Luciano Ramos de Lima, Marina Morato Stival, Silvana Schwerz Funghetto, Cris Renata Grou Volpe, Izabel Cristina Rodrigues da Silva, Calliandra Maria de Souza Silva, Alessandro de Oliveira Silva & Mani Indiana Funez
Diabetic neuropathy (DN) is one of the main complications of diabetes mellitus (DM), affecting up to 50% of patients. DN causes progressive nerve degeneration and ranges from asymptomatic to physically disabling. Patients with DN may have neuronal damage, sensory neuron changes, and peripheral nerve involvement, with pain also reported, especially in type 2 DM (T2DM) patients. However, the diagnosis is often late, contributing to ulcer formation and up to 70% of limb amputations [1, 2], affecting the DM patients’ quality of life [3, 4].
Some studies investigated DN in T2DM individuals and identified DN risk factors as DM duration, advanced age, high glycated hemoglobin levels, smoking, and obesity [5, 6]. Identifying the modifiable DN risk factors and effectively controlling them is essential for successful DM management and preventing severe consequences of the disease. Hence, risk factors must be known and evaluated to optimize patient care [7].
The relationship between inflammation, obesity, and insulin resistance is well established and may play a role in DN pathogenesis. A critical component of the inflammatory response is the increase in cytokine levels [8]. Studies show higher inflammatory cytokine levels such as tumor necrosis factor (TNF-α), IL-6, and IL-1β in DN individuals [9, 10].
TNF-α is involved in deleterious inflammatory responses in DM individuals [11]. Furthermore, polymorphisms in specific cytokine genes, such as TNF-α, may be risk factors for DN development [11–16]. Although TNF-α genetic variations have been studied in the DN context, the TNF-α-308G/A polymorphism association with DN susceptibility has been diverging [13–15]. This study investigated the relationship between TNF-α serum levels and the TNF-α-308G/A polymorphism influence on the DN presence.
