22 research outputs found

    From Normal to Obesity and Back: The Associations between Mitochondrial DNA Copy Number, Gender, and Body Mass Index.

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    Mitochondrial DNA (mtDNA) encodes core subunits of oxidative phosphorylation complexes and, as a result of intricate regulatory crosstalk between nuclear and mitochondrial genomes, the total number of mtDNA copies fits the requirements of each cell type. Deviations from the physiological number of mtDNA copies are expected to be deleterious and might cause some inherited diseases and normal ageing. We studied 46 obese patients with type 2 diabetes (T2DM) one year after a laparoscopic sleeve gastrectomy (LSG) and Roux-en-Y gastric bypass (RYGB). The results were compared with normal-weight patients without T2DM (control group 1) (body mass index (BMI) = 22.5 ± 3.01 kg/m <sup>2</sup> ) and patients with obesity without T2DM (control group 2) (BMI = 36 ± 3.45 kg/m <sup>2</sup> ). We detected an increase of mtDNA copy number in the cells of the buffy coat obtained from peripheral blood, sampled one year after bariatric surgery. We also found that average mtDNA copy number as well as its dynamics (before and after the surgery) are gender-specific. To the best of our knowledge, this is the first evidence for the restoration of mtDNA copy number in obese patients after LSG and RYGB

    CHEMERIN AS A POTENTIAL REGULATOR OF MITOCHONDRIAL QUALITY CONTROL IN OBESE PATIENTS

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    In obese patients, the relationship between the content of chemerin in blood plasma and the expression of genes TFAM, Drp1, MFN2, SOD, BAX, responsible for quality control of mitochondria, in insulin-dependent tissues (adipose tissue, liver) was revealed. The tissue-specific features of gene expression (TFAM, Drp1, MFN2, SOD, BAX), the number of mtDNA copies in the studied depots in obese patients were established. It has been proven that a change (decrease) in the number of mtDNA copies in insulin-dependent tissues can have a protective effect on mitochondria under conditions of increased oxidative stress. It was found that in patients without type 2 diabetes, an increase in chemerin production promotes the activation of the antioxidant system in the visceral adipose tissue but not in the liver. On the contrary, all obese patients with type 2 diabetes showed a decrease (compared with patients without type 2 diabetes) in the plasma level of chemerin. Thus, the low content of chemerin in the blood plasma in patients with type 2 diabetes mediates the formation of mitochondrial dysfunction in insulin-dependent tissues (adipose tissue, liver)

    HEPATIC SOD1 GENE EXPRESSION CHANGES IN THE NAFLD PATHOGENESIS IN OBESITY

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    Steatosis in the liver in obesity increases the work of mitochondria to utilize excess lipids. An overload of β-oxidation of fatty acids, the tricarboxylic acid cycle, and oxidative phosphorylation leads to a decrease in ATP and an increase in the formation of reactive oxygen species. Normally, mitochondria can efficiently remove elevated levels of reactive oxygen species using the cell's antioxidant system and metabolic adaptation to altered conditions. This study aimed to investigate the role of hepatic SOD expression in the pathogenesis of NAFLD in obesity. It was found that the level of SOD1 expression in the liver in obese patients with and without type 2 diabetes with a BMI > 40 kg/m2 was lower than in healthy donors. The copy number of mitochondrial DNA (mtDNA) in the liver in all obese patients was more than two times lower than in the control group. In the liver of obese patients without type 2 diabetes, the SOD1 protein level and the mtDNA copy number were interrelated and negatively correlated with the area of fatty inclusions. Thus, in obese patients, a decrease in antioxidant defense in the liver leads to the vulnerability of mitochondria, which, in turn, contributes to the progression of steatosis and insulin resistance

    Особенности клеточного иммунитета и цитокинового репертуара у пациентов с метаболическим синдромом

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    In the formation of metabolic syndrome there is a change of the quantitative characteristics of immunocompetent cells and blood cytokine profile. According to our study, the elevated serum content of inflammatory cytokines (IL-6, IFNγ and TGF-β), in the cases of IL-10 decrease, was detected in patients with metabolic syndrome. The level of serum IL-1 inpatients with metabolic syndrome was within normal parameters. With it, there was a significant decrease in the percentage of blood CD3- and CD4-T-lymphocytes, and, conversely, an increase in the number of activated T (CD25+) and B (CD23+)-lymphocytes and monocytes (CD14+) has been in patients with metabolic syndrome. This revealed changes, is characterized by the presence of subclinical chronic inflammation in metabolic syndrome patients. It can be the result of compensatory immune responses developing in the weakening of adaptive immunity.В процессе формирования метаболического синдрома происходит изменение количественных характеристик иммунокомпетентных клеток и цитокинового профиля крови. Согласно данным проведенного исследования, у больных метаболическим синдромом регистрировалось повышенное сывороточное содержание провоспалительных цитокинов (IL-6, IFNγ и TGF-β) при снижении IL-10. Уровень сывороточного IL-1 у лиц с метаболическим синдромом находился в пределах нормы. Вместе с тем у пациентов с метаболическим синдромом имело место достоверное уменьшение содержания в крови СD3- и СD4-Т-лимфоцитов и, напротив, повышение числа активированных Т- (СD25+) и В (СD23+)-лимфоцитов, а также моноцитов (CD14+). Выявленные изменения характеризуют наличие у больных метаболическим синдромом субклинического хронического воспаления, которое может быть следствием компенсаторных иммунных реакций, развивающихся на фоне ослабления адаптивного иммунитета

    A NEW SCHEME FOR MOTOR PROTECTION COMPRESSOR TRAINS SERIES ER2

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    The new scheme of protection of the engine DK 409 (DK406) of the compressor (EK 7B) on electric trains of series ER2 is offered. Such a scheme provides accurate and reliable protection of the electric machine, unites in itself the protection functions both under overloads with long-term currents and in case of short-circuit

    Нова схема захисту двигуна компресора на електропоїздах серії ЕР2

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    The new scheme of protection of the engine ДК 409 (ДК 406) of the compressor (ЭК 7Б) on electric trains of series ЭР2 is offered. Such a scheme provides accurate and reliable protection of the electric machine, unites in itself the protection functions both under overloads with long-term currents and in case of short-circuit.Предложена новая схема защиты двигателя ДК 409 (ДК 406) компрессора (ЭК 7Б) на электропоездах серии ЭР2. Такая схема обеспечивает четкую и надежную защиту электрической машины, объединяет в себе функции защиты как при перегрузках длительными токами, так и в случае К.З.Запропоновано нову схему захисту двигуна ДК 409 (ДК 406) компресора (ЕК 7Б) на електропоїздах серії ЕР2. Така схема забезпечує чіткий і надійний захист електричної машини, поєднує в собі функції захисту як при перевантаженні тривалими струмами, так й у випадку К.З

    Features of cellular immunity and cytokine repertoire in patients with metabolic syndrome

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    In the formation of metabolic syndrome there is a change of the quantitative characteristics of immunocompetent cells and blood cytokine profile. According to our study, the elevated serum content of inflammatory cytokines (IL-6, IFNγ and TGF-β), in the cases of IL-10 decrease, was detected in patients with metabolic syndrome. The level of serum IL-1 inpatients with metabolic syndrome was within normal parameters. With it, there was a significant decrease in the percentage of blood CD3- and CD4-T-lymphocytes, and, conversely, an increase in the number of activated T (CD25+) and B (CD23+)-lymphocytes and monocytes (CD14+) has been in patients with metabolic syndrome. This revealed changes, is characterized by the presence of subclinical chronic inflammation in metabolic syndrome patients. It can be the result of compensatory immune responses developing in the weakening of adaptive immunity
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