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Chronic (six-day) injection of insulin (im, 50 microM/animal) into BALB/c mice resulted in changes in secretory function, hypertrophy and hyperplasia of the parotid and submandibular glands. There were no significant changes in the flow rate or concentrations of proline-rich proteins, TGF alpha, or amylase in saliva when measured against constant protein levels. However, amylase enzyme activity and total saliva protein content were reduced when measured against constant saliva volume. In contrast, EGF synthesis and secretion from the submandibular gland was increased. Both the parotid and submandibular gland showed evidence of gland hypertrophy and increased rates of DNA synthesis as indicated by [3H]-thymidine incorporation in response to insulin treatment. Chronic injection of insulin did not effect the level of receptor in the plasma membrane of either gland.

Parotid gland of adult rats maintained exclusively on liquid (milk) diet for 7 or 13 days showed a 25% reduction in number of beta-adrenoceptors, and after 21 days, the reduction was 33%; with maintenance of rats on Metrecal for 7 days, the decrease was 24% for female rats and 22% for male rats. The decrease in number of muscarinic receptors after 7 or 13 days on milk was 32%, and 38% after 21 days; the decreases for rats on Metrecal for 7 days were 32% for females and 35% for males. In rats maintained on liquid (milk) diet for 7 days, and then denervated by unilateral removal of the parasympathetic and sympathetic innervations to parotid there were decreases of 39-42% in number of beta-receptors and 50-52% in muscarinic receptors at 6 or 14 days after denervation (maintenance on liquid diet for 13 and 21 days, respectively) from those of innervated glands of chow-fed rats; denervated glands of rats on chow diet showed the same reduction. Thus, it was concluded that absence of neurally mediated glandular activity, imposed by either diet or surgical removal of the nerves, caused marked decreases in number of both beta-adrenergic and muscarinic receptors, but that the presence of the nerves, even though inactive (liquid diet), provided a trophic influence that prevented the more marked decreases seen in the absence (surgical removal) of the nerves.

Three experiments were conducted to (a) determine the effect of light deprivation on submandibular flow, (b) test for accommodation in darkness-induced parotid flow-rate depression, and (c) evaluate the effects of lights of widely varying intensities on parotid flow. Light deprivation decreased submandibular flow rate from 0.146 ml/min to 0.045 ml/min, a decrease of 69%. It is suggested that photic input through the retina provides stimulation to the salivary glands in the human through the superior cervical ganglion in a system similar to that present for the pineal. This implies that the sympathetic nervous system functions in the regulation of a component of the resting flow from both the parotid and submandibular glands. Series of parotid saliva samples collected in darkness did not reveal a pattern suggestive of accommodation to darkness. The effect of darkness on flow is as strong in the first sample as in those collected later under darkness. Reinstitution of light brings immediate restoration of the routine level of unstimulated salivary flow. A light intensity as low as 0.1 fc is sufficient to maintain the usual level of resting parotid flow. Increasing intensity up to 150 fc did not significantly increase this rate of flow.