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Journal of Dental Research
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Effects of Diabetes and Insulin on {alpha}-amylase Messenger RNA Levels in Rat Parotid Glands

S.K. Kim

Research Service, VA Medical Center, Ann Arbor, Michigan 48105, Departments of Anatomy and Cell Biology, Medical School, Biologic and Material Sciences, School of Dentistry, University of Michigan, Ann Arbor

L.M. Cuzzort

Departments of Anatomy and Cell Biology, Medical School

R.K. McKean

Departments of Anatomy and Cell Biology, Medical School

E.D. Allen

Research Service, VA Medical Center, Ann Arbor, Michigan 48105

Previous studies have shown that amylase levels are reduced significantly in the pancreas and parotid gland of diabetic rats and that insulin reverses this effect and increases the secretory protein levels. In the pancreas, these changes in amylase protein levels are accompanied by parallel changes in amylase mRNA levels. In the present study, the effects of diabetes and subsequent insulin treatments on contents (per cell) of amylase protein and its mRNA in parotid glands were compared in rats rendered diabetic with an injection of a beta-cell toxin, streptozotocin (STZ). Both amylase protein and its mRNA contents were reduced significantly in diabetic rats, compared with control rats, and this reduction was reversed following insulin injections of diabetic rats. In insulin-injected diabetic rats, amylase protein contents increased before a detectable increase in amylase mRNA levels was seen. The mRNA contents of a non-secretory protein, actin, did not change during diabetogenesis or subsequent insulin treatments. The reductions in parotid contents of amylase and its mRNA in diabetic rats and the reversal of these changes by insulin are similar to those changes that occur in the pancreas under the same conditions. However, the magnitude of these changes in parotid glands was much smaller than in the pancreas, and the effect of insulin on amylase mRNA synthesis was not as immediate as in the latter gland.

Journal of Dental Research, Vol. 69, No. 8, 1500-1504 (1990)
DOI: 10.1177/00220345900690081001
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