Systemic Inflammation In Type Research Articles

Plasma concentration of visfatin is a new surrogate marker of systemic inflammation in type 2 diabetic patients

It is not clear whether plasma visfatin level is related with systemic inflammation or diabetic nephropathy in diabetic patients. In this study, we investigated the relationship between plasma visfatin levels and systemic inflammation or diabetic nephropathy in type 2 diabetic patients. In addition, we examined the physiological action of visfatin in cultured adipocytes in diabetic condition. Plasma visfatin concentrations were significantly higher in the diabetic groups than in the controls. Plasma visfatin levels were positively correlated with systolic blood pressure, body weight, fasting blood glucose, plasma levels of MCP-1, urinary albumin excretion (UAE), and carotid intima-media thickness (IMT), and were inversely correlated with plasma adiponectin, and creatinine clearance. However, plasma visfatin concentrations did not show a significant relationship with HbA1C, BMI or HOMA-IR. Regression analysis showed that plasma levels of MCP-1 and UAE were only independent determinants of plasma visfatin concentration. In cultured adipocytes, high glucose and angiotensin II stimuli markedly increased visfatin synthesis. Exogenous visfatin treatment significantly decreased differentiation of adipocytes and increased NF-κB transcriptional activity and pro-inflammatory molecules in adipocytes. These findings suggest that visfatin synthesis is activated from adipose tissue in a diabetic environment, induces NF-κB activation and leads to activation of pro-inflammatory cytokines and systemic inflammation.

Relation of abdominal fat depots to systemic markers of inflammation in type 2 diabetes.

OBJECTIVEBoth visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) have been linked to systemic inflammation in nondiabetic cohorts. We examined the relationships between VAT and SAT and systemic inflammatory markers in a large well-characterized cohort of subjects with type 2 diabetes.RESEARCH DESIGN AND METHODSThree hundred eighty-two subjects with type 2 diabetes in the CHICAGO (Carotid Intima-Media Thickness in Atherosclerosis Using Pioglitazone) study cohort underwent abdominal computed tomography to determine SAT and VAT distribution. Fasting blood was obtained for measurement of inflammatory markers. The relationships between inflammatory markers and BMI, SAT, and VAT were examined using regression models adjusted for age, sex, diabetes treatment, duration of diabetes, smoking, statin use, and A1C.RESULTSVAT was positively related to CRP, monocyte chemoattractant protein (MCP), intracellular adhesion molecule (ICAM)-1, and plasminogen activator inhibitor type 1 (PAI-1) antigen before adjustment for BMI. After adjustment for BMI, the relationship to CRP was lost but positive associations with MCP (P < 0.01), PAI-1 (P < 0.0001), ICAM-1 (P < 0.01), and vascular cell adhesion molecule (P = 0.01) were evident. BMI was positively related to CRP (P < 0.0001) and IL-6 (P < 0.01) even after adjustment for VAT and SAT. SAT was not related to any inflammatory marker after adjustment for BMI.CONCLUSIONSIn this large group of subjects with type 2 diabetes, BMI was most strongly associated with CRP and IL-6 levels. SAT was not associated with markers of systemic inflammation. The size of the VAT depot provided information additional to that provided by BMI regarding inflammatory markers that are strongly related to vascular wall remodeling and coagulation. Our findings suggest that adipose tissue distribution remains an important determinant of systemic inflammation in type 2 diabetes.