Diabetes mellitus results in neuropathy of both somatic and visceral nerves. In diabetic patients with faecal incontinence, impaired rectal sensory function, manifested by a decreased sensitivity to balloon distention is common. This may contribute to unawareness of rectal filling and incontinence. There has been little study to date of visceral mechanosensation in experimental diabetes however. We hypothesized that experimental diabetes would impair mechanosensitivity in rectal afferent nerves. Diabetes was induced in rats by i.p. injection of streptozotocin. Controls were injected with citrate. In vitro recordings were performed from rectal afferent nerves innervating isolated segments of rectum. In control animals, three distinct populations of mechanosensitive fibres were identified. Low threshold fibres responded at low intensity stretch and reached a maximal firing rate at less than 10 g of stretch (11/24 units). Wide dynamic sensitivity units responded at low intensity stretch (<2 g) but encoded stimulus intensity in a linear fashion up to 20 g (12/24 units). High threshold units responded at greater than 5 g. In diabetic animals there was a near complete loss of LT units (1/19) and most (16/29) had properties similar to WD units. However, their response threshold was significantly increased. Firing rates in response to maximal distention did not change in diabetic animals. We conclude that experimental diabetes selectively affects the detection of low threshold ‘physiologic’ rectal distention, such as that which might occur during rectal filling, prior to defaecation.