الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
Diabetes mellitus (DM) may be defined as a state of chronic hyperglycemia caused by either relative or absolute deficiency in the level of blood insulin. A huge number of people in the world suffer from diabetes; the alarming increase in incidence of DM makes it a serious health problem. The persistent hyperglycemia in diabetic patients is the inducer of DM complications, such as coronary artery disease, hyperlipidemia, cerebrovascular disease, blindness, renal failure, neurological complications, limb amputation, and premature death.
Many proinflammatory cytokines play a central role in inflammatory reaction and were shown to increase the risk of T2DM. These pro-Inflammatory cytokines can enhance insulin resistance directly in adipocytes, muscle and hepatic cells, leading to systemic disruption of insulin sensitivity and impaired glucose homeostasis. Increased levels of these pro-inflammatory cytokines lead to hepatic production and secretion of acute-phase proteins such as C-reactive protein (CRP), Tumor Necrosis Factor Alpha (TNF-α), Interleukins. These proteins appear in the early stages of T2DM, and their circulating concentrations increase as the disease progresses
Our data support the concept that subclinical activation of the immune system is involved in the pathogenesis of type 2 diabetes. We demonstrated that a specific pattern of cytokines was associated with an increased risk of type 2 diabetes, rather than isolated elevation of the respective cytokines
Diabetes itself, characterized as a state of low grade inflammation, T2DM is found to display increased transcriptional rate of C-reactive protein (CRP) and pro-inflammatory cytokines, such as tumor necrosis factor-α (TNF-α) and interleukins1 and 6 (IL-1, IL-6), which are implicated in investigating metabolic insulin resistance.