Palmitic acid as a cardiometabolic risk factor

Abstract

Current dietary recommendations are based on a reduced saturated fatty acid (SFA) consumption to prevent cardiovascular disease (CVD). The role of individual SFA in metabolic disease is not fully understandable. One type of SFA present in many common foods (dairy, meat, palm and coconut oil) is palmitic acid (16:0). A number of epidemiological studies have shown that the populations who consume large amounts of atherogenic SFA (especially palmitic, myristic, lauric) have elevated levels of LDL and HDL-cholesterol. Saturated fatty acid exert their atherogenic and thrombogenic effect through increased production of LDL, very-low-density lipoproteins particles and apolipoproteins A1, with a decrease of LDL- receptors specific activity, and an increase in platelet aggregation. The total cholesterol/ HDL-cholesterol ratio, the best overall indication of potential effects on coronary heart disease (CHD) risk is nonsignificantly affected by consumption of palmitic acid (PA). Compared with lipid effects, the influence of SFA intake on inflammation markers is less well explored. The associations between circulating and tissue PA and dietary intake of PA are diverse and most likely reflecting endogenous metabolism. Status of PA is not in intake-response relationship biomarker, probably partly due to conversion of 16:0 to 16:1 by steaoryl-CoA-desaturase (SCD-1). Increased SFA intake has been associated with increased SCD-1 activity in which may predict mortality. Palmitoylation is the process involved in protein-membrane interactions and signal transduction. Increases in dietary intake of PA decrease fat oxidation and daily energy expenditure with slight increases in adiposity. Evidence for the effects of SFA, particularly PA consumption on insulin resistance, vascular function, type 2 diabetes, and stroke is various. It is considered that circulating PA, as nonesterifiedfatty acids stimulate insulin resistance by decreasing phosphorylation of the insulin receptor and insulin receptor substrate-1. In muscle cells, PA decrease oxidation of fatty acids and glucose which elevates fatty acid and glucose levels in tissues and blood, and decreases adiponectin production, which may both promote insulin resistance. It was shown that 16:0 and 14:0 stimulate β-cells and endothelial dysfunction. The incidence of type 2 diabetes was associated with total SFA levels of plasma cholesterol esters (also demonstrated for 16:0 levels independently) and phospholipids (also for 16:0 and 18:0). In skeletal muscle phospholipids, PA has been negatively associated with insulin sensitivity and diabetes type 2. Systematic reviews on prospective cohort studies indicated that CHD risk has not been directly associated with SFA intake, although is associated with a dietary habits, high in SFA-rich foods. Taken together, there is collective convincing evidence for decreased CHD risk when replacing SFA with polyunsaturated fats. Differences in cardiometabolic risk appear greater between food groups and overall dietary patterns rather than between separate SFA.