A metabolic syndrome (MS) involves a variety of systemic clinical-biochemical processes - insulin resistance, abdominal obesity, arterial hypertension, dislipidemy [8, 9]. The MS origin has been studied insufficiently; the risk factors and pathological processes leading to this syndrome development remain disputable. There are some MS development hypotheses offered, from which the leading one is the theory of insulin resistance (IR) [7, 10]. An important role in the IR development is taken by free fatty acids (FFA). The mechanisms of glucose-insulin homeostasis and FFA interconnection predetermine the necessity to study the role of FFA and their separate components in the course of the MS formation [2, 3].
The research purpose - is to study the composition of blood plasma free fatty acids in 22 metabolic syndrome patients and 11 healthy people. The MS was diagnosed according to the criteria offered by the experts of the USA National Education Program on cholesterol [1, 12]. The investigation of carbohydrate metabolism included the glucose content determination in blood serum on an empty stomach and in 2 hours after the oral glucose load, the insulin level determination by the immunoenzyme method (the sets of the firm «DRG - diagnostics», Germany); the HOMA index was calculated (insulin on empty stomach, mUnit/ml ×glucose on empty stomach, mmol/l/22,5). The lipid exchange parameters in blood serum was determined on the biochemical analyser FP- 901М of the firm "Labsystem" (Finland) using the "Labsystem" firm sets. The A and B apolipoproteins (apo-A and apo-B) content was determined (the «DiaSys» firm sets, Germany); the apo-B/apo-A ratio was calculated. The extraction of lipids from blood plasma was executed by the method of Bly and Dyer . The methyl ethers of fatty acids (FA) were obtained by the method of Carreau и Duback , the analysis was executed on the gas-liquid chromatograph Shimadzu GC-17A. The results were stated in relative % from the total FA sum .
The FFA quality composition represented by 31 components of individual fatty acids, was analyzed with due consideration of glucose-insulin homeostasis changes in the MS patients: the 1st group - MS patients with no insulin resistance, the 2nd group - patients with the diagnosed IR. In the MS patients against the background of normoinsulinemia the lauric, myristic and palmitic acids level decrease was detected, 24:0, 16:0i acids (table 1). Against the saturated FA relative amount decrease the content of polyunsaturated fatty acids (PUFA) increased. The contents of linolic (18:2ω6) and α-linolenic (18:3ω3) acids increased twice (р<0,01), the tendency to arachidonic acid increase (20:4ω6) was registered. The sum-total fatty acids exponent Σ ω6 increased twice. The integral change exponent in fatty acids series (unsaturation index) in the first group patients compared to the control one was higher by 41% (р<0,05). In the second patient group with the IR available the FFA percentage change vector was analogous, but the disorders were less vivid than in the first patient group.
The findings testify that the disorder of transport in blood and the internalization by FFA precede the insulin resistance formation. It promotes the receptor dysfunction to insulin, the signal transfer secondary system and internalization by glucose cells [2-4]. The accumulation of PUFA in plasma is probably explained by the compensatory increase of unsaturated fatty acids passive internalization by the cells when their active transport is blocked. The adaptation of cells to such polyene fatty acids transport type arouses lipolysis, intensifies insulin release resulting in hyperinsulinemia [7, 10]. The endogenic insufficiency in PUFA cells leads to the fatty acid content change of phospholipids and physical-chemical properties of plasmalemmae, their liquidness decrease, functioning failure of receptors to insulin and glucose transportation systems . The findings affirm that the disorders of the receptor mediated FA transport, which result in plasmalemmae´s structure changes, lie in the root of IR and hyperinsulinemia formation. Thus, a significant factor of increased risk of MS development and burdening is the FFA transport failure. The diagnostics of such failures serves a signal for the MS vicious circle development beginning that includes a complex of systemic metabolic changes concerning lipidic and carbohydrate metabolism.
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