Aim: To study effects of avandia and its combination with metformine (avandamet) on secretion of fat tissue hormones.
Material And Methods: The examination protocol for 42 patients with type 2 diabetes mellitus (DM) aged 62.4 +/- 7.
The fact that fat issue is an endocrine gland secreting several hormones participating in the pathogenesis of type 2 diabetes mellitus (DM2) is universally recognized. Fat issue secretes leptin, tumor necrosis factor alpha, resistin, adiponectin, interleukin-6, free fatty acids, visfatin, omentin, perilipin, and other substances that influence the condition of insulinoresistance, one of the main factors responsible for DM2. Subcutaneous fat and visceral depot fat tissue differ in the spectrum of hormones they produce; the list of these hormones is presented in the article.
View Article and Find Full Text PDFLate complications in type 2 diabetic patients are commonly associated with accelerated development of atherosclerosis. In type 2 diabetes mellitus, non-enzymatic glycosylation of apo-B that is a function of hyperglycaemia is an efficient biochemical way of low-density lipoprotein atherogenic modification. So, proper metabolic control is needed to prevent late complications of diabetes.
View Article and Find Full Text PDFProbl Endokrinol (Mosk)
February 2007
The final glycated products forming in diabetes contribute to the higher atherogenic oxidative modification of low-density lipoproteins (LDL). The impact of glycemic control on the parameters of free radical oxidation was comparatively studied in patients with type 2 diabetes who received metformin (Glucophage, Nycomed) (Group 1, n = 40) and sulfanylurea preparations (Group 2, n - 30, out of them 15 patients took maninil and 15 had diabeton) good glycemic control caused the magnitude of oxidative stress to reduce, which appeared as the decreased levels of primary (lipid hydroperoxides) and secondary (malonic dialdehyde) products of free radical oxidation in LDL and as the enhanced activity of antioxidative defense enzymes. However, with the identical degree of glycemic control, which was determined by the level concentrations of HbA1c and lipids in both groups, the plasma levels of lipid peroxides decreased by more than 5 times in Group 1 patients receiving metformin than in Group 2 patients and the rate of LDL oxidability reduced by 4.
View Article and Find Full Text PDFAim: To study mexicor effects on functional activity of beta-cells, insulin resistance, lipid metabolism and lipid peroxidation in patients with diabetes mellitus (DM) type 2.
Material And Methods: Twenty patients with DM type 2 participated in a double blind randomized trial of mexicor vs placebo. Before and after therapy the following parameters were studied: plasma glucose before meal, immunoreactive insulin, glycosilated hemoglobin, cholesterol, triglycerides, LDLP and HDLP cholesterol, malonic dialdehyde, dienic conjugates, superoxide dismutase, catalase, glutathione peroxidase and alpha-tocopherol.
Probl Endokrinol (Mosk)
August 2005
Iodine deficiency, in addition to the development of an enlargement of the thyroid gland - goiter, leads to a number of other pathological conditions, which are commonly called iodine deficiency diseases. The spectrum of iodine deficiency diseases is wide and depends on the period of life when iodine deficiency affects the body. Iodine deficiency during pregnancy and embryonic development leads to a high prevalence of spontaneous abortion, especially in the first trimester of pregnancy; high perinatal and infant mortality, congenital malformations, congenital hypothyroidism with a lag in physical and mental development.
View Article and Find Full Text PDFOxidative stress is an imbalance in the body between prooxidants and the antioxidant defense system, which, to varying degrees of severity, accompanies insulin deficiency or insulin resistance, which are one of the essential components of the pathogenesis of vascular complications of diabetes. It has been established that oxidative stress in diabetes mellitus can be the result of several mechanisms: a) increased formation of reactive oxidants that are formed during the oxidation of both carbohydrates themselves and carbohydrates complexing with various proteins, as well as the result of autooxidation of fatty acids in triglycerides, phospholipids and esters cholesterol; b) reducing the activity of the antioxidant system in the body, which is represented by glutathione, glutathione peroxidase, catalase, superoxide dismutase, vitamins, K, E and C and other antioxidants (taurine, carotene, uric acid and ubiquinol); c) disorders of enzymes of polyol glucose metabolism, mitochondrial oxidation, metabolism of prostaglandins and leukotrienes and a decrease in glyoxalase activity; d) violation of the concentration or exchange of glutathione and ions of certain metals. In addition, ischemia, hypoxia and pseudohypoxia of tissues observed in diabetes mellitus are additional factors contributing to the increased formation of reactive oxidants in various organs and tissues.
View Article and Find Full Text PDFAim: To characterize features of immune status in patients with metabolic syndrome (MS).
Material And Methods: 41 MS patients entered the study (mean age 55.9 +/- 9.
Aim: To study a functional state of the sympathico-adrenal system in patients with diabetes mellitus (DM) in developing late complications.
Material And Methods: The study included 81 DM patients: free of late complications and diabetic autonomic neuropathy (DAN) (n = 24); with DAN (n = 6); with DAN and nonproliferative retinopathy (n = 8); with DAN and nephropathy stage 1-2; with DAN and diabetic retinopathy, sensory polyneuropathy (n = 23); with diabetic nephropathy stage 4 (n = 14). Blood levels of epinephrine, norepinephrine, dopamine were measured using liquid chromatography with electrochemical detection.
Glycosylation end-products formed during diabetes mellitus promoted atherogenic oxidative modification of low-density lipoproteins. We evaluated the effects of compensation of carbohydrate metabolism and therapy with antioxidant probucol on parameters of free radical oxidation in patients with type II diabetes mellitus. Compensation of carbohydrate metabolism reduced manifestations of oxidative stress, which was manifested in accelerated enzymatic utilization of reactive oxygen species and lipid peroxides and decreased content of free radical oxidation products in low-density lipoproteins.
View Article and Find Full Text PDFAim: To examine the effect of the alpha 1-adrenoblocker tonocardin (doxazosin) on the course of arterial hypertension (AH) and on carbohydrate and lipid metabolism and insulin resistance in patients with type 2 diabetes mellitus (DM) concurrent with AH.
Materials And Methods: 18 patients with type 2 DM concurrent with AH, treated with tonocardin for at least 12 weeks were examined; the fasting glycemia, the levels of blood glycosylated hemoglobin, serum total cholesterol and triglycerides, and the degree of insulin resistance (intravenous insulin load or insulin tolerance test and the insulin resistance index estimated by the HOMA method) were determined.
Results: Tonocardin treatment lowered systolic BP (from 159 +/- 19.
Aim: Distribution of alleles of tetranucleotide microsatellite D6S392 located nearby the gene of Mn-dependent superoxide dismutase (SOD2) was studied in healthy donors (n = 143), patients with insulin-dependent (n = 166) and insulin-independent (n = 101) diabetes mellitus (IDDM and IIDM).
Materials And Methods: Alleles of the polymorphic locus D6S392 were amplified using polymerase chain reaction (PCR) on the basis of genome DNA isolated from the venous blood of the examinees. PCR products were analysed with gel-electrophoresis in polyacrylamide gel.
Background: Graves' disease (GD) is a polygenic autoimmune thyroid syndrome. Some of the genes implicated in its pathogenesis may encode thyroid-stimulating hormone receptor (TSHR) and estrogen receptors 1 (ESR1) and 2 (ESR2). We examined dinucleotide repeat polymorphisms in the ESR1 and ESR2 genes and D727E amino acid substitution in the TSHR gene for possible association with GD in a Russian population.
View Article and Find Full Text PDFPolymorphisms of the genes for angiotensin-converting enzyme (ACE) and angiotensinogen, the proteins of the renin-angiotensin system (RAS), were tested for association with the polymetabolic syndrome (PMS) and non-insulin-dependent diabetes mellitus (NIDDM) in the Moscow population. The insertional (I) allele and genotype II of the ACE gene proved to be associated with PMS. A significant difference in allele and genotype frequency distributions of the (CA)n microsatellite of the 3'-untranslated exon of the angiotensinogen gene was revealed between randomly sampled individuals and patients with PMS and IDDM from the Moscow population.
View Article and Find Full Text PDFInsertion/deletion polymorphism of the angiotensin-converting enzyme (ACE) gene was analyzed in patients with non-insulin-dependent diabetes mellitus (NIDDM) and in the control group consisting of healthy subjects. The insertion allele (I) and genotype II were found to be associated with NIDDM. The frequencies of diabetic retinopathy and nephropathy in NIDDM patients were not associated with this polymorphism.
View Article and Find Full Text PDFThe results of examination and treatment in 129 patients with toxic goiter (TG) were analyzed. Thyroid status, stable intrathyroid iodine content, thyroid-stimulating hormone (TSH) receptor antibody titer, the volume and echostructure of thyroid tissue were studied either during their first visit and during conservative treatment. The findings suggests that the relapse rate is higher with slow reduction in thyroxine levels and prolonged suppressed TSH during treatment, with higher TSH receptor antibody titer after treatment, with large thyroid volumes when TG manifests it self and in the absence of positive changes in the volume and echostructure of thyroid tissue during treatment, with lower intrathyroid iodine content and its greater reduction during treatment.
View Article and Find Full Text PDFGraves disease is complex autoimmune thyrotoxicosis. A number of genes may contribute to the development of the disorder. Some of them may be genes that encode cytotoxic T-lymphocyte-associated serine esterase-4 (CTLA4), subunit 2 of large multifunctional protease (LMP2), thyroid-stimulating hormone receptor (TSHR), and interleukin 1 receptor antagonist (IL1RN).
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