Titov V N, Rozhkova T A, Samokhodskaya L M
Klin Lab Diagn. 2017 Feb;62(2):68-77.
The eruptive xanthomata are formed in vivo under realization of biological function of endoecology. The xanthomata are formed in tissues by early in phylogenesis resident macrophages at absorption of secreted by hepatocytes aphysiological stearic lipoproteins of very low density with high content of the same name triglycerides down to tristearate. In these lipoproteins of very low density, by force of aphysiologically high hydrophobicity, stearic triglycerides are not hydrolyzed by post-heparin lipoproteinlipase. They both do not associate apoE and form apoE/B-J00 ligands. The formation of stearic lipoproteins of very low density occurred at impairment of function of coupled biochemical reactions in synthesis of physiological ω-9 oleic mono unsaturated fatty acid in hepatocytes. To synthesize endogenous oleic mono unsaturated fatty acid the late in phylogenesis insulin expresses two enzymes of coupled biochemical reactions: palmitoyl-KoA-elongase andstearyl-KoA-desaturase, activating synthesis of fatty acids following the path glucose-endogenous palmitic unsaturated fatty acid-stearic unsaturated fatty acid-oleic mono unsaturated fatty acid. The uncoupling of enzymes of coupling synthesis forms in hepatocytes surplus of stearic mono unsaturated fatty acid, stearic triglycerides and of the same name aphysiologic lipoproteins of very low density. During inhibition of the second enzyme the first one continues to actively produce stearic unsaturated fatty acid which the second enzyme, already uncoupled, does not convert into oleic unsaturated fatty acid. By absorbing aphysiologic ligand-free stearic lipoproteins of very low density in biologic reaction of endoecology, phylogenetically early macrophages convert into foam cells initiating aphysiologic biological reaction of transcytosis, biologic reaction of inflammation, biologic reaction of apoptosis and formation of eruptive xanthomata. The lipids of eruptive xanthomata: such endogenous stearic triglycerides as tristearate, tripalmitate, exogenous carotenoids, phospholipids and unesterified cholesterol.
发疹性黄瘤是在内生态生物学功能实现的情况下于体内形成的。黄瘤是在系统发育早期由驻留巨噬细胞在吸收肝细胞分泌的具有高同名甘油三酯含量直至硬脂酸甘油三酯的极低密度生理性硬脂脂蛋白时在组织中形成的。在这些极低密度脂蛋白中，由于生理性高疏水性，硬脂酸甘油三酯不会被肝素后脂蛋白脂肪酶水解。它们既不与载脂蛋白E结合，也不形成载脂蛋白E/B-J00配体。极低密度硬脂脂蛋白的形成发生在肝细胞中生理ω-9油酸单不饱和脂肪酸合成中偶联生化反应功能受损时。为了合成内源性油酸单不饱和脂肪酸，系统发育后期的胰岛素表达两种偶联生化反应的酶：棕榈酰辅酶A延长酶和硬脂酰辅酶A去饱和酶，激活沿葡萄糖-内源性棕榈酸不饱和脂肪酸-硬脂酸不饱和脂肪酸-油酸单不饱和脂肪酸途径的脂肪酸合成。偶联合成酶的解偶联在肝细胞中形成了过量的硬脂酸单不饱和脂肪酸、硬脂酸甘油三酯和同名的极低密度生理性脂蛋白。在第二种酶受到抑制时，第一种酶继续活跃地产生硬脂酸不饱和脂肪酸，而已经解偶联的第二种酶不会将其转化为油酸不饱和脂肪酸。在系统发育早期的巨噬细胞通过在内生态生物学反应中吸收无生理性配体的极低密度硬脂脂蛋白，转化为泡沫细胞，引发转胞吞作用的生理性生物学反应、炎症生物学反应、凋亡生物学反应以及发疹性黄瘤形成。发疹性黄瘤的脂质包括：如硬脂酸甘油三酯、三棕榈酸甘油酯等内源性硬脂酸甘油三酯以及外源性类胡萝卜素、磷脂和未酯化胆固醇。
