Titov V N, Krylin V V, Shiriaeva Iu K
Klin Lab Diagn. 2011 Feb(2):4-15.
Unity of the pathogenesis of atherosclerosis, type 2 diabetes mellitus, and metabolic syndrome gives rise to impaired biological function of adaptation, altered biological function of exotrophy (external feeding) and endoecology ("purity" of the intercellular medium). Biological reactions of inflammation and hydrodynamic pressure, or blood pressure, are in vivo activated to compensate for intercellular debris accumulation by endogenous phlogogens--ligand-free low density lipoproteins (LDL). The biological reactions jointly remove LDL from blood to the intima of elastic type arteries, to interstitial tissue for the local pool of the intravascular medium. The causes of formation of aphysiological LDLs are a preponderance of palmitate-oleate-palmitate triglycerides in the latter and impaired hydrolysis upon exposure to post-heparin lipase to give rise to small, dense LDLs; intimal macrophages utilize the debris only partially and develop atheromatosis from polyenic fatty acids (FA) etherified by cholesterol alcohol. Excess of palmitic saturated fatty acid (sFA) is responsible for the lowered permeability of the plasma membrane, cell death via the mechanism similar to apoptosis. Aphysiological protein palmitoylation (covalent interaction with palmitic sFA) increased the debris accumulation of the intercellular medium and the activity of both biological reactions. Elevated plasma palmitic sFA and its enhanced passive absorption in the form of unetherified FA, as well as high C-reactive protein levels are a cause of insulin resistance. The only way to prevent atherosclerosis in the population is to normalize the biological function of exotrophy when the energy value ratio of FA, proteins and carbohydrates is 1:1:1 and that of sFA, monoenic, and polyenic FA is also 1:1:1. The lower amount of palmitic sFA and the higher concentration of essential polyenic FA, the lower blood levels of cholesterol alcohol and triglycerides are. At the same time, simultaneously activations and the biological function of locomotion are a level of physical activity.
动脉粥样硬化、2型糖尿病和代谢综合征发病机制的统一性导致适应的生物学功能受损、外营养（外部进食）生物学功能改变以及内环境生态（细胞间介质的“纯净度”）改变。炎症和流体动力压力（即血压）的生物学反应在体内被激活，以内源致炎物质——无配体低密度脂蛋白（LDL）来补偿细胞间碎片的积累。这些生物学反应共同将LDL从血液中清除至弹性型动脉内膜，再到血管内介质局部池的间质组织。非生理性LDL形成的原因在于其中棕榈酸 - 油酸 - 棕榈酸甘油三酯占优势，且暴露于肝素后脂肪酶时水解受损，从而产生小而致密的LDL；内膜巨噬细胞仅部分利用这些碎片，并由胆固醇醇醚化的多烯脂肪酸（FA）引发动脉粥样化。棕榈饱和脂肪酸（sFA）过量导致质膜通透性降低，通过类似于细胞凋亡的机制导致细胞死亡。非生理性蛋白质棕榈酰化（与棕榈sFA的共价相互作用）增加了细胞间介质的碎片积累以及两种生物学反应的活性。血浆棕榈sFA升高及其以未醚化FA形式增强的被动吸收，以及高C反应蛋白水平是胰岛素抵抗的原因。在人群中预防动脉粥样硬化的唯一方法是当FA、蛋白质和碳水化合物的能量值比为1:1:1且sFA、单烯和多烯FA的能量值比也为1:1:1时，使外营养的生物学功能正常化。棕榈sFA含量越低，必需多烯FA浓度越高，胆固醇醇和甘油三酯的血液水平就越低。同时，运动的激活和生物学功能是身体活动的一个水平。
