People with diabetes mellitus (DM) suffer from a series of medical complications, including the indigestion of foodstuffs. This is due to the inability of the exocrine pancreas to secrete an adequate amount of pancreatic juice. The medical term used to describe this dysfunction is ‘pancreatic insufficiency’. Like the pancreas, the parotid is also an exocrine gland that secretes mainly α-amylase, which is required for the digestion of carbohydrates. Since the parotid is similar in structure and function to the exocrine pancreas, the aim was to investigate whether DM may also produce ‘salivary insufficiency’. DM was induced in adult male Wistar rats by a single (I.P.) injection of streptozotocin (STZ) (60 mg kg^-1 body weight; Sharma et al. 1985). Age-matched control animals were injected with a similar volume of citrate buffer. The animals were tested for DM 4 days after STZ injection and 2 months later when they were humanely killed for the experiment. Isolated parotid glands from control and diabetic rats were used to measure amylase secretion and intracellular free calcium concentrations [Ca²⁺], and to study any morphological changes in the tissues, employing established fluorimetric and light microscopic techniques (Francis et al. 1990; Singh et al. 1999).

After 2 months of STZ treatment diabetic rats weighed significantly (Student’s unpaired t test; P < 0.001) less (232 ± 7.2 g; mean ± S.E.M.; n = 8) than controls (381 ± 12.53 g, n = 8). Similarly, blood glucose level was much higher in diabetic rats (407.50 ± 35.90 mg dl^-1, n = 8, compared with control 81.20 ± 3.1 mg dl^-1, n = 8). Basal amylase secretion (expressed as U ml^-1 (100 mg tissue)^-1) by parotid glands from control and diabetic rats was 14.36 ± 0.89 (n = 38) and 2.36 ± 0.27 (n = 38), respectively. These results show that DM can elicit a significant (P < 0.001) decrease in amylase secretion compared with control. When control parotid segments were stimulated with either acetylcholine (10^-5 M ACh) or noradrenaline (10^-5 M NA), there was a marked increase in amylase secretion. Typically, amylase output in the presence of ACh and NA was 25.43 ± 1.47 (n = 6) and 64.10 ± 9.9 (n = 9), respectively. The output elicited by both ACh and NA from diabetic parotid segments was significantly (P < 0.05) reduced compared with that elicited from controls. Values with 10^-5 M ACh and 10^-5 M NA were 14.88 ± 2.49 (n = 5) and 36.60 ± 6.7 (n = 4), respectively. Basal [Ca²⁺]_i in fura-2-loaded acinar cells from control parotid glands was 93.10 ± 6.73 nM (n = 8). Stimulation of acinar cells with 10^-5 M ACh resulted in no significant change in the initial peak Ca²⁺ transient in diabetic compared with control acinar cells. In contrast, the plateau phase of the Ca²⁺ transient was markedly decreased in diabetic acinar cells compared with controls, suggesting that DM may be associated with a decrease in Ca²⁺ entry into parotid acinar cells. Light microscopic studies of diabetic and age-matched control parotid glands showed striking differences in morphology. Diabetic parotid glands contained a large number of lipid vacuoles, whereas glands from control animals displayed normal structure and with few or no lipid vacuoles. The results have shown that DM can lead to the infiltration of numerous lipid vacuoles and a reduction in amylase secretion (salivary insufficiency) in the rat parotid gland.

All procedures accord with current UK legislation.