The regulation of metabolism of glucose is billions years older than system of insulin and biological function of locomotion (function of motion). Hence hypoglycemiс effect of hormone is mediated by alteration of metabolism of fatty acids. The insulin in physiological way deprives mitochondrions a possibility to metabolize ketone bodies, short chain, medium chain and long chain fatty acids and forces them to oxidize glucose which phylogenetically is not an optimal substrate. The relationships between fatty acids and glucose in the Rendle cycle have an effect only on autocrine level (in cell) determining alternation of biological reactions of exotrophia (after food intake) and endotrophia (beyond food intake) in biological function of alimentation (trophology). The most anti-diabetic pharmaceuticals are as insulin hyperlipemiс by their mechanism of action. The decrease content of lipid substrates of oxidation in cytosol of cells and mitochondrions “are forced” to oxidize glucose. In these conditions, insulin enhances absorption of glucose by cells through glucose carriers GLUT4. The derivatives of sulfonil-urea increase secretion of insulin by β-cells of islets. The biguanidines bond in cytosol covalently and irreversibly ketone bodies taking them away from oxidation in mitochondrions. The fibrates, glitazones, flavonoids and flavones, lipoic tio-fatty acids. The endogenous eicosanoids, derivatives ω-3 and ω-6 of essential polyolefinic fatty acids and conjugated unsaturated fatty acids are the antagonists of receptors of activation of proliferation of peroxisomes. In peroxisomes, they enhance α-, βand ω-oxidation of all exogenous aphysiological fatty acids and excess of palmitic saturated fatty acid forming hypolipidemia in cytozol. The hypolipidemic pharmaceuticals with effect of β-blocker of oxidation stop absorption of fatty acids by mitochondrions. The Ω-3 essential polyolefinic fatty acids, simultaneously with hypolipidemic effect, activate function of GLUT4. In patients of middle age, the diabetes mellitus type II is a symptom of syndrome of atherosclerosis. The reason is that in cells the deficiency of essential polyolefinic fatty acids and is determined by derangement of synthesis of phospholipids and function of GLUT4. It is valid to consider diabetes mellitus primarily as a pathology of metabolism of fatty acids and secondly as a pathology of content of glucose. It is necessary to take into account both under treatment (tactic activities) and strategic program of prevention of diabetes mellitus in population.
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