Analysis of Established Dyslipidemia-Associated Loci in the Diabetes Prevention Program. / Varga, Tibor V; Winters, Alexandra H; Jablonski, Kathleen A; Horton, Edward S; Khare-Ranade, Prajakta; Knowler, William C; Marcovina, Santica M; Renström, Frida; Watson, Karol E; Goldberg, Ronald; Florez, José C; Pollin, Toni I; Franks, Paul W.

I: Circulation. Cardiovascular genetics, Bind 9, Nr. 6, 12.2016, s. 495-503.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Varga, TV, Winters, AH, Jablonski, KA, Horton, ES, Khare-Ranade, P, Knowler, WC, Marcovina, SM, Renström, F, Watson, KE, Goldberg, R, Florez, JC, Pollin, TI & Franks, PW 2016, 'Comprehensive Analysis of Established Dyslipidemia-Associated Loci in the Diabetes Prevention Program', Circulation. Cardiovascular genetics, bind 9, nr. 6, s. 495-503. https://doi.org/10.1161/CIRCGENETICS.116.001457

APA

Varga, T. V., Winters, A. H., Jablonski, K. A., Horton, E. S., Khare-Ranade, P., Knowler, W. C., Marcovina, S. M., Renström, F., Watson, K. E., Goldberg, R., Florez, J. C., Pollin, T. I., & Franks, P. W. (2016). Comprehensive Analysis of Established Dyslipidemia-Associated Loci in the Diabetes Prevention Program. Circulation. Cardiovascular genetics, 9(6), 495-503. https://doi.org/10.1161/CIRCGENETICS.116.001457

Vancouver

Varga TV, Winters AH, Jablonski KA, Horton ES, Khare-Ranade P, Knowler WC o.a. Comprehensive Analysis of Established Dyslipidemia-Associated Loci in the Diabetes Prevention Program. Circulation. Cardiovascular genetics. 2016 dec.;9(6):495-503. https://doi.org/10.1161/CIRCGENETICS.116.001457

Author

Varga, Tibor V ; Winters, Alexandra H ; Jablonski, Kathleen A ; Horton, Edward S ; Khare-Ranade, Prajakta ; Knowler, William C ; Marcovina, Santica M ; Renström, Frida ; Watson, Karol E ; Goldberg, Ronald ; Florez, José C ; Pollin, Toni I ; Franks, Paul W. / Comprehensive Analysis of Established Dyslipidemia-Associated Loci in the Diabetes Prevention Program. I: Circulation. Cardiovascular genetics. 2016 ; Bind 9, Nr. 6. s. 495-503.

Bibtex

@article{dafb5978dee54181b2e30bebfc6fe4e6,
title = "Comprehensive Analysis of Established Dyslipidemia-Associated Loci in the Diabetes Prevention Program",
abstract = "BACKGROUND: We assessed whether 234 established dyslipidemia-associated loci modify the effects of metformin treatment and lifestyle intervention (versus placebo control) on lipid and lipid subfraction levels in the Diabetes Prevention Program randomized controlled trial.METHODS AND RESULTS: We tested gene treatment interactions in relation to baseline-adjusted follow-up blood lipid concentrations (high-density lipoprotein [HDL] and low-density lipoprotein-cholesterol, total cholesterol, and triglycerides) and lipoprotein subfraction particle concentrations and size in 2993 participants with pre-diabetes. Of the previously reported single-nucleotide polymorphism associations, 32.5% replicated at P<0.05 with baseline lipid traits. Trait-specific genetic risk scores were robustly associated (3×10-4>P>1.1×10-16) with their respective baseline traits for all but 2 traits. Lifestyle modified the effect of the genetic risk score for large HDL particle numbers, such that each risk allele of the genetic risk scores was associated with lower concentrations of large HDL particles at follow-up in the lifestyle arm (β=-0.11 µmol/L per genetic risk scores risk allele; 95% confidence interval, -0.188 to -0.033; P=5×10-3; Pinteraction=1×10-3 for lifestyle versus placebo), but not in the metformin or placebo arms (P>0.05). In the lifestyle arm, participants with high genetic risk had more favorable or similar trait levels at 1-year compared with participants at lower genetic risk at baseline for 17 of the 20 traits.CONCLUSIONS: Improvements in large HDL particle concentrations conferred by lifestyle may be diminished by genetic factors. Lifestyle intervention, however, was successful in offsetting unfavorable genetic loading for most lipid traits.CLINICAL TRIAL REGISTRATION: URL: https://www.clinicaltrials.gov. Unique Identifier: NCT00004992.",
keywords = "Cholesterol, HDL/blood, Cholesterol, LDL/blood, Dyslipidemias/blood, Gene-Environment Interaction, Genetic Loci, Genetic Markers, Genetic Predisposition to Disease, Heredity, Humans, Hypoglycemic Agents/therapeutic use, Lipids/blood, Metformin/therapeutic use, Particle Size, Phenotype, Polymorphism, Single Nucleotide, Prediabetic State/blood, Risk Assessment, Risk Factors, Risk Reduction Behavior, Triglycerides/blood, United States/epidemiology",
author = "Varga, {Tibor V} and Winters, {Alexandra H} and Jablonski, {Kathleen A} and Horton, {Edward S} and Prajakta Khare-Ranade and Knowler, {William C} and Marcovina, {Santica M} and Frida Renstr{\"o}m and Watson, {Karol E} and Ronald Goldberg and Florez, {Jos{\'e} C} and Pollin, {Toni I} and Franks, {Paul W}",
note = "{\textcopyright} 2016 American Heart Association, Inc.",
year = "2016",
month = dec,
doi = "10.1161/CIRCGENETICS.116.001457",
language = "English",
volume = "9",
pages = "495--503",
journal = "Circulation: Cardiovascular Genetics",
issn = "1942-325X",
publisher = "Lippincott Williams & Wilkins",
number = "6",

}

RIS

TY - JOUR

T1 - Comprehensive Analysis of Established Dyslipidemia-Associated Loci in the Diabetes Prevention Program

AU - Varga, Tibor V

AU - Winters, Alexandra H

AU - Jablonski, Kathleen A

AU - Horton, Edward S

AU - Khare-Ranade, Prajakta

AU - Knowler, William C

AU - Marcovina, Santica M

AU - Renström, Frida

AU - Watson, Karol E

AU - Goldberg, Ronald

AU - Florez, José C

AU - Pollin, Toni I

AU - Franks, Paul W

N1 - © 2016 American Heart Association, Inc.

PY - 2016/12

Y1 - 2016/12

N2 - BACKGROUND: We assessed whether 234 established dyslipidemia-associated loci modify the effects of metformin treatment and lifestyle intervention (versus placebo control) on lipid and lipid subfraction levels in the Diabetes Prevention Program randomized controlled trial.METHODS AND RESULTS: We tested gene treatment interactions in relation to baseline-adjusted follow-up blood lipid concentrations (high-density lipoprotein [HDL] and low-density lipoprotein-cholesterol, total cholesterol, and triglycerides) and lipoprotein subfraction particle concentrations and size in 2993 participants with pre-diabetes. Of the previously reported single-nucleotide polymorphism associations, 32.5% replicated at P<0.05 with baseline lipid traits. Trait-specific genetic risk scores were robustly associated (3×10-4>P>1.1×10-16) with their respective baseline traits for all but 2 traits. Lifestyle modified the effect of the genetic risk score for large HDL particle numbers, such that each risk allele of the genetic risk scores was associated with lower concentrations of large HDL particles at follow-up in the lifestyle arm (β=-0.11 µmol/L per genetic risk scores risk allele; 95% confidence interval, -0.188 to -0.033; P=5×10-3; Pinteraction=1×10-3 for lifestyle versus placebo), but not in the metformin or placebo arms (P>0.05). In the lifestyle arm, participants with high genetic risk had more favorable or similar trait levels at 1-year compared with participants at lower genetic risk at baseline for 17 of the 20 traits.CONCLUSIONS: Improvements in large HDL particle concentrations conferred by lifestyle may be diminished by genetic factors. Lifestyle intervention, however, was successful in offsetting unfavorable genetic loading for most lipid traits.CLINICAL TRIAL REGISTRATION: URL: https://www.clinicaltrials.gov. Unique Identifier: NCT00004992.

AB - BACKGROUND: We assessed whether 234 established dyslipidemia-associated loci modify the effects of metformin treatment and lifestyle intervention (versus placebo control) on lipid and lipid subfraction levels in the Diabetes Prevention Program randomized controlled trial.METHODS AND RESULTS: We tested gene treatment interactions in relation to baseline-adjusted follow-up blood lipid concentrations (high-density lipoprotein [HDL] and low-density lipoprotein-cholesterol, total cholesterol, and triglycerides) and lipoprotein subfraction particle concentrations and size in 2993 participants with pre-diabetes. Of the previously reported single-nucleotide polymorphism associations, 32.5% replicated at P<0.05 with baseline lipid traits. Trait-specific genetic risk scores were robustly associated (3×10-4>P>1.1×10-16) with their respective baseline traits for all but 2 traits. Lifestyle modified the effect of the genetic risk score for large HDL particle numbers, such that each risk allele of the genetic risk scores was associated with lower concentrations of large HDL particles at follow-up in the lifestyle arm (β=-0.11 µmol/L per genetic risk scores risk allele; 95% confidence interval, -0.188 to -0.033; P=5×10-3; Pinteraction=1×10-3 for lifestyle versus placebo), but not in the metformin or placebo arms (P>0.05). In the lifestyle arm, participants with high genetic risk had more favorable or similar trait levels at 1-year compared with participants at lower genetic risk at baseline for 17 of the 20 traits.CONCLUSIONS: Improvements in large HDL particle concentrations conferred by lifestyle may be diminished by genetic factors. Lifestyle intervention, however, was successful in offsetting unfavorable genetic loading for most lipid traits.CLINICAL TRIAL REGISTRATION: URL: https://www.clinicaltrials.gov. Unique Identifier: NCT00004992.

KW - Cholesterol, HDL/blood

KW - Cholesterol, LDL/blood

KW - Dyslipidemias/blood

KW - Gene-Environment Interaction

KW - Genetic Loci

KW - Genetic Markers

KW - Genetic Predisposition to Disease

KW - Heredity

KW - Humans

KW - Hypoglycemic Agents/therapeutic use

KW - Lipids/blood

KW - Metformin/therapeutic use

KW - Particle Size

KW - Phenotype

KW - Polymorphism, Single Nucleotide

KW - Prediabetic State/blood

KW - Risk Assessment

KW - Risk Factors

KW - Risk Reduction Behavior

KW - Triglycerides/blood

KW - United States/epidemiology

U2 - 10.1161/CIRCGENETICS.116.001457

DO - 10.1161/CIRCGENETICS.116.001457

M3 - Journal article

C2 - 27784733

VL - 9

SP - 495

EP - 503

JO - Circulation: Cardiovascular Genetics

JF - Circulation: Cardiovascular Genetics

SN - 1942-325X

IS - 6

ER -

ID: 242837079