Abstract
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. Narrative review study conducted at a research center. This was a review on the effect of fat intake on inflammatory gene expression in humans. 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. 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.
Highlights
Inflammation is a physiological response triggered by infection and injury that has the purposes of eliminating irritating agents and accelerating tissue regeneration.[1,2] In this process, several inflammatory mediators are released, including cell adhesion molecules, cytokines, chemokines and other inflammatory agents.[3]
We identified 14 studies that investigated the effect of fatty acid intake on inflammatory gene expression (Table 2)
In order to assist comparisons between the studies, dietary interventions were compared according to fat content source (SFA, monounsaturated fatty acid (MUFA) or polyunsaturated fatty acid (PUFA)) and its respective proportion of total energy intake (E%)
Summary
Inflammation is a physiological response triggered by infection and injury that has the purposes of eliminating irritating agents and accelerating tissue regeneration.[1,2] In this process, several inflammatory mediators are released, including cell adhesion molecules, cytokines, chemokines and other inflammatory agents (e.g. nitrogen and reactive oxygen species).[3] In order to maintain the homeostatic balance, a controlled inflammatory response is required. Excessive or inappropriate inflammation leads to a pathological inflammatory status.[1] Increasingly, there is evidence to suggest that a deregulated inflammatory response plays a pivotal role in the onset and progression of atherosclerosis.[4]. Excessive adiposity and adiposity-related metabolic diseases (metabolic syndrome, diabetes and atherosclerosis) are attributed to a chronic state of low-grade inflammation. Diet-induced weight loss is an important factor for reducing pro-inflammatory markers.[5,6,7] besides lipid storage, fat cells are capable of producing and secreting chemoattractants such as monocyte chemotactic protein-1 (MCP-1) and pro-inflammatory mediators such as interleukins (IL), for instance IL-1β, IL-6 and tumor necrosis factor (TNF)-α, during adipose tissue expansion, thereby resulting in inflammatory and metabolic deregulation.[8]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
