Laurine Fatty Acids, Medium Fatty Acids and Triglycerides, Hyperlipidemia, Resistance to Insulin, Prevention of Atherosclerosis and Ateromatosis

Abstract

Although the biochemistry of the positive effects of medium-chain fatty acids (FA) and triglycerides (TG) of the same name in vivo is not fully understood, food enriched with medium-chain LC and the same TG is effective in patients with type I diabetes, insulin resistance syndrome and in neurodegenerative pathology. Lauric C12 LC is half the FA in coconut oil. Residents of southeast Asia with constant use of coconut oil, have a low level of diseases of the cardiovascular system in the population. With a regulatory intake with food C12:0 laurin FA formed moderate ketosis and neuroprotective effect. Unlike long-chain LC, medium-chain TG cells are not deposited either in visceral fat cells, or in insulin-dependent adipocytes. Medium-chain fatty acids rapidly oxidize mitochondria; the formation of acetyl-CoA cells is used to form ketone bodies, activating thermogenesis in orange and brown adipocytes. Experiments with animals and observations in the clinic showed that taking medium-chain TG with food is more physiological than long-chain oils. This significantly increases the level of cholesterol in high-density lipoproteins. Food enriched with medium chain TG is optimal for increasing the ketone content in blood plasma, cerebrospinal fluid without limiting the carbohydrate content in food. The formation of excess ketone bodies by cells can be achieved by activating the metabolic transformations of medium-chain FAs, without fasting and preserving carbohydrates in food. Coconut oil has a positive effect on the cardiovascular system, preventing the formation of atherosclerosis and atheromatosis. Effective in the prevention of the pathology of the cardiovascular system is a decrease in food amounts of palmitic acid, an increase in oleic acid, polyene FA with a simultaneous increase in the proportion of medium-chain FA.

Multi-Omics Approach Reveals miR-SNPs Affecting Muscle Fatty Acids Profile in Nelore Cattle

“…Additionally, C12:0 is the most potent antimicrobial saturated FA [65,66]. Food enriched with medium-chain FA can increase the ketone content, positively impacting the ratio between total and high-density lipoprotein cholesterol [67,68]. Hwang and Joo [69] have shown that high-fat and highmarbled muscles, such as LT, have a higher proportion of C12:0 that is positively correlated with sensorial traits.…”

Effect of dietary fats on endogenous oleic acid biosynthesis in rat liver

“…The active form of oleic acid (oleyl-CoA) acylates various alcohol acceptors: monoglycerides, diglycerides, glycerophosphate, cholesterol [9], forming triglycerides in the greatest amount. From triglycerides in the liver, very low density lipoproteins (VLDL) are formed, which are increted by the liver into the blood and carried throughout the body, providing energy material to many organs and tissues, especially muscle tissue.…”

Clinical Significance of Retinol Binding Protein-4 (Rbp-4) in Patients With Type 2 Diabetes Mellitus and Non-Alcoholic Fatty Liver Disease

“…Функциональная недостаточность инсулиновых рецепторов приводит к развитию инсулинорезистентных форм сахарного диабета, к снижению числа рецепторов к инсулину и обусловлена, главным образом, ожирением и эндотоксин-опосредованным хроническим субклинически протекающим воспалением. Именно абдоминальный тип ожирения определяет степень ИР [13][14][15][16].…”

“…Наиболее выраженная патогенетическая связь определяется у больных, имеющих НАЖБП на фоне СД 2-го типа [20,22]. НАЖБП в 95% случаев протекает на фоне ожирения и СД 2-го типа или нарушения толерантности к глюкозе (НТГ), артериальной гипертензии и сердечной недостаточности [13,14,16,17,21,[30][31][32].…”

“…Значения липокалина 2 (LCN2) были выше у пациентов с сердечно-сосудистыми заболеваниями, чем у других участников исследования, но эта разница не достигла статистической значимости (p=0,46). LCN2 представляет собой 25 кДа гликопротеин, который выделяется обильно жировыми тканями и, следовательно, повышен в условиях ожирения и СД 2-го типа [16,26]. Клинические исследования демонстрируют его провоспалительные свойства и причинное участие в связанных с ожирением метаболических аномалиях, в том числе и НАЖБП [8,16,26,28].…”