ssociation between serum visfatin and carotid atherosclerosis in diabetic and non-diabetic patients on maintenance hemodialysis

Abstract

IntroductionAdipose tissue releases bioactive factors termed adipokines. Visfatin is an adipokine that plays an active role promoting vascular inflammation and atherosclerosis. The purpose of this study was to determine the association between serum visfatin levels and carotid atherosclerosis in diabetic and non-diabetic patients on maintenance hemodialysis (HD) in order to clarify the role of serum visfatinas, a risk factor for cardiovascular complications in HD patients.MethodsForty patients on maintenance hemodialysis were enrolled in this case-control study in 2015. They were subdivided into two groups, i.e., a diabetic group (n = 20) and a non-diabetic group (n = 20). Twenty healthy subjects who were age and gender matched were included as a control group. Carotid Duplex studies were performed on all patients, and serum visfatin was determined by a competitive enzyme immunoassay.ResultsHD patients showed a highly significant increase in serum visfatin, urea, creatinine, Ca×Ph, K, fasting glucose, triglycerides, LDL levels, and a significant decrease in eGFR, Na, HDL, and Hb compared to the control group. Also, serum visfatin levels showed a highly significant increase in the diabetic HD group compared to both the non-diabetic HD and control groups. Serum visfatin showed a highly significant increase in non-diabetic HD patients compared to the control group. Carotid intima-media thickness (IMT) showed a highly significant increase in HD group compared to the control group. Serum visfatin correlated positively with serum urea, creatinine, glucose, and IMT, but it was negatively correlated with eGFR, Na, and HDLConclusionWe concluded that serum visfatin is increased in HD patients with and without diabetes. Moreover, its association with IMT may be involved in the pathogenesis of atherosclerosis in CRF patients.

Antioxidative, anti-inflammatory and anti-apoptotic effects of ellagic acid in liver and brain of rats treated by D-galactose

“…It has been demonstrated that oxidative stress is one of the key factors responsibl e for liver damage and brain ageing via oxidative injury, as revealed by the over-production of the lipid peroxidation marker MDA and the increasing antioxidant activities of CAT, GSH-Px, SOD, and T-AOC. SOD is the first gatekeeper in the antioxidant defence system by catalysing the dismutation of the superoxide anion to oxygen and hydrogen peroxide (H 2 O 2 ), the latter of which is further metabolized by CAT or GSH-Px 43 – 45 . T-AOC is representative of all antioxidants, and MDA is well-recognized not only as an indicator of ageing but also as the most important product of membrane lipid peroxidation, and thus, it indirectly reflects the level of cell oxidative damage.…”

The evaluation of serum biomarkers in patients with sarcoidosis: Can visfatin be a new biomarker for sarcoidosis?

“…Under different conditions including metabolic syndrome, type 2 DM, rheumatic disease, and hemodialysis, visfatin had a positive correlation with the presence and severity of the disease [33,34].…”

Visfatin/eNampt induces endothelial dysfunction in vivo: a role for Toll-Like Receptor 4 and NLRP3 inflammasome

“…*p < 0.05 vs respective basal values in the absence of visfatin/eNampt. Indeed, the link between visfatin/eNampt and cardiovascular diseases has been even reinforced by more recent reports 28,29 , both in the presence or in the absence or metabolic alterations 19,30,31 . A common ground of clinical studies linking visfatin/eNampt with cardiovascular diseases highlights the clear relationship between this adipokine and a pro-inflammatory context [32][33][34] .…”