Gastric emptying was measured in normal and insulin-treated spontaneously diabetic BB rats using the retention of an acaloric methylcellulose gel containing phenol red delivered by garage. Dye content in stomachs removed after killing 20 rain later was determined spectroscopically, and was compared to that in rats killed immediately after gavage to assess emptying. Diabetic rats had a markedly greater gastric emptying (90.3 + 1.7 % passed) compared to normal Harlan Sprague Dawley rats (49.1 + 4.7 % passed; p < 0.001) and non-diabetic BB rats (61.1 + 9.2 % passed; p < 0.001). The pancreatic beta-cell peptide, amylin, which is deficient in insulin-dependent diabetes mellitus, dose-dependently inhibited gastric emptying in both normal and diabet-ic rats. The EDs0 of the response in normal rats measured by phenol red and novel [3-3H]glucose gavage techniques was approximately 0.4 ~g. This dose was estimated to increase plasma amylin concentration by a mean of approximately 20 pmol/1 to concentrations within the range observed in vivo. It is proposed that amylin could participate in the physiological control of nutrient entry into the duodenum, and that the accelerated gastric emptying seen in BB rats could be related to their lack of amylin secretion. [Diabetologia (1995) 38: 642-648] Key words BB rat, gastric emptying, amylin, incretins, [3-3H]glucose islet amyloid polypeptide.
Disturbances of gastric emptying are a common feature of diabetes mellitus. However, with incomplete information about the natural history of disordered gastric motor function in diabetes, the literature on gastric emptying in diabetes is acknowledged to be confusing [1]. Many reports do not distinguish between juvenile-onset insulin-dependent (IDDM) and maturity-onset non-insulin-dependent (NIDDM) forms of diabetes. Further, as it is often difficult to do so, many reports do not distinguish between gas-