Biological activity of immunoreactive insulin like activity extracted from rat submandibular gland. Taouis, Mohammed, Deville De Periere Dominique, Hillaire-Buys Dominique, Derouet Michel, Gross Ren[acute]e, Simon Jean, and Ribes G[acute]erard. Institut National de la Recherche Agronomique, Station de Recherches Avicoles, Endocrinologie de la Croissance et du M[acute]etabolisme, 37380 Nouzilly, France, Laboratoire de Physiologie, Facult[acute]e d'Odontologie, 34000 Montpellier, France, Laboratoire de Pharmacologie, Facult[acute]e de M[acute]edecine et UMR 9921 du Centre National de la Recherche Scientifique, 34000 Montpellier, France.
APStracts 2:0084E, 1995.
Earlier studies indicate the presence of an insulin-like immunoreactivity (ILI) in rat submandibular salivary glands (SSG). Previous observations also showed that streptozotocin (STZ) induced diabetes was accompanied by an increase in SSG-ILI concentrations. In the present work we studied the effect of SSG-ILI from normal and streptozotocin diabetic rats (ILI-N and ILI-D respectively) on insulin receptor binding and function in LMH cell line. ILI-N and ILI-D inhibited 125I-insulin binding to intact cells and WGA-purified insulin receptors with a high affinity. Furthermore, ILI-N and ILI-D activated, although weakly, the [beta]-subunit autophosphorylation of solubilized and WGA-purified insulin receptors. An ATP hydrolytic activity was present in ILI-N and, at a greater extent, in ILI-D extracts which can, at least in part, explain their low potency at activating autophosphorylation and kinase activity of insulin receptors in vitro. However, following ILI treatment of intact cells and immunoprecipitations of insulin receptors, ILI induced a dose -dependent tyrosine phosphorylation of the insulin receptor [beta] subunit. Finally, ILI-N and ILI-D stimulated amino acid uptake and lipogenesis in LMH cells. These findings suggest that SSG-ILI is biologically active and can participate to metabolic regulations. 

Received 14 February 1994; accepted in final form 22 March 1995.
APS Manuscript Number E64-4.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 25 April 1995.