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Recently except as energy depot fat is seen as an endocrine organ. As such it produces bioactive molecules, so called. adipokines, tattoo arm which are not only involved in both physiological and pathological processes in the adipose tissue, and deploying their effect in other organs. tattoo arm
Adipokines regulate glucose and lipid metabolism, hemostasis, hemodynamics, and immune processes in the CNS appetite. Obesity is associated with a chronic inflammatory reaction, which originate primarily in adipose tissue. Adipose tissue is infiltrated by inflammatory cells, primarily macrophages which secrete enhanced inflammatory adipokines. For example, obesity is measured in increased systemic levels of high-sensitivity C-reactive protein (hsCRP), interleukin 6 (IL-6) and tumor necrosis factor-alpha (TNF-α). tattoo arm 1, 2
The study Framingham Heart Study is one of the first epidemiological studies that establish the primeval relationship between obesity and cardiovascular disease. tattoo arm 3 For some of the existing adipose tissue inflammatory adipokines secreted has been demonstrated pathogenetic role in the occurrence of insulin resistance, type 2 diabetes, atherosclerosis and coronary heart disease (CVD).
Atherosclerosis is an inflammatory process, in which the base of the stand endothelial dysfunction. It is characterized by an imbalance between the endothelium-dependent vasodilation and vasoconstriction, as well as between the pro-and antithrombotic factors. Protein-1 (MCP-1, monocyte chemoattractant) is an inflammatory tattoo arm adipokines, whose concentrations in the blood and adipose tissue are increased in obesity. In its operation of the signal molecule to the cells of the immune system, MCP-1 stimulates the migration of leukocytes to the endothelium. 4
Acute phase protein prothrombotic - plasminogen activator inhibitor-1 (PAI-1) is produced by both the platelet and the adipose tissue and is elevated in the plasma of patients with obesity. PAI-1 blocks fibrinolysis by inhibiting plasminogen activation. Positively correlated with cardiovascular risk and mortality, as well as the emergence of type 2 diabetes mellitus. 5
Other adipokines tattoo arm known long involved in endothelial dysfunction and atherogenesis are IL-6, TNF-α, leptin, but CRP, which in addition to the liver, and is produced in adipose tissue. CRP is not limited to a predictive marker of cardiovascular event, but also directly affects the function of the endothelium, it increases the expression of adhesion tattoo arm molecules such as VCAM-1 and ICAM-1, which enhances the potency of other inflammatory adipokines as PAI-1, and blocks the production of vasodilator nitrogen monoxide (NO). Conversely 6 - adiponectin appears to have anti-inflammatory action ateroprotektivno. Low concentrations of adiponectin in the serum, they were measured in humans with obesity are independent prognostic tattoo arm indicator of endothelial dysfunction. 7
The open recently increased adipokines resistin expression tattoo arm of IL-6 and TNF-α in the adipose tissue of mice and induce insulin resistance in skeletal muscle tattoo arm and liver. The effect of resistin on glucose metabolism in humans has not yet been clarified unambiguously due to conflicting clinical data. Rezistinat stimulates the release of the strongest endogenous vasoconstrictor endothelin in endothelial cells, and induces the proliferation of cells of the vascular musculature. Thus, this also appears tattoo arm adipokines involved in pathogenic mechanisms that give rise to endothelial dysfunction. 2, 6
Initially osteopontinat is found in bone, wherein the form of the matrix protein is involved in mineralization, but also in their absorption. It has long been investigating its role in the occurrence of various inflammatory diseases such as rheumatoid arthritis, multiple sclerosis, but also in atherosclerosis. 8 Osteopontinat identified as adipokines until 2008, it is produced in adipose tissue almost exclusively of inflammatory macrophages. 9 In studies tattoo arm with genetically engineered mice showed that the absence of osteopontin improves insulin sensitivity in obesity. 10 Neutralization of osteopontin by special
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