Abstract
Hyperglycemia is the hallmark of diabetes mellitus [DM]; it activates certain biochemical pathways leading to micro- and macrovascular complications in diabetic patients. Moreover, hyperglycemia generates oxidative stress and causes free radicalmediated lipid peroxidation. In turn, the oxidative stress causes endothelial dysfunction, and has been suggested as one of the important mechanisms underlying the onset and progression of diabetic vascular complications.
Highlights
Hyperglycemia is the hallmark of diabetes mellitus [DM]; it activates certain biochemical pathways leading to micro- and macrovascular complications in diabetic patients [1]
It has been reported that the prevalence of vascular complications in diabetic patients with Gilbert syndrome, a congenital hyperbilirubinemia, is lower compared with in those without this syndrome [7]
In accordance with the results of this previous animal study, several literatures have reported the association between diabetic microvascular complications and bilirubin by comparing serum bilirubin concentrations in diabetic patients with and without microvascular complications such as neuropathy [9], nephropathy [10], and retinopathy [11,12]
Summary
Hyperglycemia is the hallmark of diabetes mellitus [DM]; it activates certain biochemical pathways leading to micro- and macrovascular complications in diabetic patients [1]. Hyperglycemia generates oxidative stress and causes free radicalmediated lipid peroxidation [2,3]. The oxidative stress causes endothelial dysfunction, and has been suggested as one of the important mechanisms underlying the onset and progression of diabetic vascular complications [4].
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