Difference between revisions of "Saturated fatty acids"
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Revision as of 19:53, 30 November 2019
Saturated fatty acids
Saturated fatty acids are fats that contain no double bonds between the carbon atoms, so it is saturated with hydrogen. Consumption of a Western diet rich in saturated fats is associated with obesity and insulin resistance. In some insulin-resistant phenotypes, this is associated with accumulation of skeletal muscle fatty acids. Direct examination in muscle cells in vitro indicates that saturated fatty acids cause insulin resistance whereas unsaturated fatty acids exert a protective effect or even improve insulin sensitivity. Saturated fats are less readily oxidized and accumulate as DAG and ceramide in vitro, whereas mono- and polyunsaturated fats accumulate as IMTG or free fatty acids (FFA), thus providing a link between fatty acid subtype and insulin resistance.
In cell culture when telomeres are shortened past a key length or state, the Arf/Ink gene system (p16/p14 humans, p16/p19 mice) switches on and activates p53, which suppresses further cell division. The p53 gene is a key tumor suppressor and its deletion or mutation allows cancerous growth. The switching on of p53 also causes changes in fatty acid metabolism, especially down-regulation of both fatty acid synthase and stearoyl-CoA (delta-9) desaturase. The co-suppression of these genes together with enhanced uptake of extracellular fatty acids, leads to raised levels of cellular palmitate and induction of either apoptosis or senescence. In senescent cells, the fatty acid composition of the cellular membranes alters and leads to changes in both structure and function of organelles, especially mitochondria.
Lipids, and especially omega-3 fatty acids, provided the first coherent experimental demonstration of the effect of diet (nutrients) on the structure and function of the brain. In fact the brain, after adipose tissue, is the organ richest in lipids, whose only role is to participate in membrane structure. Increased levels of low density lipoprotein (LDL) and cholesterol-enriched very low density lipoprotein (VLDL) have been shown to increase atherosclerosis susceptibility and lead to clinical sequelae such as coronary heart disease and stroke, the major causes of morbidity and mortality in much of the world today (1). In humans it has been shown that dietary cholesterol and saturated fatty acids (SFA) increase the levels of these atherogenic lipoproteins, and current recommendations include decreasing their intake as part of a heart-healthy diet.