Increased Serum WISP1 Levels are Associated with Lower Extremity Atherosclerotic Disease in Patients with Type 2 Diabetes Mellitus

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Abstract

Background Serum wnt1-induced signaling pathway protein 1 (WISP1) levels are increased with obesity, which is a common complication associated with lower extremity atherosclerotic disease (LEAD). However, to date, the relationship between elevated WISP1 levels and the incidence of lower extremity atherosclerotic disease (LEAD) in type 2 diabetes mellitus (T2DM) remains unclear.

Methods 174 newly diagnosed type 2 diabetic patients were enrolled in our study. Patients were divided into two groups, LEAD group (n=100) and control group (n=74). Anthropometric parameters, blood pressure and some biochemical parameters were obtained. Body composition was detected by bioelectrical impedance analysis (BIA). Levels of serum insulin were determined by radioimmunoassay. Serum WISP1 and interleukin 6 (IL-6) levels were determined using an enzyme-linked immunosorbent assay.

Results It was shown that serum WISP1 levels in diabetic patients with LEAD were higher than those without LEAD (P<0.001). Serum WISP1 levels were positively related with waist circumference (r=0.237, P=0.003), waist-hip ratio (r=0.22, P=0.006), visceral fat area (r=0.354, P<0.001), serum creatinine (r=0.192, P=0.012), interleukin 6 (r=0.182, P=0.032), c-reactive protein (r=0.681, P<0.001), triglycerides (r=0.119, P<0.001), fasting glucose (r=0.196, P=0.011), glycated hemoglobin (r=0.284, P<0.001), and HOMA-IR (r=0.285, P<0.026). Compared with the lowest tertile, the odds ratio of the middle tertile for LEAD incidence was 3.27 (95% CI, 1.24–8.64) and 4.46 (95% CI, 1.62–12.29) for the highest tertile after adjusting confounding factors.

Conclusion The results suggest that increased serum WISP1 levels independently contribute to the incidence of LEAD in patients with newly diagnosed T2DM.

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Victor Aboyans, Jean-Baptiste Ricco, Marie-Louise E L Bartelink … (2018)

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Atherosclerosis and inflammation: overview and updates

Glaucylara Reis Geovanini, Peter Libby (2018)

The concept that inflammation participates pivotally in the pathogenesis of atherosclerosis and its complications has gained considerable attention, but has not yet entered clinical practice. Experimental work has elucidated molecular and cellular pathways of inflammation that promote atherosclerosis. The recognition of atherogenesis as an active process rather than a cholesterol storage disease or a repository of calcium has highlighted some key inflammatory mechanisms. For example, mononuclear phagocytes contribute to all stages of this disease, illustrating the link between inflammation and atherosclerosis. From a clinical perspective, harnessing inflammation may now help target therapeutics, change guidelines, and enter daily practice. Multiple lines of incontrovertible evidence have proven a causal role for low-density lipoprotein (LDL) cholesterol in atherosclerosis, and we have highly effective tools for lowering LDL, consequently reducing events. Yet, even with intense LDL reduction, events still occur. Inflammation can explain some of this residual risk. An anti-inflammatory intervention has now proven capable of improving outcomes in individuals well treated with LDL-lowering agents. A suite of trials are now pursuing anti-inflammatory therapies in this context. Assessment and treatment of residual inflammatory risk are poised to provide new inroads into preventive cardiology. This brief review aims to explore the potential mechanisms underlying the association of inflammation and atherogenesis, and their clinical consequences.