Pathogenesis of insulin resistance in metabolic obesity

Litvinova, L. S.; Kirienkova, E. V.; Мазунин, И. О.; Vasilenko, M. A.; Fattakhov, Nikolai

doi:10.1134/s1990750814030093

Cited by 7 publications

(7 citation statements)

References 100 publications

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“…In obesity, the increased production of inflammation mediators in the adipose tissue, liver, pancreas and skeletal muscles causes subclinical metabolic inflammation [ 5 , 8 , 9 ]. This inflammation affects the metabolic and secretory function of adipose tissue and plays a leading role in the development of obesity accompanying MS, type 2 diabetes mellitus and atherosclerosis [ 10 – 12 ]. The main source of proinflammatory mediators in this process are CD14 + cells [ 11 ].…”

Section: Introductionmentioning

confidence: 99%

Role of adiponectin and proinflammatory gene expression in adipose tissue chronic inflammation in women with metabolic syndrome

Litvinova

Atochin

Vasilenko

et al. 2014

Diabetol Metab Syndr

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BackgroundThe purpose of this research was to study the gene expression of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), nuclear factor kappa B (NF-κB), vascular endothelial growth factor A (VEGF-A) and adiponectin (AdipoQ) genes in the visceral (omental, mesenteric) and subcutaneous adipose tissue depots in metabolic syndrome (MS).We studied 23 women with MS, with a mean age of 50.7 ± 4.5 years and mean body mass index (BMI) of 45.6 ± 9.8 kg/m2. The control group included 10 women, with a mean age of 40.6 ± 8.7 years and normal BMI (22.3 ± 3.7 kg/m2). The gene expression levels in the omental (OAT), mesenteric (MAT) and subcutaneous (SAT) adipose tissues were assessed by quantitative real-time PCR.FindingsIncreased gene expression levels of IL-6 and TNF-α were detected in MAT in patients with MS, compared with the control group (p < 0.05 and p < 0.005, respectively). Significant positive correlations were observed between IL-6 mRNA expression levels in OAT and the content of CD14 + cells in the peripheral blood (r = 0.55, p < 0.05), as well as between NF-κB and VEGF-A mRNA levels in OAT (r = 0.43, p < 0.05) in patients with MS. The AdipoQ gene expression levels in OAT were significantly decreased in women with MS compared with the control group (p < 0.05). In addition, there were inverse correlations between AdipoQ gene levels in MAT and serum CRP levels (r = −0.63, p < 0.05), as well as between AdipoQ gene levels in MAT and serum IL-6 levels (r = −0.46, p < 0.05).ConclusionThese data demonstrate that proinflammatory gene expression of MAT in women with MS was increased compared with the control group. The AdipoQ gene expression levels in OAT were significantly decreased in women with MS compared with the control group.

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Section: Introductionmentioning

confidence: 99%

Role of adiponectin and proinflammatory gene expression in adipose tissue chronic inflammation in women with metabolic syndrome

Litvinova

Atochin

Vasilenko

et al. 2014

Diabetol Metab Syndr

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“…This results in autophosphorylation and activation of its tyrosine kinase function. The β-subunit can autophosphorylate, and it can phosphorylate other proteins or intracellular substrates, such as insulin receptor substrate 1 (IRS-1), insulin receptor substrate 2 (IRS-2), and the Src homology collagen (Shc) family of proteins (Hirabara et al, 2014;Litvinova et al, 2014).…”

Section: Etiologic Factors Of Insulin Resistancementioning

confidence: 99%

“…The action of insulin is mediated by three main signaling cascades: the phosphatidyl inositol 3-kinase (PI3K)/protein kinase B (Akt) pathway, the Cbl associated protein (CAP)/Cbl pathway, and the Ras/mitogen-activated protein kinase (MAPK) pathway. These pathways regulate relevant cellular processes, such as glucose uptake, protein synthesis, and the expression of genes involved in cellular proliferation and differentiation (Litvinova et al, 2014).…”

Section: Etiologic Factors Of Insulin Resistancementioning

confidence: 99%

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The role of selenium in insulin resistance

Fontenelle

Feitosa

Morais

et al. 2018

Braz. J. Pharm. Sci.

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In recent years, there has been growing interest in clarifying the pathogenesis of some chronic diseases, such as obesity and type 2 diabetes mellitus. Metabolic alterations in these diseases are characterized by chronic hyperglycemia and insulin resistance. Studies have demonstrated the participation of minerals in the pathogenesis of insulin resistance, more specifically their involvement in the synthesis and regulation of insulin. Selenium is an anti-inflammatory and antioxidant micronutrient that is essential for the activity of selenoproteins. Two selenoproteins (glutathione peroxidase and selenoprotein P) are known to be involved in the insulin signaling pathway. The aim of this review is to provide an update on the role of selenium in insulin resistance mechanisms. Evidence shows that adequate concentrations of selenium play a key role in the secretion and action of insulin, but an excess of selenium in the body is associated with the pathogenesis of insulin resistance and the development of diabetes mellitus.

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“…It is still unclear whether mitochondrial dysfunction results from or causes insulin resistance (Martin and McGee, 2014 ). One of the key pathophysiological factors underlying the formation of insulin resistance may be the dysregulation of energy metabolism in insulin-sensitive tissues such as skeletal muscle, liver, and adipose (Litvinova et al, 2014 ). Particularly, in skeletal muscle, decreased mitochondrial respiration capacity, reduced ATP production, and increased ROS levels lead to reduced fatty acid oxidation and increased cytosolic free fatty acid levels, resulting in insulin resistance and T2DM (Pagel-Langenickel et al, 2010 ).…”

Section: Metabolic Syndrome and Mitochondrial Dysfunctionmentioning

confidence: 99%

Nitric oxide and mitochondria in metabolic syndrome

et al. 2015

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Metabolic syndrome (MS) is a cluster of metabolic disorders that collectively increase the risk of cardiovascular disease. Nitric oxide (NO) plays a crucial role in the pathogeneses of MS components and is involved in different mitochondrial signaling pathways that control respiration and apoptosis. The present review summarizes the recent information regarding the interrelations of mitochondria and NO in MS. Changes in the activities of different NO synthase isoforms lead to the formation of metabolic disorders and therefore are highlighted here. Reduced endothelial NOS activity and NO bioavailability, as the main factors underlying the endothelial dysfunction that occurs in MS, are discussed in this review in relation to mitochondrial dysfunction. We also focus on potential therapeutic strategies involving NO signaling pathways that can be used to treat patients with metabolic disorders associated with mitochondrial dysfunction. The article may help researchers develop new approaches for the diagnosis, prevention and treatment of MS.

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Pathogenesis of insulin resistance in metabolic obesity

Cited by 7 publications

References 100 publications

Role of adiponectin and proinflammatory gene expression in adipose tissue chronic inflammation in women with metabolic syndrome

Role of adiponectin and proinflammatory gene expression in adipose tissue chronic inflammation in women with metabolic syndrome

The role of selenium in insulin resistance

Nitric oxide and mitochondria in metabolic syndrome

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