The Relationship between Dietary Fatty Acids and Inflammatory Genes on the Obese Phenotype and Serum Lipids
Abstract
:1. Introduction
2. Relationship between Inflammation, Obesity and Lipid Metabolism
3. Dietary Fatty Acids and Inflammation
4. Tumor Necrosis Factor-α
4.1. TNFα and Dietary Fatty Acids
4.2. TNFA Gene Variants, Obesity and Serum Lipids
Study type | Dietary fatty acid | Effect on gene expression | Effect on plasma levels | Reference | |
---|---|---|---|---|---|
TNFα | |||||
3T3-L1 adipocytes. Incubation at 24 and 48 h with 50 or 500 μM fatty acid | Cell culture | SFA (PA) | Increase | Increase | [62] |
MUFA (OA) | No effect | No effect | |||
Human macrophages treated with n-3 PUFA | Cell culture | EPA & DHA | Decrease | Decrease | [77] |
Male Wistar rats, high fat diet, 1 g/kg per day EPA, 5 weeks | Rodent | n-3 PUFA (EPA) | Prevent over expression | Not examined | [64] |
NZB/NZW F1 Lupus-prone female mice, 10% fat, fed ad lib for lifespan | Rodent | n-3 PUFA | Decrease | Not examined | [63] |
Caucasians. Supplemented normal diet with 18 g fish oil daily for 6 weeks | Human intervention (9) | n-3 PUFA | Decrease | [66] | |
Caucasians. Supplemented normal diet with 6 g fish oil daily for 12 weeks | Human intervention (111) | n-3 PUFA | Decrease in subjects with lower levels of TNFα before supplementation | [67] | |
Caucasians. Supplemented normal diet with flaxseed oil, and flaxseed oil and butter spread for 8 weeks. At week 4, diets were supplemented with fish oil, (1.62 g EPA, 1.08 g DHA)/day | Human intervention (28) | n-3 PUFA (EPA & DHA) | Decrease | [65] | |
IL-6 | |||||
3T3-L1 adipocytes. Incubation at 24 h with 250 μM fatty acid | Cell culture | SFA (PA) | Increase | Increase | [31] |
SFA (DA) | No effect | No effect | |||
n-3 PUFA (DHA) | No effect | No effect | |||
Human macrophages treated with n-3 PUFA | Cell culture | EPA & DHA | Decrease | Decrease | [77] |
Male c57bl/10sCn mice fed ad lib either high fat control diet (soybean oil) or a high PA diet for 16 weeks | Rodent | SFA (PA) | Increase | Not examined | [78] |
Male Sprague-Dawley rats fed ad lib one of 3 diets: SFA, MUFA, or PUFA for 4 weeks | Rodent | SFA (coconut oil) | Not examined | Increase IL-6 release from adipocytes | [79] |
MUFA (olive oil) | Not examined | Decrease IL-6 release from adipocytes | |||
PUFA (sunflower oil) | Not examined | Moderate IL-6 release from adipocytes | |||
Abdominally overweight Caucasians. Fed either SFA-rich diet (19% SFA and 11% MUFA) or MUFA-rich diet (20% MUFA and 11% SFA) for 8 weeks | Human intervention (20) | SFA | Increase IL-6 gene expression | [80] | |
MUFA | Decrease IL-6 gene expression | ||||
African Americans, Caucasians, Chinese and Hispanics men and women. Relationship between dietary intake (food frequency questionnaire) and biomarkers of inflammation and endothelial activation | Human (5677) | n-3 PUFA | Decrease in IL-6 levels | [81] | |
Relationship between plasma fatty acids and inflammatory marker levels | Human (1123) | n-3 PUFA (DHA) | Low plasma levels of DHA associated with increased IL-6 levels | [82] | |
n-6 PUFA (AA) | Low plasma levels of AA associated with increased IL-6 levels |
SNP | Study cohort | Genotype frequency | Result | Reference |
---|---|---|---|---|
TNFA | ||||
Obesity | ||||
TNFA –308 G > A | Caucasian N-W (154) and obese (154) | N-W, GG: 75.8%; GA + AA: 24.2% Obese, GG: 70.8%; GA + AA: 29.2% |
| [71] |
Caucasian women (378) | GG: 72.2%; GA + AA: 27.7% |
| [70] | |
Caucasian BMI < 27.3 (44), BMI 27.3–31.9 (44), BMI 31.9–36.5 (44) and BMI > 36.5 (44) | BMI < 27.3, GG: 75%; GA + AA: 25% BMI 27.3–31.9, GG: 68.2%; GA + AA: 31.8% BMI 31.9–36.5, GG: 77%; GA + AA: 33% BMI > 36.5, GG: 47.7%; GA + AA: 52.3% |
| [68] | |
Caucasian (1392) | GG: 67.6%; GA + AA: 32.3% |
| [69] | |
Caucasian normal wt. (79) and obese (115) | N-W, GG: 73.4%; GA + AA: 24.2% Obese, GG: 75.6%; GA + AA: 26% |
| [83] | |
Korean normal wt. (82) and obese (153) | N-W, GG: 82.9%; GA + AA: 17% Obese, GG: 84.3%; GA + AA: 15.7% |
| [84] | |
Caucasian normotensive (113) and hypertensive (62) | Normotensive, GG: 84.8%; GA + AA: 15% Hypertensive, GG: 67.7%; GA + AA: 32.3% |
| [74] | |
Caucasian normal weight (64) and overweight (65) | Not shown |
| [72] | |
Caucasian men (262) | GG: 56.4%; GA + AA: 43.5% |
| [73] | |
Meta-analysis (48 eligible studies) |
| [21] | ||
TNFA –238 G > A | N-W (107) and obese (120) black, and N-W (89) and obese (62) white SA women | Black, GG: 60%; GA: 40%; AA: 0%; A allele: 20% White, GG: 78.5%; GA: 21%; AA: 0.5%; A allele: 11% |
| [5] |
TNFA –308 G > A & –238 G > A | Iranian men and women (BMI < 25, 25 ≤ BMI < 30, BMI ≥ 30) (239) | Under 18 years, BMI < 85%, GG: 80.8%; GA: 19.2% BMI > 85%, GG: 81.2%; GA: 12.5%; AA: 6.2%. Above 18 years, BMI < 25, GG: 89.3%; GA: 10.7% 25 ≤ BMI < 30, GG: 87.7%; GA: 12.3% BMI ≥ 30, GG: 80.4%; 15.2%; 4.3% |
| [85] |
Caucasian and African-American non-diabetics (424) | –308 G > A BMI < 25, GG: 73.2%; GA: 22.5%, AA: 4.3% BMI 25–29.9, GG: 66.7%; GA: 27%, AA: 6.3% BMI 30–40, GG: 67.2%; GA: 30.2%; AA: 2.6% BMI > 40, GG: 73.4%; GA: 24.3%; AA: 2.4% –238 G > A BMI < 25, GG: 90.4%; GA: 9.1%, AA: 0.5% BMI 25–29.9, GG: 90.5%; GA: 7.9%, AA: 1.6% BMI 30–40, GG: 85.9%; GA: 14.1% BMI > 40, GG: 91.1%; GA: 8.9% |
| [86] | |
Serum lipids | ||||
TNFA –308 G > A | Caucasian obese women (136) and obese men (34) | Obese women, GG: 57.3%; GA + AA: 42.6% Obese men, GG: 64.7%; GA + AA: 35.3% |
| [75] |
Caucasian obese men (38) and obese women (83) | Obese men, GG: 50%; GA + AA: 50% Obese women, GG: 54.2%; GA + AA: 45.7% |
| [76] | |
IL-6 | ||||
Obesity | ||||
IL-6 –174 G > C | Finnish men and women (1334) | GG: 19.3%; GC: 51.3%; CC: 29.3% | In men BMI was higher in the –174 CC genotype compared to GC and GG | [87] |
Meta-analysis (48 eligible studies) |
| [21] | ||
Meta-analysis Caucasians, diabetic and non-diabetic (25635) |
| [88] | ||
IL-6 –174 G > C & IVS3 +281 G > T and IVS4 +869 A > G | Health men (980) and women (2255) and Meta-analysis (26944) |
| [89] | |
IL-6 –174 G > C IVS3 +281 G > T & IVS4 +869 A > G | N-W (108) and obese (124) black, and N-W (89) and obese (63) white SA women | -174 G > C N-W black: GG: 97%; GC: 3% Obese black: GG: 95%; GC: 3%; CC: 2% N-W white: GG: 30%; GC: 58%; CC: 11% Obese white: GG: 32%; GC: 46%; CC: 22% IVS3 +281 G > T N-W black: GG: 54%; GT: 38%; TT: 8% Obese black: GG: 55%; GT: 37%; TT:9% N-W white: GG: 35%; GT: 48%; TT: 17% Obese white: GG: 30%; GT: 51%; TT: 19% IVS4 +869 A > G N-W black: AA: 51%; AG: 39%; GG: 10% Obese black: AA: 54%; AG: 40%; GG: 6% N-W white: AA: 42%; AG: 57%; GG: 1% Obese white: AA: 37%; AG: 63% |
| [90] |
Serum lipids | ||||
IL-6 –174 G > C | Caucasian men (245) and women (252) | Women, GG: 28%; GC: 47%; CC: 24% Men, GG: 30%; GC: 46%; CC: 24% |
| [91] |
Finnish men and women (1334) | GG: 19.3%; GC: 51.3%; CC: 29.3% |
| [87] | |
Spanish Caucasian men (15) and women (17) | GG: 25%; GC: 40.6%; CC: 34.4% |
| [92] | |
Finnish men and women (2228) | GG: 20.8%; GC: 50.4%; CC: 28.8% |
| [93] | |
IL-6 -174 G > C, IVS3 +281 G > T & IVS4 +869 A > G | N-W (108) and obese (124) black, and N-W (89) and obese (63) white SA women | –174 G > C N-W black: GG: 97%; GC: 3% Obese black: GG: 95%; GC: 3%; CC: 2% N-W white: GG: 30%; GC: 58%; CC: 11% Obese white: GG: 32%; GC: 46%; CC: 22% IVS3 +281 G > T N-W black: GG: 54%; GT: 38%; TT: 8% Obese black: GG: 55%; GT: 37%; TT:9% N-W white: GG: 35%; GT: 48%; TT: 17% Obese white: GG: 30%; GT: 51%; TT: 19% IVS4 +869 A > G N-W black: AA: 51%; AG: 39%; GG: 10% Obese black: AA: 54%; AG: 40%; GG: 6% N-W white: AA: 42%; AG: 57%; GG: 1% Obese white: AA: 37%; AG: 63% |
| [90] |
4.3. TNFA Gene and Diet Interactions on Obesity and Serum Lipids
SNP | Study cohort | Genotype frequency | Diet assessment and fats | Diet-gene association | Reference |
---|---|---|---|---|---|
TNFA | |||||
Obesity | |||||
TNFA –308 G > A | Caucasian N-W (154) and obese (154) | Normal weight, GG: 75.8%; GA + AA: 24.2% Obese, GG: 70.8%; GA + AA: 29.2% | Food frequency questionnaire measured energy and dietary fatty acid intake. |
| [71] |
Black South African N-W (105) and obese (118) | Black, GG: 69%; GA: 28%; AA: 3%; A allele: 17% | Food frequency questionnaire measured dietary fatty acid intake. |
| [3] | |
TNFA –238 G > A | N-W (107) and obese (120) black, and N-W (89) and obese (62) white SA women | Black, GG: 60%; GA: 40%. A allele: 20% White, GG: 78.5%; GA: 21%; AA: 0.5%; A allele: 11% | Food frequency questionnaire measured dietary fatty acid intake. | In black women:
| [5] |
Serum lipids | |||||
TNFA –308 G > A | Black South African N-W (105) and obese (118) | Black, GG: 69%; GA: 28%; AA: 3%; A allele: 17% | Food frequency questionnaire measured dietary fatty acid intake. |
| [3] |
Caucasian South African N-W (88) and obese (60) white SA women | White, GG: 56%; GA: 42%; AA: 2%; A allele: 23% | Food frequency questionnaire measured dietary fatty acid intake. |
| [4] | |
TNFA –238 G > A | N-W (107) and obese (120) black, and N-W (89) and obese (62) white SA women | Black, GG: 60%; GA: 40%. A allele: 20% White, GG: 78.5%; GA: 21%; AA: 0.5%; A allele: 11% | Food frequency questionnaire measured dietary fatty acid intake. |
| [5] |
TNFA –308 G > A & –238 G > A | Ethnoracially diverse Canadian diabetic men (53) and women (56) | –308 G > A GG: 63.3%; GA: 32%; AA: 0.05% –238 G > A GG: 75.2%; GA: 21.1%; AA: 0.04% | Three-day food record measured dietary fat intake. |
| [94] |
TNFA –308 G > A & –238 G > A | Ethnoracially diverse Canadian healthy men (202) and women (393) | –308 G > A, 11% for A allele –238 G > A, 5% for A allele | Food frequency questionnaire measured dietary intake. |
| [95] |
IL-6 | |||||
Obesity | |||||
IL-6 –174 G > C | Obese Caucasians men (181) and women (541) | GG: 28.8%; GC: 50.2%, CC: 18%. | Test meal consisted of 95%E from fat, of which 60% SFA. |
| [96] |
737 Spanish men and women | GG: 37.6%; GC: 46.8%; CC: 15.6% | Three years diet intervention assigned to low-fat diet; Mediterranean diet supplemented with virgin olive oil or with nuts. |
| [97] | |
IL-6 –174 G > C, IVS3 +281 G > T & IVS4 +869 G > A | N-W (107) and obese (120) black, and N-W (89) and obese (62) white SA women | –174 G > C N-W black: GG: 97%; GC: 3% Obese black: GG: 95%; GC: 3%; CC: 2% N-W white: GG: 30%; GC: 58%; CC: 11% Obese white: GG: 32%; GC: 46%; CC: 22% IVS3 +281 G > T N-W black: GG: 54%; GT: 38%; TT: 8% Obese black: GG: 55%; GT: 37%; TT:9% N-W white: GG: 35%; GT: 48%; TT: 17% Obese white: GG: 30%; GT: 51%; TT: 19% IVS4 +869 A > G N-W black: AA: 51%; AG: 39%; GG: 10% Obese black: AA: 54%; AG: 40%; GG: 6% N-W white: AA: 42%; AG: 57%; GG: 1% Obese white: AA: 37%; AG: 63% | Food frequency questionnaire measured dietary fatty acid intake. |
| [98] |
Serum lipids | |||||
IL-6 –174 G > C | Spanish Caucasian men and women (32) | GG: 25%; GC: 40.6%; CC: 34.4% | Measured fasting and post-glucose load plasma lipids. |
| [92] |
IL-6 –174 G > C, IVS3 +281 G > T & IVS4 +869 G > A | N-W (107) and obese (120) black, and N-W (89) and obese (62) white SA women | –174 G > C N-W black: GG: 97%; GC: 3% Obese black: GG: 95%; GC: 3%; CC: 2% N-W white: GG: 30%; GC: 58%; CC: 11% Obese white: GG: 32%; GC: 46%; CC: 22% IVS3 +281 G > T N-W black: GG: 54%; GT: 38%; TT: 8% Obese black: GG: 55%; GT: 37%; TT:9% N-W white: GG: 35%; GT: 48%; TT: 17% Obese white: GG: 30%; GT: 51%; TT: 19% IVS4 +869 A > G N-W black: AA: 51%; AG: 39%; GG: 10% Obese black: AA: 54%; AG: 40%; GG: 6% N-W white: AA: 42%; AG: 57%; GG: 1% Obese white: AA: 37%; AG: 63% | Food frequency questionnaire measured dietary fatty acid intake. |
| [98] |
5. Interleukin-6
5.1. IL-6 and Dietary Fatty Acids
5.2. IL-6 Gene Variants, Obesity and Serum Lipids
5.3. IL-6 Gene and Diet Interactions on Obesity and Serum Lipids
6. The Role of Ethnicity and Gender as Confounders
Ensemble 1000 Genomes: phase 1 | ||||
---|---|---|---|---|
EUR | GBR | AFR | ASW | |
TNFA –308 G > A rs1800629 | ||||
GG | 0.75 | 0.80 | 0.81 | 0.87 |
GA | 0.24 | 0.17 | 0.18 | 0.13 |
AA | 0.02 | 0.03 | 0.00 | 0.00 |
A allele | 0.14 | 0.12 | 0.10 | 0.10 |
TNFA –238 G > A rs361525 | ||||
GG | 0.87 | 0.81 | 0.93 | 0.90 |
GA | 0.13 | 0.19 | 0.07 | 0.10 |
AA | 0.00 | 0.00 | 0.00 | 0.00 |
A allele | 0.07 | 0.10 | 0.03 | 0.05 |
IL-6 –174 G > C rs1800795 | ||||
GG | 0.36 | 0.39 | 0.95 | 0.78 |
GC | 0.44 | 0.42 | 0.05 | 0.21 |
CC | 0.20 | 0.19 | 0.0 | 0.0 |
C allele | 0.41 | 0.40 | 0.02 | 0.11 |
IL-6 IVS3 +281 G > T rs1554606 | ||||
GG | 0.34 | 0.36 | 0.48 | 0.39 |
GT | 0.45 | 0.44 | 0.46 | 0.57 |
TT | 0.20 | 0.19 | 0.05 | 0.03 |
T allele | 0.43 | 0.41 | 0.28 | 0.32 |
IL-6 IVS4 +869 A > G rs2069845 | ||||
AA | 0.34 | 0.36 | 0.46 | 0.37 |
GA | 0.45 | 0.44 | 0.47 | 0.57 |
GG | 0.20 | 0.19 | 0.05 | 0.04 |
G allele | 0.43 | 0.41 | 0.29 | 0.33 |
7. Conclusions
Conflict of Interest
References
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Joffe, Y.T.; Collins, M.; Goedecke, J.H. The Relationship between Dietary Fatty Acids and Inflammatory Genes on the Obese Phenotype and Serum Lipids. Nutrients 2013, 5, 1672-1705. https://doi.org/10.3390/nu5051672
Joffe YT, Collins M, Goedecke JH. The Relationship between Dietary Fatty Acids and Inflammatory Genes on the Obese Phenotype and Serum Lipids. Nutrients. 2013; 5(5):1672-1705. https://doi.org/10.3390/nu5051672
Chicago/Turabian StyleJoffe, Yael T., Malcolm Collins, and Julia H. Goedecke. 2013. "The Relationship between Dietary Fatty Acids and Inflammatory Genes on the Obese Phenotype and Serum Lipids" Nutrients 5, no. 5: 1672-1705. https://doi.org/10.3390/nu5051672
APA StyleJoffe, Y. T., Collins, M., & Goedecke, J. H. (2013). The Relationship between Dietary Fatty Acids and Inflammatory Genes on the Obese Phenotype and Serum Lipids. Nutrients, 5(5), 1672-1705. https://doi.org/10.3390/nu5051672