Diabetic peripheral neuropathy (DPN) is the most common complication of diabetes. Half of DPN patients experience sensory deficits including loss of sensation and pain. Loss of sensation increases the risk of unnoticed foot injuries which combined with poor circulation and healing lead to amputation. Type 2 diabetes accounts for 50% of foot amputation highlighting the significant impact sensory loss can have on patients' quality of life. However, the cellular basis underlying sensory loss in DPN remains unclear. We characterised diabetes-induced neuronal loss and damage in dorsal root ganglia (DRG) in the db/db mouse model of type 2 diabetes. Morphometric characterisation was carried out on two neuronal populations in lumbar DRGs of 32-week diabetic (db/db) mice. These are the N200-positive neurons, a marker for low and high-threshold mechanosensitive sensory and proprioceptive neurons, and peripherin (PRPH)-positive neurons, a marker for pain sensing neurons. In diabetic mice, N200-positive neurons were reduced by 30%. Furthermore, diabetes increased the percentage of N200-positive neurons with cytoplasmic vacuoles, a sign of damage and stress, by 2.44 fold. In addition, the average number of vacuoles was 1.6 fold higher in diabetic mice. Therapies aimed at reducing this loss could help patients better protect their limbs from injuries and thus reduce amputations.