Abstract
AimTo evaluate the serum concentrations of inflammatory mediators in patients with type 2 diabetes mellitus (T2DM) with or without renal alteration (RA) function.MethodsSerum samples from 76 patients with T2DM and 24 healthy individuals were selected. Patients with T2DM were divided into two groups according to eGFR (> or < 60mL/min/1.73m2). Cytokines, chemokines and adipokines levels were evaluated using the Multiplex immunoassay and ELISA.ResultsTNFR1 and leptin were higher in the T2DM group with RA than in the T2DM group without RA and control group. All patients with T2DM showed increased resistin, IL-8, and MIP-1α compared to the control group. Adiponectin were higher and IL-4 decreased in the T2DM group with RA compared to the control group. eGFR positively correlated with IL-4 and negatively with TNFR1, TNFR2, and leptin in patients with T2DM. In the T2DM group with RA, eGFR was negatively correlated with TNFR1 and resistin. TNFR1 was positively correlated with resistin and leptin, as well as resistin with IL-8 and leptin.ConclusionIncreased levels of TNFR1, adipokines, chemokines and decrease of IL-4 play important role in the inflammatory process developed in T2DM and decreased renal function. We also suggest that TNFR1 is a strong predictor of renal dysfunction in patients with T2DM.
Highlights
Type 2 diabetes mellitus (T2DM) is one of the most prevalent subtypes of diabetes mellitus (DM)
tumor necrosis factor receptor-1 (TNFR1) and leptin were higher in the T2DM group with renal alteration (RA) than in the T2DM group without RA and control group
Adiponectin were higher and IL-4 decreased in the T2DM group with RA compared to the control group. estimated glomerular filtration rate (eGFR) positively correlated with IL-4 and negatively with TNFR1, TNFR2, and leptin in patients with T2DM
Summary
Type 2 diabetes mellitus (T2DM) is one of the most prevalent subtypes of diabetes mellitus (DM). It is a metabolic disorder resulting from the relative deficiency of insulin production and/or its action, which leads to increased serum glucose levels, which is considered the main cause of chronic kidney disease (CKD) [1, 2]. Hyperglycemia in T2DM is strongly associated with the development of macrovascular and microvascular complications, which may result in decreased renal function.[3] Studies suggest that low-grade inflammation, characterized by the production of cytokines, chemokines, and adipokines, is involved in the pathogenic processes that cause T2DM and its complications [4,5,6,7]. Diabetes and inflammation are simultaneously involved, feeding a positive feedback loop [8]
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