The role of dietary fatty acid intake in inflammatory gene expression: a critical review

Rocha, Daniela Mayumi; Bressan, Josefina; Hermsdorff, Helen Hermana

doi:10.1590/1516-3180.2016.008607072016

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Sao Paulo Medical Journal

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Review Article • Sao Paulo Med. J. 135 (02) • Mar-Apr 2017 • https://doi.org/10.1590/1516-3180.2016.008607072016 copy

The role of dietary fatty acid intake in inflammatory gene expression: a critical review

O papel da ingestão dos ácidos graxos da dieta na expressão de genes inflamatórios: uma revisão crítica

Authorship SCIMAGO INSTITUTIONS RANKINGS

ABSTRACT

CONTEXT AND OBJECTIVE:

Diet is an important modifiable factor involved in obesity-induced inflammation. We reviewed clinical trials that assessed the effect of consumption of different fatty acids on the expression of inflammation-related genes, such as cytokines, adipokines, chemokines and transcription factors.

DESIGN AND SETTING:

Narrative review study conducted at a research center.

METHODS:

This was a review on the effect of fat intake on inflammatory gene expression in humans.

RESULTS:

Consumption of saturated fatty acids (SFAs) was related to postprandial upregulation of genes associated with pro-inflammatory pathways in peripheral blood mononuclear cells (PBMCs), in comparison with monounsaturated fatty acid (MUFA) or polyunsaturated fatty acid (PUFA) intake. In addition, acute intake of a high-SFA meal also induced a postprandial pro-inflammatory response for several inflammatory genes in subcutaneous adipose tissue. Both high-MUFA and high-PUFA diets showed anti-inflammatory profiles, or at least a less pronounced pro-inflammatory response than did SFA consumption. However, the results concerning the best substitute for SFAs were divergent because of the large variability in doses of MUFA (20% to 72% of energy intake) and n3 PUFA (0.4 g to 23.7% of energy intake) used in interventions.

CONCLUSIONS:

The lipid profile of the diet can modulate the genes relating to postprandial and long-term inflammation in PBMCs and adipose tissue. Identifying the optimal fat profile for inflammatory control may be a promising approach for treating chronic diseases such as obesity.

KEY WORDS:
Dietary fats; Fatty acids; Gene expression; Inflammation; Dietary fats, unsaturated

Database	Search	Filters		Results
Cochrane Library	("gene expression" OR "RNA" OR "mRNA" OR "gene") AND (("saturated fatty acid" OR "saturated fatty acids" OR "SFA" OR "SFAs") OR ("monounsaturated fatty acid" OR "monounsaturated fatty acids" OR "MUFA" OR "MUFAs") OR ("polyunsaturated fatty acid" OR "polyunsaturated fatty acids" OR "PUFA" OR "PUFAs")) AND ("inflammation" OR "inflammatory" OR "proinflammatory")	Title, abstract, keywords in trials	48 articles	2 animal/in vitro studies 3 poster session abstracts 43 clinical trials
LILACS	("gene expression" OR "RNA" OR "mRNA" OR "gene") AND (("saturated fatty acid" OR "saturated fatty acids" OR "SFA" OR "SFAs") OR ("monounsaturated fatty acid" OR "monounsaturated fatty acids" OR "MUFA" OR "MUFAs") OR ("polyunsaturated fatty acid" OR "polyunsaturated fatty acids" OR "PUFA" OR "PUFAs")) AND ("inflammation" OR "inflammatory" OR "proinflammatory")	No filter	2 articles	2 reviews
PubMed	("gene expression" OR "RNA" OR "mRNA" OR "gene") AND (("saturated fatty acid" OR "saturated fatty acids" OR "SFA" OR "SFAs") OR ("monounsaturated fatty acid" OR "monounsaturated fatty acids" OR "MUFA" OR "MUFAs") OR ("polyunsaturated fatty acid" OR "polyunsaturated fatty acids" OR "PUFA" OR "PUFAs")) AND ("inflammation" OR "inflammatory" OR "proinflammatory")	Title/abstract in clinical trials on humans	44 articles	4 animal/in vitro studies 40 clinical trials

Year, authors	Subjects	Study design	Dietary intervention	Duration	Postprandial intervention	Inflammatory gene markers
2009, Bouwens et al.²⁹29. Bouwens M, van de Rest O, Dellschaft N, et al. Fish-oil supplementation induces antiinflammatory gene expression profiles in human blood mononuclear cells. Am J Clin Nutr. 2009;90(2):415-24.	n = 111 M/F: 66/45 Age: 66-80 years	Clinical trial, randomized, double-blind, controlled, parallel	3 groups (N/A E% from fat): - High n3 PUFA (EPA/DHA): 1.8 g/day - Control (sunflower oil): 4.0 g/day	26 weeks	-	RNA microarray analysis (encoding 17,699 genes) in PBMCs, measured in fasting period at baseline and after the intervention period.
2009, van Dijk et al.³³33. van Dijk SJ, Feskens EJ, Bos MB, et al. A saturated fatty acid-rich diet induces an obesity-linked proinflammatory gene expression profile in adipose tissue of subjects at risk of metabolic syndrome. Am J Clin Nutr. 2009;90(6):1656-64.	n = 20 M/F: 10/10 Mean age: 45-60 years	Clinical trial, parallel	2 groups (N/A E% from fat): - SFA: 19 E% - MUFA: 20 E%	8 weeks	-	RNA microarray analysis (encoding 17,699 genes) in SAT, measured in fasting period at baseline and after the intervention period.
2009, Jiménez-Gómez et al.²⁴24. Jiménez-Gómez Y, López-Miranda J, Blanco-Colio LM, et al. Olive oil and walnut breakfasts reduce the postprandial inflammatory response in mononuclear cells compared with a butter breakfast in healthy men. Atherosclerosis. 2009;204(2):e70-6.	n = 20 M/F: 20/0 Mean age: N/A	Clinical trial, randomized, crossover, postprandial	3 groups: High fat (38 E% from fat): - SFA: 22 E% - MUFA: 24 E% Low fat (< 30% E% from fat): - n3 PUFA (ALA): 2 E%	4 weeks	Breakfast (60 E% from fat): - SFA: 35 E% - MUFA: 36 E% - n3 PUFA (ALA): 4 E%	TNF-α, IL-6 and MCP-1 in PBMCs, measured in fasting period and 3, 6 and 9 h after the breakfast.
2011, Meneses et al.²⁵25. Meneses ME, Camargo A, Perez-Martinez P, et al. Postprandial inflammatory response in adipose tissue of patients with metabolic syndrome after the intake of different dietary models. Mol Nutr Food Res. 2011;55(12):1759-70.	n = 39 M/F: 14/25 Mean age: ~ 57 years	Clinical trial, randomized, controlled, parallel, postprandial	4 groups: High fat (38 E% from fat): - SFA: 16 E% - MUFA: 20 E% Low fat (28 E% from fat): - LFHCC n3: supplement with 1.24 g/day of n3 PUFA - LFHCC: 1.2 g/day supplement of control (sunflower oil)	12 weeks	Breakfast (65 E% from fat): - SFA: 38 E% - MUFA: 43 E% - LFHCC n3: supplement with 1.24 g of n3 PUFA - LFHCC: supplement with placebo capsules	p65, IκBα, IκBβ2, IL-6, MCP-1 and IL-1β in SAT, measured in fasting period and 4 h after the breakfast.
2011, Pietraszek et al.²³23. Pietraszek A, Gregersen S, Hermansen K. Acute effects of dietary fat on inflammatory markers and gene expression in first-degree relatives of type 2 diabetes patients. Rev Diabet Stud. 2011;8(4):477-89.	n = 34 M/F: 11/23 Mean age: ~ 50 years	Clinical trial, randomized, crossover, postprandial	Standard diet: 24 E% from fat	1 day	Breakfast (87 E% from fat): - SFA: 79 E%^§ - MUFA: 72 E%	ADIPOR1, ADIPOR2, MCP-1, IL-1β, IL-6, IL-6R, CD16A, LEP, LEPR, RBP4, TLR4, TNF-α AND TNFRSF1A in muscle and SAT, measured in fasting period and 3 h 30 min after the breakfast. Also, ADIPQ was determined in SAT.
2011, Rudkowska et al.³⁴34. Rudkowska I, Ponton A, Jacques H, et al. Effects of a supplementation of n-3 polyunsaturated fatty acids with or without fish gelatin on gene expression in peripheral blood mononuclear cells in obese, insulin-resistant subjects. J Nutrigenet Nutrigenomics. 2011;4(4):192-202.	n = 16 M/F: 7/9 Mean age: 57 years	Clinical trial, randomized, crossover	2 groups: - n3 PUFA: 1.8 g/day - n3 PUFA FP: 1.8 g/day + fish protein	8 weeks	-	RNA microarray analysis (encoding 37,804 genes) in PBMCs, measured at baseline and after the intervention period.
2012, Camargo et al.²⁶26. Camargo A, Delgado-Lista J, Garcia-Rios A, et al. Expression of proinflammatory, proatherogenic genes is reduced by the Mediterranean diet in elderly people. Br J Nutr. 2012;108(3):500-8.	n = 20 M/F: 10/10 Mean age: 67 years	Clinical trial, randomized, crossover, postprandial	3 groups: High fat (38 E% from fat): - SFA: 22 E% - MUFA: 24 E% Low fat (< 30% E% from fat): - n3 PUFA (ALA): 2 E%	4 weeks	Breakfast (60 E% from fat): - SFA: 35 E% - MUFA: 36 E% - n3 PUFA (ALA): 4 E%	p65, IκBα, MCP-1, MIF-1, MMP-9 and IL-6 in PBMCs, measured in fasting period and 1, 2 and 4 h after the breakfast.
2012, Cruz-Teno et al.²⁷27. Cruz-Teno C, Pérez-Martínez P, Delgado-Lista J, et al. Dietary fat modifies the postprandial inflammatory state in subjects with metabolic syndrome: the LIPGENE study. Mol Nutr Food Res. 2012;56(6):854-65.	n = 75 M/F: 28/47 Mean age: ~ 56 years	Clinical trial, randomized, controlled, parallel, postprandial	4 groups: High fat (38 E% from fat): - SFA: 16 E% - MUFA: 20 E% Low fat (28 E% from fat): - LFHCC n3: supplement with 1.24 g/day of n3 PUFA - LFHCC: 1.0 g/day supplement of control (sunflower oil)	12 weeks	Breakfast (65 E% from fat): - SFA: 38 E% - MUFA: 43 E% - LFHCC n3: supplement with 1.24 g of n3 PUFA - LFHCC: supplement with placebo capsules	TNF-α, IL-6, IκB-α, p65, MCP-1, MIF, MMP-9 in PBMCs, measured in fasting period and 2 and 4 h after the breakfast.
2012, van Dijk et al.³⁰30. van Dijk SJ, Feskens EJ, Bos MB, et al. Consumption of a high monounsaturated fat diet reduces oxidative phosphorylation gene expression in peripheral blood mononuclear cells of abdominally overweight men and women. J Nutr. 2012;142(7):1219-25.	n = 49 M/F: 22/27 Mean age: ~ 55 years	Clinical trial, parallel	3 groups (37-40 E% from fat): - SFA: 19 E% - MUFA: 20% E% - MED^*: 21 E% from MUFA	8 weeks	-	RNA microarray analysis (encoding 17,699 genes) in PBMCs, measured in fasting period at baseline and after the intervention period.
2012, van Dijk et al.²²22. van Dijk SJ, Mensink M, Esser D, et al. Responses to high-fat challenges varying in fat type in subjects with different metabolic risk phenotypes: a randomized trial. PLoS One. 2012;7(7):e41388.	n = 42 M/F: 42/0 Age: 50-70 years	Clinical trial, randomized, double-blind, crossover, postprandial	Low-fat meal: N/A	1 day	Shake (87 E% from fat): - SFA: 46.5 E% - MUFA: 72 E% - n3 PUFA (EPA/DHA): 23.7 E%	IL-1β, IL-8, MCP-1, NFkB1 and TNF-α in PBMCs, measured in fasting period and 2 and 4 h after the breakfast.
2012, Schmidt et al.³⁶36. Schmidt S, Stahl F, Mutz KO, et al. Different gene expression profiles in normo- and dyslipidemic men after fish oil supplementation: results from a randomized controlled trial. Lipids Health Dis. 2012;11:105.	n = 40 M/F: 40/0 Mean age: ~ 40 years	Clinical trial, randomized, double-blind, controlled, parallel, postprandial	2 groups: - n3 PUFA (EPA/DHA): 2.7 g/day - Control (n6 PUFA): 3.05 g/day (LA)	12 weeks	Consumption of capsules of the dietary intervention.	RNA microarray analyses from whole blood at baseline, after 1 and 12 weeks of supplementation (long-term effect). Also 4 h after intake of capsules (postprandial response).
2012, Itariu et al.³¹31. Itariu BK, Zeyda M, Hochbrugger EE, et al. Long-chain n-3 PUFAs reduce adipose tissue and systemic inflammation in severely obese nondiabetic patients: a randomized controlled trial. Am J Clin Nutr. 2012;96(5):1137-49.	n = 55 M/F: 46/9 Mean age: ~ 38 years	Clinical trial, randomized, controlled, parallel	2 groups (30 E% from fat): - n3 PUFA (EPA/DHA): 3.36 g/day - Control (butter): 5 g/day	8 weeks	-	MCP-1, MIP-1α, IL-6, ADIPOQ, HIF1A and TGF-β1, CD68, CD163, MRC1 and CD40 in SAT and VAT, after the intervention period.
2013, Kratz et al.³²32. Kratz M, Kuzma JN, Hagman DK, et al. n3 PUFAs do not affect adipose tissue inflammation in overweight to moderately obese men and women. J Nutr. 2013;143(8):1340-7.	n = 24 M/F: 8/16 Mean age: ~ 39 years	Clinical trial, randomized, single-blind, controlled, parallel	2 groups (~34 E% from fat): - n3 PUFA: 3.5 E% - Control: 0.5 E% from n3 PUFA	14 weeks	-	TNF-α, IL-6, ICAM-1, CD14, CD206, CD284, MCP-1 and SAA1 in SAT, collected at baseline and after the intervention period.
2013, Labonté et al.³⁵35. Labonté MÈ, Couture P, Tremblay AJ, et al. Eicosapentaenoic and docosahexaenoic acid supplementation and inflammatory gene expression in the duodenum of obese patients with type 2 diabetes. Nutr J. 2013;12(1):98.	n = 12 M/F: 12/0 Mean age: 54 years	Clinical trial, randomized, double-blind, controlled, crossover	2 groups: - n3 PUFA (EPA/DHA): 3.0 g/day - Control: blend of corn and soybean oil	8 weeks	-	IL-6, IL-18, TNF-α in duodenal samples, collected in fasting period at the end of each intervention.

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[1] Address for correspondence: Helen Hermana Miranda Hermsdorff Departamento de Nutrição e Saúde, Universidade Federal de Viçosa (UFV) Av. P. H. Rolfs, s/n^o Campus Universitário - Viçosa (MG) - Brasil CEP 36570-900 Tel. (+55 31) 3899-1269 Fax: (+55 31) 3899-2541 E-mail: helenhermana@ufv.br