Cross-cultural validation of the sports performance questionnaire in Chinese adolescent football players: a confirmatory factor analysis study.

Diabetic neuropathy is among the most common complications in type 1 and type 2 diabetes mellitus (T1DM & T2DM) (). According to the International Diabetes Federation (IDF) in 2025, an estimated 589 million adults (11.1% of world population) aged 20–79 years worldwide are living with diabetes mellitus (DM). By 2050, the total number of adults living with DM is projected to rise to 853 million (13% of world population) (). Diabetic polyneuropathy (DPN) is the most prevalent chronic complication of T1DM and T2DM, involving over half of all diabetic persons, significantly compromising patients’ quality of life and contributing to elevated morbidity and mortality rates (). DPN develops within 10 years of the onset of diabetes in T1DM patients, while for T2DM patients, DPN may already be present at the time of diagnosis or preceding this, in the prediabetes stage (). For example, in patients diagnosed with diabetes, it is estimated that over 20% already have DPN (). DPN imposes a substantial economic burden on healthcare systems, patients and families (). The disorder is characterized by a degenerative symmetrical loss of distal axons, starting in the extremities, recognized as a ‘glove and stocking syndrome’, leading to sensory loss and neuropathic pain. Autonomic dysfunction and later motor dysfunction are also features, not discussed here. DPN is a leading cause of foot ulceration and lower limb amputations. Key pathogenic pathways or mechanisms identified include activation of the polyol pathway resulting in sorbitol accumulation, increased oxidative stress, mitochondrial dysfunction, accumulation of advanced glycation end products (AGEs) and perhaps microvascular impairment (). While DPN can sometimes be prevented or delayed with careful glycemic control, established DPN is often irreversible (). In work to date, interventions to reverse neuronal metabolic targeting include aldose reductase inhibitors, sodium-glucose cotransporter 2 (SGLT2) inhibitors, glucagon-like peptide-1 (GLP-1) receptor agonists or others. These have all had varying but not robust impacts on DPN (–). Current management strategies primarily focus on controlling hyperglycemia, alleviating symptoms of diabetes and controlling pain. Disease-modifying treatments capable of arresting or reversing progressive axon loss in DPN remain elusive. The most prevalent diabetic neuropathy is distal symmetric polyneuropathy (diabetic polyneuropathy; referred to here as DPN), accounting for approximately 75% of patients with diabetic neuropathy (). Symptoms of DPN include ‘stocking and glove’ pattern numbness, pain, with weakness of distal extremities in more advanced disease. Approximately 10% to 30% patients diagnosed with DPN have neuropathic pain depending on the populations studied (–). DPN is associated with unrecognized injuries, ulcerations, and amputations, as individuals may not detect harmful stimuli, leading to increased mortality: 5-year mortality rates of patients with diabetic foot ulcers was 2.5 times higher than in patients without foot ulcers (). According to a study conducted among Chinese and European persons, painful DPN may be particularly prevalent in patients diagnosed with diabetes of durations less than 10 years or alternatively longer, in those with DM of more than 15 years. Older age, female gender, and BMI ≥ 30 kg/m were also risk factors of painful diabetic neuropathy (PDN) (). Early small fiber involvement is associated with burning pain, painful paraesthesiae, pinprick insensitivity, hyperalgesia, and allodynia. Large fiber involvement can cause numbness, loss of vibration and proprioception, paraethesiae, motor weakness, and imbalance with unintentional injury (, , ).