The nicotinic acid as an inhibitor of lipolysis in the phylogenetically early visceral cells; insulin also blocks hydrolysis of triglycerides in the phylogenetically late adipocytes.

Abstract

It is valid to consider effect of nicotinic acid as an insulin-mimetic one. The uniformity of biologic effect of exogenous nicotinic acid and endogenous insulin permits to become aware that a) the hypo-lipidemic activity of insulin, inhibition of lipolysis in phylogenetically late insulin-dependent adipocytes and decreasing of content of unesterified fatty acids in blood plasma are considered as a basis of hypoglycemic effect of insulin; b) nicotinic acid similar to insulin blocks lipolysis too but in hormoneindependent visceral fatty cells. The counter-insular effect is manifested in vivo by exogenous and endogenous palmitic saturated fatty acid by force of physical chemical characteristics. The biological role of insulin consists in regulation of metabolism of fatty acids mainly unesterified fatty acids and in absorption of glucose by all insulin-dependent cells. It is supposed that contractile cells (myocytes and cardiomyocytes) cumulate glycogen for implementing glucose as a substrate in synthesis in situ de novo of ῲ-9 oleic mono-saturated fatty acid. The insulin initiates synthesis because mitochondria process this mono-saturated fatty to β-oxidation with the highest constant of reaction velocity. This is conditioned by physical chemical characteristics of oleic mono-saturated fatty acid, positioning of double bond in the chain of fatty acid; this ensures maximal efficiency of ATP gaining. In phylogenesis, the low efficient palmitic alternative of metabolism of fatty acids is formed the earliest. At the later stages of phylogenesis the cells, under becoming of motion function, worked out more efficient alternative of ATP synthesis from exogenous ῲ-9 oleic monosaturated fatty acid. At the late stages of phylogenesis, under becoming of biological function of locomotion (motion at the expense of contraction of cross-striated skeletal myocytes) insulin began to activate absorption of glucose by cells with subsequent synthesis of endogenous ῲ-9 oleic mono-saturated fatty acid out of it. The aphysiological effect of environment factors in the form of derangement of biological function of trophology (feeding), surplus of palmitic unesterified fatty acids in food serve as a main cause of such a high rate of functional derangement - insulin resistance syndrome in populations. Hence, there is no reason to call it diabetes mellitus type II.