Abstract
This study investigated the relationship between serum xanthine oxidase (XOD) activity and the occurrence of diabetic peripheral neuropathy (DPN) in type 2 diabetes mellitus (T2DM) patients. Serum XOD activity, ischemia-modified albumin (IMA), uric acid (UA), albumin, glycated hemoglobin (HbA1c), advanced glycation end products (AGE), total free thiols, atherogenic index of plasma (AIP), and body mass index (BMI) were measured in 80 T2DM patients (29 with and 51 without DPN), and 30 nondiabetic control subjects. Duration of diabetes, hypertension, medication, and microalbuminuria was recorded. Serum XOD activities in controls, non-DPN, and DPN were 5.7 ± 2.4 U/L, 20.3 ± 8.6 U/L, and 27.5 ± 10.6 U/L (p < 0.01), respectively. XOD activity was directly correlated to IMA, UA, BMI, HbA1c, and AGE, while inversely correlated to serum total free thiols. A multivariable logistic regression model, which included duration of diabetes, hypertension, AIP, HbA1c, UA, and XOD activity, revealed HbA1c [OR = 1.03 (1.00–1.05); p = 0.034] and XOD activity [OR = 1.07 (1.00–1.14); p = 0.036] as independent predictors of DPN. Serum XOD activity was well correlated to several other risk factors. These results indicate the role of XOD in the development of DPN among T2DM patients.
Highlights
Diabetic peripheral neuropathy (DPN) is a late-stage microvascular complication that develops in nearly 50% patients during the course of type 2 diabetes mellitus (T2DM), affecting low extremities
There were no significant differences between control and groups with DM, in terms of age and sex distribution, smoking status, presence of hypertension, serum creatinine, and total protein levels (Table 1)
Serum xanthine oxidase (XOD) activity was well correlated to the levels of ischemia-modified albumin (IMA) and some other biomarkers of increased reactive oxygen species (ROS) formation
Summary
Diabetic peripheral neuropathy (DPN) is a late-stage microvascular complication that develops in nearly 50% patients during the course of type 2 diabetes mellitus (T2DM), affecting low extremities. Metabolic-vascular interactions in DPN are highly complex and include diverse molecular pathways, like activation of protein kinase C and polyol metabolism, glycation and glycoxidation, low-grade inflammation, and excessive formation of reactive oxygen species (ROS), such as superoxide and hydrogen peroxide [4]. In vascular compartment these ROS can react with intrinsic vasodilator nitric oxide, and while the fall of nitric oxide levels would cause vasoconstriction, the resulting peroxynitrite could trigger the downstream events leading to nerve damage [5]
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