Common Variants in Lipid Metabolism-Related Genes Associate with Fat Mass Changes in Response to Dietary Monounsaturated Fatty Acids in Adults with Abdominal Obesity.
adiposity
dietary fatty acids
fat quality
fatness
gene–nutrient interaction
genotype
Journal
The Journal of nutrition
ISSN: 1541-6100
Titre abrégé: J Nutr
Pays: United States
ID NLM: 0404243
Informations de publication
Date de publication:
01 10 2019
01 10 2019
Historique:
received:
21
04
2019
revised:
06
05
2019
accepted:
23
05
2019
pubmed:
11
7
2019
medline:
24
6
2020
entrez:
11
7
2019
Statut:
ppublish
Résumé
Different fatty acids (FAs) can vary in their obesogenic effect, and genetic makeup can contribute to fat deposition in response to dietary FA composition. However, the antiobesogenic effects of the interactions between dietary MUFAs and genetics have scarcely been tested in intervention studies. We evaluated the overall (primary outcome) and genetically modulated (secondary outcome) response in body weight and fat mass to different levels of MUFA consumption. In the Canola Oil Multicenter Intervention Trial II, a randomized, crossover, isocaloric, controlled-feeding multicenter trial, 44 men and 71 women with a mean age of 44 y and an increased waist circumference (men ∼108 cm and women ∼102 cm) consumed each of 3 oils for 6 wk, separated by four 12-wk washout periods. Oils included 2 high-MUFA oils-conventional canola and high-oleic canola (<7% SFAs, >65% MUFAs)-and 1 low-MUFA/high-SFA oil blend (40.2% SFAs, 22.0% MUFAs). Body fat was measured using DXA. Five candidate single-nucleotide polymorphisms (SNPs) were genotyped using qualitative PCR. Data were analyzed using a repeated measures mixed model. No significant differences were observed in adiposity measures following the consumption of either high-MUFA diet compared with the low-MUFA/high-SFA treatment. However, when stratified by genotype, 3 SNPs within lipoprotein lipase (LPL), adiponectin, and apoE genes influenced, separately, fat mass changes in response to treatment (n = 101). Mainly, the LPL rs13702-CC genotype was associated with lower visceral fat (high-MUFA: -216.2 ± 58.6 g; low-MUFA: 17.2 ± 81.1 g; P = 0.017) and android fat mass (high-MUFA: -267.3 ± 76.4 g; low-MUFA: -21.7 ± 102.2 g; P = 0.037) following average consumption of the 2 high-MUFA diets. Common variants in LPL, adiponectin, and apoE genes modulated body fat mass response to dietary MUFAs in an isocaloric diet in adults with abdominal obesity. These findings might eventually help in developing personalized dietary recommendations for weight control. The trial was registered at clinicaltrials.gov as NCT02029833 (https://www.clinicaltrials.gov/ct2/show/NCT02029833?cond=NCT02029833&rank=1).
Sections du résumé
BACKGROUND
Different fatty acids (FAs) can vary in their obesogenic effect, and genetic makeup can contribute to fat deposition in response to dietary FA composition. However, the antiobesogenic effects of the interactions between dietary MUFAs and genetics have scarcely been tested in intervention studies.
OBJECTIVE
We evaluated the overall (primary outcome) and genetically modulated (secondary outcome) response in body weight and fat mass to different levels of MUFA consumption.
METHODS
In the Canola Oil Multicenter Intervention Trial II, a randomized, crossover, isocaloric, controlled-feeding multicenter trial, 44 men and 71 women with a mean age of 44 y and an increased waist circumference (men ∼108 cm and women ∼102 cm) consumed each of 3 oils for 6 wk, separated by four 12-wk washout periods. Oils included 2 high-MUFA oils-conventional canola and high-oleic canola (<7% SFAs, >65% MUFAs)-and 1 low-MUFA/high-SFA oil blend (40.2% SFAs, 22.0% MUFAs). Body fat was measured using DXA. Five candidate single-nucleotide polymorphisms (SNPs) were genotyped using qualitative PCR. Data were analyzed using a repeated measures mixed model.
RESULTS
No significant differences were observed in adiposity measures following the consumption of either high-MUFA diet compared with the low-MUFA/high-SFA treatment. However, when stratified by genotype, 3 SNPs within lipoprotein lipase (LPL), adiponectin, and apoE genes influenced, separately, fat mass changes in response to treatment (n = 101). Mainly, the LPL rs13702-CC genotype was associated with lower visceral fat (high-MUFA: -216.2 ± 58.6 g; low-MUFA: 17.2 ± 81.1 g; P = 0.017) and android fat mass (high-MUFA: -267.3 ± 76.4 g; low-MUFA: -21.7 ± 102.2 g; P = 0.037) following average consumption of the 2 high-MUFA diets.
CONCLUSIONS
Common variants in LPL, adiponectin, and apoE genes modulated body fat mass response to dietary MUFAs in an isocaloric diet in adults with abdominal obesity. These findings might eventually help in developing personalized dietary recommendations for weight control. The trial was registered at clinicaltrials.gov as NCT02029833 (https://www.clinicaltrials.gov/ct2/show/NCT02029833?cond=NCT02029833&rank=1).
Identifiants
pubmed: 31291447
pii: S0022-3166(22)16464-3
doi: 10.1093/jn/nxz136
pmc: PMC7443768
doi:
Substances chimiques
Dietary Fats
0
Fatty Acids, Monounsaturated
0
Banques de données
ClinicalTrials.gov
['NCT02029833']
Types de publication
Journal Article
Multicenter Study
Randomized Controlled Trial
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1749-1756Subventions
Organisme : NIA NIH HHS
ID : T32 AG033534
Pays : United States
Informations de copyright
Copyright © American Society for Nutrition 2019. All rights reserved.
Références
Exp Mol Med. 2008 Oct 31;40(5):523-32
pubmed: 18985010
Obesity (Silver Spring). 2015 Oct;23(10):1980-6
pubmed: 26331956
Epidemiol Health. 2011;33:e2011003
pubmed: 21603224
Hum Mol Genet. 2003 Nov 15;12(22):2923-9
pubmed: 14506127
Obesity (Silver Spring). 2009 Mar;17(3):510-7
pubmed: 19238139
FASEB J. 2017 Mar;31(3):989-997
pubmed: 27895108
Genet Test Mol Biomarkers. 2017 Jan;21(1):53-57
pubmed: 28085496
Endocrine. 2014 Nov;47(2):500-5
pubmed: 24504765
Nutrients. 2014 Oct 20;6(10):4452-71
pubmed: 25333200
Obesity (Silver Spring). 2016 Nov;24(11):2261-2268
pubmed: 27804268
Diabetologia. 2002 Mar;45(3):369-77
pubmed: 11914742
J Clin Invest. 1993 Nov;92(5):2124-30
pubmed: 8227328
Obesity (Silver Spring). 2012 Jun;20(6):1313-8
pubmed: 22282048
Mol Cell Biochem. 2010 Apr;337(1-2):307-15
pubmed: 19915960
Mol Nutr Food Res. 2014 Apr;58(4):821-9
pubmed: 24173768
Am J Hum Genet. 2013 Jan 10;92(1):5-14
pubmed: 23246289
Am J Clin Nutr. 2013 Apr;97(4):689-97
pubmed: 23446891
J Nutr. 2019 Mar 1;149(3):471-478
pubmed: 30773586
Br J Nutr. 2003 Sep;90(3):717-27
pubmed: 13129479
Diabetes. 2001 Mar;50(3):686-9
pubmed: 11246892
J Mol Med (Berl). 2002 Dec;80(12):753-69
pubmed: 12483461
Int J Obes Relat Metab Disord. 2002 Jun;26(6):814-21
pubmed: 12037652
Metabolism. 2012 Nov;61(11):1598-605
pubmed: 22698766
Curr Obes Rep. 2015 Dec;4(4):401-10
pubmed: 26374640
J Acad Nutr Diet. 2015 Feb;115(2):249-63
pubmed: 25636220
Gene. 2012 Nov 10;509(2):282-5
pubmed: 22921891
Biomed Res Int. 2014;2014:658913
pubmed: 25110685
J Diabetes Metab Disord. 2012 Oct 08;11(1):18
pubmed: 23497440
Obes Rev. 2005 May;6(2):155-68
pubmed: 15836466
Diabetes Care. 2004 Jun;27(6):1276-80
pubmed: 15161775
Int J Obes (Lond). 2013 Sep;37(9):1211-20
pubmed: 23357958
Ann Nutr Metab. 2010;57(3-4):242-50
pubmed: 21150196
Obesity (Silver Spring). 2014 Jun;22(6):1422-9
pubmed: 24639419
Eur J Nutr. 2006 Dec;45(8):454-62
pubmed: 17080261
J Nutr. 2004 Oct;134(10):2517-22
pubmed: 15465740
Nutr Metab Cardiovasc Dis. 2014 Dec;24(12):1323-9
pubmed: 25156894
Am J Physiol Endocrinol Metab. 2009 Aug;297(2):E271-88
pubmed: 19318514
Food Funct. 2015 Jan;6(1):204-10
pubmed: 25347552
J Nutrigenet Nutrigenomics. 2014;7(4-6):243-51
pubmed: 25968937
Diabetologia. 2007 Dec;50(12):2451-60
pubmed: 17898990
Obesity (Silver Spring). 2008 Jan;16(1):29-33
pubmed: 18223608
Am J Clin Nutr. 2015 Aug;102(2):505-13
pubmed: 26085515
Mol Nutr Food Res. 2015 Feb;59(2):334-43
pubmed: 25381750
Eur J Nutr. 2014 Apr;53(3):691-710
pubmed: 24363161
Clin Nutr. 2008 Feb;27(1):133-41
pubmed: 17765364
In Vivo. 2009 Jan-Feb;23(1):33-9
pubmed: 19368122
Arch Med Res. 2012 Feb;43(2):145-53
pubmed: 22374249
Mol Nutr Food Res. 2011 Dec;55(12):1771-9
pubmed: 22102511
J Clin Endocrinol Metab. 2005 Aug;90(8):4816-23
pubmed: 15928243
Nutr Hosp. 2006 May-Jun;21(3):317-31
pubmed: 16771114
Lipids. 2017 Oct;52(10):803-822
pubmed: 28889206
Mol Cell Endocrinol. 2014 Jan 25;382(1):740-757
pubmed: 22963884