Fatty Acids Consumption: The Role Metabolic Aspects Involved in Obesity and Its Associated Disorders

Abstract

Obesity and its associated disorders, such as insulin resistance, dyslipidemia, metabolic inflammation, dysbiosis, and non-alcoholic hepatic steatosis, are involved in several molecular and inflammatory mechanisms that alter the metabolism. Food habit changes, such as the quality of fatty acids in the diet, are proposed to treat and prevent these disorders. Some studies demonstrated that saturated fatty acids (SFA) are considered detrimental for treating these disorders. A high fat diet rich in palmitic acid, a SFA, is associated with lower insulin sensitivity and it may also increase atherosclerosis parameters. On the other hand, a high intake of eicosapentaenoic (EPA) and docosahexaenoic (DHA) fatty acids may promote positive effects, especially on triglyceride levels and increased high-density lipoprotein (HDL) levels. Moreover, polyunsaturated fatty acids (PUFAs) and monounsaturated fatty acids (MUFAs) are effective at limiting the hepatic steatosis process through a series of biochemical events, such as reducing the markers of non-alcoholic hepatic steatosis, increasing the gene expression of lipid metabolism, decreasing lipogenic activity, and releasing adiponectin. This current review shows that the consumption of unsaturated fatty acids, MUFA, and PUFA, and especially EPA and DHA, which can be applied as food supplements, may promote effects on glucose and lipid metabolism, as well as on metabolic inflammation, gut microbiota, and hepatic metabolism.

Keywords: chronic diseases; fatty acids; obesity; obesity-related metabolic dysfunction.

Figure 1

Different metabolic changes involved after consumption of different types of fatty acids: saturated (SFA), monounsaturated (MUFA), and polyunsaturated (PUFA) fatty acids. Different types of fatty acids have different effects on the major metabolic organs of the body. Diets with high levels of SFA, especially high fat (HF), modulate the inflammatory process with the infiltration of macrophages and other immunological cells, promoting higher production of type M2 macrophages, considered pro-inflammatory, with a reduction in type M1 macrophages, which are anti-inflammatory, in addition to the expression of inflammatory cytokines and circulating endotoxins, which promote insulin resistance. This inflammatory process is related to the microbiota, which also has a greater expression of inflammatory endotoxins and cytokines, as well as transitions in intestinal colonization, with increase of strains of the genus Firmicutes, and decrease of Bacteroidetes and Lactobacillus genus after consumption of HF diets rich in SFA. On the other hand, the consumption of MUFA and PUFA has positive effects on glucose metabolism, with a reduction in some parameters related to type II diabetes mellitus (DM II), such as hemoglobin A1c (HbA1c) and glycaemia, and a reduction of hepatic steatosis and related parameters. Intake of PUFA is linked to increased expression of adiponectin, an anti-inflammatory cytokine, which promotes hepatic metabolic enhancement, and reduces the risk of atherosclerosis, such as increased high density lipoprotein (HDL) and decreased triacyclglycerols (TAG). LDL; very low density lipoprotein (VLDL); glucagon-like peptide-1 (GLP-1) receptor; peroxisome proliferator-activated receptor-γ (PPAR-γ); free fatty acids (FFA); sterol regulatory element-binding protein -1C (SREBP-1C); Non-alcoholic fatty liver disease (NAFLD); interleukin (IL); tumor necrosis factor (TNF); lipopolyssacharide (LPS); high fat (HF).