Replication of the Association of BDNF and MC4R Variants With Dietary Intake in the Diabetes Prevention Program

for the Diabetes Prevention Program Research Group

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

OBJECTIVES: Genomewide association studies (GWAS) have identified consistent associations with obesity, with a number of studies implicating eating behavior as a primary mechanism. Few studies have replicated genetic associations with dietary intake. This study evaluates the association between obesity susceptibility loci and dietary intake. METHODS: Data were obtained as part of the Diabetes Prevention Program (DPP), a clinical trial of diabetes prevention in persons at high risk of diabetes. The association of 31 genomewide association studies identified obesity risk alleles with dietary intake, measured through a food frequency questionnaire, was investigated in 3,180 participants from DPP at baseline. RESULTS: The minor allele at BDNF, identified as protective against obesity, was associated with lower total caloric intake (β = −106.06, SE = 33.13; p = .0014) at experimentwide statistical significance (p = .0016), whereas association of MC4R rs571312 with higher caloric intake reached nominal significance (β = 61.32, SE = 26.24; p = .0194). Among non-Hispanic white participants, the association of BDNF rs2030323 with total caloric intake was stronger (β = −151.99, SE = 30.09; p < .0001), and association of FTO rs1421085 with higher caloric intake (β = 56.72, SE = 20.69; p = .0061) and percentage fat intake (β = 0.37, SE = 0.08; p = .0418) was also observed. CONCLUSIONS: These results demonstrate with the strength of independent replication that BDNF rs2030323 is associated with 100 to 150 greater total caloric intake per allele, with additional contributions of MC4R and, in non-Hispanic white individuals, FTO. As it has been argued that an additional 100 kcal/d could account for the trends in weight gain, prevention focusing on genetic profiles with high dietary intake may help to quell adverse obesity trends.Clinical Trial Registration: Clinicaltrials.gov,NCT00004992.

Original languageEnglish (US)
JournalPsychosomatic Medicine
DOIs
StateAccepted/In press - Aug 20 2016

Fingerprint

Brain-Derived Neurotrophic Factor
Energy Intake
Obesity
Alleles
Clinical Trials
Feeding Behavior
Weight Gain
Fats
Intake
Replication
Diabetes
Food

ASJC Scopus subject areas

  • Medicine(all)
  • Developmental and Educational Psychology
  • Arts and Humanities (miscellaneous)
  • Applied Psychology
  • Psychiatry and Mental health

Cite this

Replication of the Association of BDNF and MC4R Variants With Dietary Intake in the Diabetes Prevention Program. / for the Diabetes Prevention Program Research Group.

In: Psychosomatic Medicine, 20.08.2016.

Research output: Contribution to journalArticle

@article{41efb4e54a264f5ebedc5de56697bf11,
title = "Replication of the Association of BDNF and MC4R Variants With Dietary Intake in the Diabetes Prevention Program",
abstract = "OBJECTIVES: Genomewide association studies (GWAS) have identified consistent associations with obesity, with a number of studies implicating eating behavior as a primary mechanism. Few studies have replicated genetic associations with dietary intake. This study evaluates the association between obesity susceptibility loci and dietary intake. METHODS: Data were obtained as part of the Diabetes Prevention Program (DPP), a clinical trial of diabetes prevention in persons at high risk of diabetes. The association of 31 genomewide association studies identified obesity risk alleles with dietary intake, measured through a food frequency questionnaire, was investigated in 3,180 participants from DPP at baseline. RESULTS: The minor allele at BDNF, identified as protective against obesity, was associated with lower total caloric intake (β = −106.06, SE = 33.13; p = .0014) at experimentwide statistical significance (p = .0016), whereas association of MC4R rs571312 with higher caloric intake reached nominal significance (β = 61.32, SE = 26.24; p = .0194). Among non-Hispanic white participants, the association of BDNF rs2030323 with total caloric intake was stronger (β = −151.99, SE = 30.09; p < .0001), and association of FTO rs1421085 with higher caloric intake (β = 56.72, SE = 20.69; p = .0061) and percentage fat intake (β = 0.37, SE = 0.08; p = .0418) was also observed. CONCLUSIONS: These results demonstrate with the strength of independent replication that BDNF rs2030323 is associated with 100 to 150 greater total caloric intake per allele, with additional contributions of MC4R and, in non-Hispanic white individuals, FTO. As it has been argued that an additional 100 kcal/d could account for the trends in weight gain, prevention focusing on genetic profiles with high dietary intake may help to quell adverse obesity trends.Clinical Trial Registration: Clinicaltrials.gov,NCT00004992.",
author = "{for the Diabetes Prevention Program Research Group} and McCaffery, {Jeanne M.} and Jablonski, {Kathleen A.} and Franks, {Paul W.} and Delahanty, {Linda M.} and Vanita Aroda and David Marrero and Hamman, {Richard F.} and Horton, {Edward S.} and Samuel Dagogo-Jack and Judith Wylie-Rosett and Elizabeth Barrett-Connor and Abbas Kitabchi and Knowler, {William C.} and Wing, {Rena R.} and Florez, {Jose C.}",
year = "2016",
month = "8",
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journal = "Psychosomatic Medicine",
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T1 - Replication of the Association of BDNF and MC4R Variants With Dietary Intake in the Diabetes Prevention Program

AU - for the Diabetes Prevention Program Research Group

AU - McCaffery, Jeanne M.

AU - Jablonski, Kathleen A.

AU - Franks, Paul W.

AU - Delahanty, Linda M.

AU - Aroda, Vanita

AU - Marrero, David

AU - Hamman, Richard F.

AU - Horton, Edward S.

AU - Dagogo-Jack, Samuel

AU - Wylie-Rosett, Judith

AU - Barrett-Connor, Elizabeth

AU - Kitabchi, Abbas

AU - Knowler, William C.

AU - Wing, Rena R.

AU - Florez, Jose C.

PY - 2016/8/20

Y1 - 2016/8/20

N2 - OBJECTIVES: Genomewide association studies (GWAS) have identified consistent associations with obesity, with a number of studies implicating eating behavior as a primary mechanism. Few studies have replicated genetic associations with dietary intake. This study evaluates the association between obesity susceptibility loci and dietary intake. METHODS: Data were obtained as part of the Diabetes Prevention Program (DPP), a clinical trial of diabetes prevention in persons at high risk of diabetes. The association of 31 genomewide association studies identified obesity risk alleles with dietary intake, measured through a food frequency questionnaire, was investigated in 3,180 participants from DPP at baseline. RESULTS: The minor allele at BDNF, identified as protective against obesity, was associated with lower total caloric intake (β = −106.06, SE = 33.13; p = .0014) at experimentwide statistical significance (p = .0016), whereas association of MC4R rs571312 with higher caloric intake reached nominal significance (β = 61.32, SE = 26.24; p = .0194). Among non-Hispanic white participants, the association of BDNF rs2030323 with total caloric intake was stronger (β = −151.99, SE = 30.09; p < .0001), and association of FTO rs1421085 with higher caloric intake (β = 56.72, SE = 20.69; p = .0061) and percentage fat intake (β = 0.37, SE = 0.08; p = .0418) was also observed. CONCLUSIONS: These results demonstrate with the strength of independent replication that BDNF rs2030323 is associated with 100 to 150 greater total caloric intake per allele, with additional contributions of MC4R and, in non-Hispanic white individuals, FTO. As it has been argued that an additional 100 kcal/d could account for the trends in weight gain, prevention focusing on genetic profiles with high dietary intake may help to quell adverse obesity trends.Clinical Trial Registration: Clinicaltrials.gov,NCT00004992.

AB - OBJECTIVES: Genomewide association studies (GWAS) have identified consistent associations with obesity, with a number of studies implicating eating behavior as a primary mechanism. Few studies have replicated genetic associations with dietary intake. This study evaluates the association between obesity susceptibility loci and dietary intake. METHODS: Data were obtained as part of the Diabetes Prevention Program (DPP), a clinical trial of diabetes prevention in persons at high risk of diabetes. The association of 31 genomewide association studies identified obesity risk alleles with dietary intake, measured through a food frequency questionnaire, was investigated in 3,180 participants from DPP at baseline. RESULTS: The minor allele at BDNF, identified as protective against obesity, was associated with lower total caloric intake (β = −106.06, SE = 33.13; p = .0014) at experimentwide statistical significance (p = .0016), whereas association of MC4R rs571312 with higher caloric intake reached nominal significance (β = 61.32, SE = 26.24; p = .0194). Among non-Hispanic white participants, the association of BDNF rs2030323 with total caloric intake was stronger (β = −151.99, SE = 30.09; p < .0001), and association of FTO rs1421085 with higher caloric intake (β = 56.72, SE = 20.69; p = .0061) and percentage fat intake (β = 0.37, SE = 0.08; p = .0418) was also observed. CONCLUSIONS: These results demonstrate with the strength of independent replication that BDNF rs2030323 is associated with 100 to 150 greater total caloric intake per allele, with additional contributions of MC4R and, in non-Hispanic white individuals, FTO. As it has been argued that an additional 100 kcal/d could account for the trends in weight gain, prevention focusing on genetic profiles with high dietary intake may help to quell adverse obesity trends.Clinical Trial Registration: Clinicaltrials.gov,NCT00004992.

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DO - 10.1097/PSY.0000000000000380

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