Delayed stomach to caecum transit time in the diabetic rat. Possible role of hyperglucagonaemia.

Disturbances of gastrointestinal motility are a common feature of diabetes mellitus and are usually ascribed to autonomic neuropathy. In order to assess the role of other factors on changes in motility in diabetes we have studied the stomach to caecum transit time (SCTT) during the progression of streptozotocin induced diabetes in the rat. Rats were used one, two, four, and eight weeks after a single injection of streptozotocin and age matched animals were used as controls. In further experiments non-diabetic rats received a bolus injection of pancreatic glucagon (50 or 75 micrograms intraperitoneally) or its diluent. SCTT was estimated using the non-invasive hydrogen excretion method. SCTT was unaffected by the age of the animal (mean (SEM) value: 101 (5) min), but was significantly delayed at one week (139 (11) min, p less than 0.01), two weeks (163 (16) min, p less than 0.01), four weeks (148 (9) min, p less than 0.01), and eight weeks (171 (13) min, p less than 0.01) after streptozotocin. SCTT was also slower during hyperglucagonaemia (control 96 (6) min; glucagon treated 50 micrograms: 120 (7) min, p less than 0.05 and 75 micrograms: 127 (8), p less than 0.05). Since autonomic neuropathy is not a recognised feature of the initial stages of diabetes hyperglucagonaemia may be responsible, at least in part, for diabetes induced changes in gastrointestinal motility.