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Biomedical subjects

E I Sokolov

Publications and source records attributed to E I Sokolov.

At least 19 recordsLinked to original sources
PubMed2006

[Clinical value of detection of insulin resistance in woman with metabolic syndrome].

Hyperinsulinemic and euglycemic clamp studies were done in 17 women selected from 64 postmenopausal female patients aged 46-67 years with clinical picture of metabolic syndrome, and in 7 control women. Clamp test made it possible to follow dynamics of insulin and other hormones in the process of regulation of glucose level. This method allowed to prove quantitatively the presence of resistance to insulin and hormonal disintegration in patients with metabolic syndrome. Elevation of activity of sympathoadrenal system plays an important role in the pathogenesis of hypertension in metabolic syndrome at the account of augmented sensitivity of receptor apparatus. Lowering of somatotropic hormone level in patients with metabolic syndrome is associated with disturbed somatotropic function of the hypophysis which regulates blood pressure.

Aged↗
PubMed2006

[Hormonal regulation of lipoprotein metabolism: the role in pathogenesis of coronary heart disease].

The character and role of hormonal dysregulation of lipoprotein metabolism during postprandial hyperlipemia were studied in patients with coronary heart disease (CHD) and hyperthyroidism as compared with healthy subjects. Pronounced hypertriglyceridemia alongside with the decreased high density lipoprotein cholesterol (HDL C) after standard fat load were associated with increased level of insulin and decreased level of cortisol. Moreover, in CHD patients fasting hyperinsulinemia becoming even stronger postprandially resulted in prevalence of antilipolytic action of insulin over lipid-mobilizing effect of cortisol; and an extended postprandial hypertriglyceridemia took place. Patients with hyperthyroidism and low cholesterol level both in atherogenic LDL and antiatherogenic HDL, demonstrated decreased level of apo AI (as in CHD patients) and apo B (three times lower than in CHD patients). Very low ratio of apo B/AI in patients with hyperthyroidism both in fasting and postprandial state was a clear indication of their lipoprotein profile antiatherogeneity. Thus, in patients with hyperthyroidism despite of low HDL C and apo AI levels, antiatherogenic properties of lipoprotein profile are probably determined by very low apo B/AI ratio induced by thyroid hormones, and might be explained by the influence of thyroid hormones on the expression of genes coding these apoproteins.

Apolipoprotein A-I↗
PubMed2005

[Small dense low density lipoprotein particles: mechanisms of formation, atherogenic properties, possibilities of modification of their content in blood plasma].

Atherogenic low density lipoproteins (LDL) consist of subfractions of particles with different dimensions, density, proportion of various lipid components, affinity to apo B/E receptors, susceptibility to oxidation, and other properties. As a rule spectrum of LDL particles has one predominant central peak and several (up to 6) additional peaks containing particles which are smaller or larger than particles of the main peak. There are also smaller and bigger particles within the main peak itself. In normolipidemia average diameter of particles of the predominant main peak exceeds 25.5 hm (profile A), in combined hyperlipidemia main peak consists of smaller (<25.5 hm) particles (profile B). It has been shown in many studies that because of several characteristics (lower affinity to apo B/E receptors, prolonged presence in blood stream, susceptibility to oxidation and uncontrolled entrapment by macrophages) small dense LDL particles play significant role in atherogenesis. The authors of this review have demonstrated that in subjects with abdominal obesity and concomitant metabolic risk factors in postprandial period after standard meal LDL spectrum shifts towards small particles and this shift persists during 6 hours after meal. An apparently atherogenic subfraction of large cholesterol ester loaded particles is also described in this paper.

Cholesterol, VLDL↗
PubMed2004

[Hormonal dysregulation of lipid metabolism in pathogenesis of ischemic heart disease].

The aim of the study was to specify postprandial hyperlipidemia (PHL) and the level of hormones which regulate metabolism, lipids in particular, in patients with ischemic heart disease (IHD) vs those in healthy persons and patients with thyrotoxicosis as well as to clarify whether IHD pathogenesis correlates with fat metabolism disturbance. Lipid and apoprotein parameters of dyslipoproteinemia, concentrations of insulin, hydrocortisone, T3, T4 and thyrotropic hormone were tested before and 3, 6 hours after fat loading in IHD patients with angiographically documented coronary atherosclerosis, in healthy persons and patients with diffuse toxic goiter. In IHD patients postprandial PHL differed from that in healthy persons and thyrotoxicosis patients by higher and growing up to hour 6 after fat loading hypertriglyceridemia associated with lowering of antiatherogenic cholesterol of HDLP. In thyrotoxicosis both fasting and afterload lipid and apoprotein indices of the lipoprotein spectrum continued at low level except triglycerides the level of which returned to normal level. The hormonal spectrum in IHD patients was characterized by higher fasting insulin and its noticeable rise after fat loading. As healthy persons and patients with thyrotoxicosis had no significant changes in hormones levels after fat loading, it is suggested that development of atherogenic postprandial PHL caused primarily by hormone dysregulation of fat metabolism with a leading role of hyperinsulinemia contributes much to pathogenesis of IHD.

Adult↗
PubMed2004

[Lowering of antiatherogenic significance of high density lipoproteins in obese persons].

Protein and lipid components of blood serum high density lipoproteins (HDL) responsible for their functional activity were studied before and after fat load in subjects with normal body mass and various types of obesity. Subjects with abdominal obesity compared with those with gluteo-femoral obesity and normal body mass initially had pronounced disturbances in components of HDL and their acceptor capacity. Fat load caused changes of HDL composition in all study groups. Postprandial effect in persons with normal body mass became obvious 6 hours after load while in those with excess mass it occurred earlier - 3 hours after fatty meal. In subjects with gluteo-femoral obesity this effect remained on the same level while in those with abdominal obesity it became more pronounced by hour 6. Contrary to subjects with normal body mass and gluteo-femoral obesity fat load induced changes of HDL components in persons with abdominal obesity were not associated with augmented acceptor capacity of HDL what could be considered as proatherogenic effect.

Adolescent↗
PubMed2004

[Serum lipoproteins in different types of obesity in lipid loading challenge].

The impact of food fat load on plasmic lipid transport system (LTS) was studied in persons with abdominal and gluteofemoral obesity by the standard fat test proposed by J. Patsch. The lipoprotein spectrum in abdominally obese patients was characterized by high atherogenicity of lipoprotein spectrum on an empty stomach aggravating under fat intake: prolongation of postprandial lipemia up to 6 hours with growing apoB and apoB/A1. Patients with gluteofemoral obesity differed from normal weight persons only by higher fasting values of triglycerides. They showed no atherogenic trend in changes in response to food fat.

Abdomen↗
PubMed2003

Low-density lipoprotein subfractions during abdominal and gluteofemoral obesity.

Subfractional spectrum of plasma low-density lipoproteins in people with normal body weight and patient with obesity was studied by gradient electrophoresis (3-12%) in polyacrylamide gel. Low-density lipoprotein subfractions in fasting patients with abdominal and gluteofemoral obesity were primarily presented by small particles (compared to people with normal body weight). The composition of low-density lipoprotein subfractions underwent most pronounced changes in patients with abdominal obesity after single fat load.

Abdomen↗
PubMed2003

[Diabetic dyslipidemia and pathogenesis of ischemic heart disease].

BACKGROUND: Type II diabetes is associated with high risk of ischemic heart disease (IHD), diabetes and IHD have similar risk factors, abdominal obesity as well as interrelated disturbances of lipid and carbohydrate metabolism play important roles in pathogenesis of both diseases. AIM: To elucidate characteristics of metabolism and transport of lipids and carbohydrates in patients with type II diabetes and IHD with normal and excessive body mass with abdominal type of fat distribution. MATERIAL AND METHODS: Parameters of carbohydrate metabolism, blood serum levels of free fatty acids, lipid and apoprotein (apo-) parameters of lipoprotein spectrum were evaluated in subjects without diabetes or IHD (group 1), patients with IHD and normal body mass (group 2), patients with IHD combined with diabetes with normal body mass (group 3), patients with IHD, diabetes and abdominal obesity (group 4). RESULTS: Patients with combination of diabetes and IHD compared with those of groups 1 and 2 in addition to higher blood glucose had lower growth hormone, higher triglycerides, lower high density lipoprotein cholesterol (CH) and apo-A1, higher low/high density lipoprotein CH and apo-B/apo-A1 ratios. These atherogenic changes were more pronounced in patients of group 4 who had highest levels of insulin, free fatty acids, low density lipoprotein CH and apo-B and lowest glucose/insulin ratio and level of apo-A1. CONCLUSION: Insulin resistance and hyperinsulinemia are most important features of disturbed carbohydrate and lipid metabolism. Insulin resistance and hyperinsulinemia are most pronounced in subjects with abdominal obesity in whom they create conditions for impaired glucose utilization, development of atherogenic dyslipidemia and eventually emergence of IHD.

Adult↗
PubMed2002

[Hyperinsulinemia and insulin resistance in pathogenesis of atherosclerosis and ischemic heart disease].

AIM: To confirm the pathogenetic relationship of hyperinsulinemia, insulin resistance, and coronary disease. MATERIAL AND METHODS: Thirty-nine coronary patients (male) were examined using lipid loading test, bicycle ergometry, coronarography, and measurements of insulin, cholesterol (CS), triglycerides (TG), very low density lipoproteins (VLDL), low density lipoproteins (LDL), high density lipoprotein (HDL) CS, apoA-1, and apoB. RESULTS: Blood levels of CS, TG, VLDL, LDL, HDL CS, apoA-1, apoB, and insulin were measured before and 3, 6, and 9 h after lipid loading in 39 coronary patients and 20 normal subjects. Coronarography showed initially high levels of insulin in coronary patients with pronounced changes. Insulin level drastically increased after insulin loading; increases in TG and apoB levels were the most pronounced, while the concentrations of HDL CS and apoA-1 decreased and did not normalize 6 h after lipid loading. CONCLUSION: The results confirmed the relationship between hyperinsulinemia, insulin resistance, and coronary disease.

Arteriosclerosis↗
PubMed2001

[Myocardial and vascular impairment in diabetes mellitus].

AIM: To study relations between ischemic heart disease (IHD) and hormonal and metabolic disorders in patients with diabetes mellitus and IHD. MATERIAL AND METHODS: Cuff test was used to study functional activity of the vessels. Platelet aggregation, prostacyclin, antithrombin III were studied in 168 healthy subjects, diabetes mellitus (DM) patients (n = 98) and DM type 2 patients (n = 118). RESULTS: Microscopic examinations of the myocardium (endomyocardial biopsy) were made and the results were compared to antithrombogenic activity of vascular wall in DM. Myocardial vessels in the patients have undergone morphological alterations. Antithrombogenic activity of the vessels in DM patients was studied under compression. CONCLUSION: Microcirculation was found changed: vascular walls were thick and homogenized, endothelyocytes underwent edema and destruction with enlargement of the basal membrane. Platelet hypersensitivity was proved in DM as well as more active metabolism of arachidonic acid, low prostacyclin endothelial activity.

Adult↗
PubMed1997

[Affection of myocardium in diabetes mellitus].

Echocardiography was performed in 67 patients with compensated diabetes mellitus (DM) type I and II. No signs of cardiovascular failure were noted. 20 patients have undergone myocardial scintigraphy. The patients were found to have hyperkinetic central hemodynamics resultant in DM type I from tachycardia, high rate of circulatory shortening of myocardial fibers, in DM type II from compensatory myocardial hypertrophy. In both diabetic types the function of myocardial relaxation was deteriorated as indicated by increased end diastolic volume and slow left ventricular relaxation. This evidences for initial cardiac failure. Myocardial scintigraphy registered perfusion defects in all the examinees, more profound in diabetes mellitus type II. The above findings explain the existence of marked coronarogenic and metabolic myocardial defects in DM.

Adult↗
PubMed1993

[Detection of risk factors for hemodynamic dysadaptation under physical loading by data of genetic studies (the beta-adrenoreceptor blockade test) (Part 3)].

Examinations in 28 pairs of twins who were studied by bicycle ergometry during a "pure" graded exercise and an exercise during oral administration of anapriline have shown that the functional features of the heart make some contribution to cardiovascular implementation of the "pure" graded exercise. When given exercise and anapriline, energy processes play a role in its implementation. It is suggested that exercise + anapriline will cause substantial metabolic changes which can be essential in cardiac decompensation if exercise is not limited in the use of beta-blockers.

Adaptation, Physiological↗
PubMed1992

[The effect of anaprilin on the reaction of the sympathetic-adrenal system to graded physical loading in healthy subjects and patients with ischemic heart disease].

The specific features of responses of the sympathoadrenal system during its activation by graded exercise (E), including that along with anaprilin induced blockade of beta-adrenoceptors, were determined from the urinary excretion of norepinephrine, epinephrine, dopamine, and dioxyphenylalanine in 54 healthy males and 22 patients with postinfarction cardiosclerosis concurrent with Functional Class I-II angina pectoris on effort. E caused hyperreactivity of the sympathoadrenal system, as appeared as significantly greater increases in the levels of catecholamines and their precursors in the patients than in the healthy persons. A single anaprilin dose of 40 mg abolished the responsiveness to exercise and improved its tolerance. The revealed features of sympathoadrenal responsiveness to exercise with and without anaprilin suggest that the patients with coronary heart disease have sympathoadrenal dysfunction, which shows one of the possible mechanisms responsible for the cardioprotective effect of beta-adrenoblockers in this disease.

Adrenal Glands↗