Effect of Metformin and Sulfonylurea on C-Reactive Protein Level in Well-Controlled Type 2 Diabetics with Metabolic Syndrome

Abstract

The objective of this study was to examine the effect of the antihyperglycemic agents metformin (insulin sensitizer) and glibenclamide (insulin secretory agent) on the serum level of C-reactive protein (CRP) in well-controlled type 2 diabetics with metabolic syndrome. The participants were diabetic patients being followed in the medical outpatient clinic of King Abdulaziz University Hospital. The inclusion criteria were type 2 diabetics with the metabolic syndrome, well-controlled blood glucose on metformin alone or glibenclamide alone, and exclusion of major medical illness. Patients were divided into two groups according to the antihyperglycemic agent used. CRP level was measured 4-wk apart and the mean was calculated. The following data were collected from the study groups: age, sex, body mass index (BMI), duration of diabetes, smoking history, presence of hypertension, hyperlipidemia, and mean CRP level. A total of 110 patients were studied, 65 using metformin and 45 using glibenclamide. CRP level was significantly lower in patients using metformin for blood glucose control compared with those using glibenclamide, 5.56 and 8.3 mg/L, respectively (p = 0.01). A significantly higher level was observed in hypertensive and hyperlipidemic patients compared with normotensive and normolipidemic, 5.3 vs 3.2 mg/L and 7.1 vs 4.3 mg/L, respectively (p = 0.02, 0.01). There was a statistically significant correlation between CRP and BMI (r = 0.37) and age (r = 0.36) (all p = 0.01). The data showed that metformin decreases the level of circulating CRP, a marker of inflammation, more than glibenclamide.

Both slow-release and regular-form metformin improve glycemic control without altering plasma visfatin level in patients with type 2 diabetes mellitus

“…Decreased CRP levels have been seen in type 2 diabetes mellitus after treatment with thiazolidinedione (TZD) [23,28], sulfonylurea [29], and metformin [14,23,[30][31][32]. However, one study reported that metformin did not reduce CRP levels [29].…”

AMP-activated protein kinase: an emerging drug target to regulate imbalances in lipid and carbohydrate metabolism to treat cardio-metabolic diseases

“…while metformin affects hsCRP levels in much greater extent than insulin secretagoge glibenclamide ( 185,187 ), both metformin and PPAR-␥ agonist rosiglitazone, which also promotes AMPK activity ( 29 ), were similarly effective in controlling infl ammatory markers in addition to metabolic parameters ( 186 ).…”

An immune origin of type 2 diabetes?

“…Here, again, polymorphisms in immune genes modulate risk, implying a pathogenetic significance for immune gene products Table 4 Interventions that have an impact on the inflammatory state Inflammatory mediators whose concentrations are reduced by weight loss and/or physical exercise [190][191][192][193][194][195][196][197][198][199][200][201][202][203][204][205][206][207] CRP, TNF-α, soluble TNF-α receptor 2, IL-6, IL-18, MCP-1, PAI-1, t-PA, soluble ICAM-1, soluble VCAM-1, P-selectin Inflammatory mediators whose concentrations are reduced by glucose-lowering drugs [186,188,[208][209][210][211][212][213][214][215][216][217] Sulphonylurea: TNF-α Metformin: CRP Glitazones: CRP, SAA, TNF-α, soluble CD40 ligand, PAI-1 Insulin: CRP, IL-1, IL-6, TNF-α, soluble ICAM-1, MCP-1, PAI-1 SAA Serum amyloid A, t-PA tissue plasminogen activator, VCAM-1 vascular cell adhesion molecule-1 [171][172][173]. Where studied, the upregulation of inflammatory mediators was linked to increased oxidative stress, impaired mitochondrial function and abnormal cholesterol metabolism [174][175][176].…”