Common Variants in Lipid Metabolism-Related Genes Associate with Fat Mass Changes in Response to Dietary Monounsaturated Fatty Acids in Adults with Abdominal Obesity

Abstract

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).

Keywords: adiposity; dietary fatty acids; fat quality; fatness; gene–nutrient interaction; genotype.

Copyright © American Society for Nutrition 2019. All rights reserved.

Figures

FIGURE 1

LPL rs13702 genotypes determine the effect of high- compared with low-MUFA consumption on 6-wk changes in VAT mass (A), android fat (B), total fat mass (C), and body weight (D) in adults with abdominal obesity. Changes were calculated by subtracting the baseline value of the selected fat mass from its corresponding 6-wk end-point value. Total participants = 101: n = 50 LPL rs13702-TT, n = 45 LPL rs13702-CT, and n = 6 LPL rs13702-CC. Values are least-squares means ± SEMs. PROC MIXED (SAS Institute, Inc.) with repeated-measures procedure was used to assess the effect of gene–MUFA interactions on fat mass changes, using participants’ identification code as a repeated factor. P < 0.05 was considered significant. *Statistical significance in the response of a specific fat mass to different concentrations of dietary MUFAs within the same genotype. †Trend toward statistical significance (0.06 > P > 0.05) in the response of a specific fat mass to different concentrations of dietary MUFAs within the same genotype. ¥Statistically significant (P = 0.017) greater reduction in VAT mass following high-MUFA consumption in CC carriers compared with TT carriers of LPL rs13702. LPL, lipoprotein lipase gene; VAT, visceral adipose tissue.

FIGURE 2

ADIPOQ rs266729 genotypes determine the effect of high- compared with low-MUFA consumption on 6-wk changes in SCAT (A) and android fat mass (B) in adults with abdominal obesity. Changes were calculated by subtracting the baseline value of the selected fat mass from its corresponding 6-wk end-point value. Total participants = 101: n = 91 ADIPOQ rs266729-CC + CG and n = 10 ADIPOQ rs266729-GG. Values are least-squares means ± SEMs. PROC MIXED (SAS Institute, Inc.) with repeated-measures procedure was used to assess the effect of gene–MUFA interactions on fat mass changes, using participants’ identification code as a repeated factor. P < 0.05 was considered significant. *Statistical significance in the response of a specific fat mass to different concentrations of dietary MUFAs within the same genotype. ¥Statistical significance of the greater reduction in SCAT mass and android fat mass following low-MUFA consumption in C carriers (P = 0.012 and 0.022, respectively) compared with GG carriers of ADIPOQ rs266729. Recessive model (CC + CG compared with GG) was analyzed because the simple effect of heterozygous-by-MUFA showed a significant interaction on ≥1 compartmental fat masses. ADIPOQ, adiponectin gene; SCAT, subcutaneous adipose tissue.

FIGURE 3

APOE genotypes determine the effect of high- compared with low-MUFA consumption on 6-wk changes in total fat mass in adults with abdominal obesity. Changes were calculated by subtracting the baseline value of the total fat mass from its corresponding 6-wk end-point value. Total participants = 101: n = 35 non-E4 and n = 66 E4. Values are least-squares means ± SEMs. PROC MIXED (SAS Institute, Inc.) with repeated-measures procedure was used to assess the effect of gene–MUFA interactions on fat mass changes, using participants’ identification code as a repeated factor. P < 0.05 was considered significant. *Statistical significance in the response of a specific fat mass to different concentrations of dietary MUFAs within the same genotype. APOE, apoE gene.