Intestinal mucin secretion in streptozotocin-diabetic rats |
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Authors: | Dr Michèle Mantle PhD Ela Thakore BSc Ronald Mathison PhD Joseph S Davison PhD |
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Institution: | (1) Gastrointestinal Research Group, Department of Medical Biochemistry, Health Sciences Centre, University of Calgary, 3330, Hospital Dr. N.W., T2N 1N4 Calgary, Alberta, Canada;(2) Department of Medical Physiology, Health Sciences Centre, University of Calgary, Alberta, Canada |
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Abstract: | In diabetic rats, intestinal mucin secretion is unusually high compared with that in normal rats. These studies demonstrate that mucin synthesis is also increased in the diabetic intestine. - and -adrenergic agonists or antagonists did not affect mucin output in either normal or diabetic animals, suggesting that altered release in diabetes was not due to goblet cells responding abnormally to adrenergic agents. The cholinergic agonist bethanechol caused a dose-dependent and atropine-sensitive increase in mucin secretion from the normal intestine but had no effect on mucin release from diabetic tissue. Atropine alone did not reduce mucin secretion from the diabetic intestine to levels found in normal tissue. Cholera toxin caused an approximately fivefold increase in mucin output from normal rats but had no effect on mucin secretion from diabetic animals. Thus, goblet cell responses to cholinergic stimulation and cholera toxin in the diabetic intestine are markedly impaired. However, loss of cholinergic control does not appear to be responsible for altered baseline mucin secretion in diabetes.This work was supported by the Medical Research Council of Canada. M.M. holds a Scholarship Award and J.S.D. a Professorship from the Alberta Heritage Foundation for Medical Research. |
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Keywords: | mucin intestine secretion diabetes adrenergic cholinergic cholera toxin |
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