Diabetic neuropathy is a painful consequence of diabetes mellitus that affects millions of people. It is characterized by nerve injury resulting from elevated blood glucose levels. Numerous symptoms, including pain, numbness, muscular weakness, autonomic dysfunction, and foot ulcers, may be brought on by diabetic neuropathy, which can seriously impact a person's quality of life. According to estimates, the incidence of neuropathy is above 50% in patients with chronic illness and around 8% in people with a recent diagnosis. Sensorimotor and autonomic neuropathies are the two most common forms of diabetic neuropathy. Pain, paraesthesia, and a lack of sensation are symptoms of sensorimotor neuropathy, while myocardial infarction, arrhythmia, and unexpected death are symptoms of autonomic neuropathy. In addition to glycaemic management, there is no other treatment for preventing sensorimotor and autonomic neuropathies. Patients with cardiovascular autonomic neuropathy should undergo extensive diabetic treatment, multifactorial cardiovascular risk reduction, and lifestyle modification. Tricyclic antidepressants, serotonin and norepinephrine reuptake inhibitors, gabapentin, pregabalin, and opioids are used to alleviate sensory neuropathy. The goal of this chapter is to provide a comprehensive analysis of the pathophysiology of diabetic neuropathy, along with a discussion of the underlying molecular mechanisms and pathways. This includes the influence of hyperglycemiaon nerve function, aberrant glucose metabolism, the involvement of advanced glycation end products (AGEs), and inflammatory and immune-mediated processes.