“…The diabetic duration, homeostasis model assessment for insulin resistance, haemoglobin A 1c , and increased glycaemic variability assessed by the mean amplitude of glycaemic excursions are all independent contributors to diabetic peripheral neuropathy in type 2 diabetic (T2D) patients. 3 The pathological mechanisms of diabetic neuropathy are nearly the same as diabetic retinopathy and nephropathy, such as oxidative stress, increased advanced glycation end products and their receptors, activation of the polyol pathway, inducible nitric oxide synthase, and activation of mitogen-activated protein kinases and protein kinase C. Moreover, increased cytokines (eg, nerve growth factor, tumour necrosis factor [TNF] α, and interleukin 6), hypoxia, and ischaemia deficiency are crucial etiologic roles for diabetic neuropathy. 4 Consistent with these findings, dysfunctional metabolic pathways in diabetes result in functional disorder, damage, and cell death, which are inherent to the peripheral nervous system (eg, Schwann cells, dorsal root ganglia neurons, and vasa nervorum).…”