TY - JOUR
T1 - Alkaline phosphatase activity in chronic streptozotocin-induced insulin deficiency in the rat
T2 - Effect of insulin replacement
AU - Hough, Stephen
AU - Avioli, Louis V.
AU - Teitelbaum, Steven L.
AU - Fallon, Michael D.
N1 - Funding Information:
From the Division of Bone and Mineral Metabolism, Department of Medicine, The Jewish Hospital of St. Louis, Washington Vniver-sity School of Medicine. St. Louis. Missouri, and the Department of Pathology and Laboratory Medicine, The Jewish Hospital of St. Louis. Washington University School of Medicine. St. Louis, Missouri. Supported in part by National Institutes of Health Grants AMI 1674 and AM2052I; The Saint Louis Shriners Hospital for Crippled Children and a post-doctoral South African Medical Research Council grant to Stephen Hough. Received for publication December 24. 1980. Address reprint requests to Michael D. Fallon, M.D., Department of Pathology, The Jewish Hospital of St. Louis, 216 South Kings Highway, St. Louis. Missouri 631 IO. 0 1981 by Grune & Stratton, Inc. 0026-0495/81/3012-0008801.00/0
PY - 1981/12
Y1 - 1981/12
N2 - Alterations in circulating alkaline phosphatase have been described in both man and the experimental animal with chronic insulin deficiency. We evaluated plasma and tissue alkaline phosphatase levels in freely-fed control, streptozotocin-induced diabetic and insulin-treated diabetic rats, seven weeks after the induction of diabetes. Circulating alkaline phosphatase activity was markedly elevated in the insulin deficient animal (p < 0.001) and completely normalized following insulin administration. The elevated plasma alkaline phosphatase activity observed in the insulin deficient animals was heat-resistant and phenylalanine-sensitive, a pattern typical of the intestinal isoenzyme. Small intestinal alkaline phosphatase activity was significantly higher (p < 0.01) in the diabetic animals, but comparable in the insulin-replaced and control rats. The intestinal isoenzyme activity was found to be strikingly insulin-sensitive; withholding insulin therapy for 36 hr prior to sacrifice resulted in an abrupt rise in both plasma and intestinal alkaline phosphatase values comparable to those observed in the insulin-deficient state. In contrast to these observations, skeletal alkaline phosphatase activity was decreased in the insulin deficient animal (p < 0.01) and this abnormality was corrected by insulin replacement. Neither insulin deficiency nor insulin replacement resulted in any significant changes in the hepatic alkaline phosphatase isoenzyme.
AB - Alterations in circulating alkaline phosphatase have been described in both man and the experimental animal with chronic insulin deficiency. We evaluated plasma and tissue alkaline phosphatase levels in freely-fed control, streptozotocin-induced diabetic and insulin-treated diabetic rats, seven weeks after the induction of diabetes. Circulating alkaline phosphatase activity was markedly elevated in the insulin deficient animal (p < 0.001) and completely normalized following insulin administration. The elevated plasma alkaline phosphatase activity observed in the insulin deficient animals was heat-resistant and phenylalanine-sensitive, a pattern typical of the intestinal isoenzyme. Small intestinal alkaline phosphatase activity was significantly higher (p < 0.01) in the diabetic animals, but comparable in the insulin-replaced and control rats. The intestinal isoenzyme activity was found to be strikingly insulin-sensitive; withholding insulin therapy for 36 hr prior to sacrifice resulted in an abrupt rise in both plasma and intestinal alkaline phosphatase values comparable to those observed in the insulin-deficient state. In contrast to these observations, skeletal alkaline phosphatase activity was decreased in the insulin deficient animal (p < 0.01) and this abnormality was corrected by insulin replacement. Neither insulin deficiency nor insulin replacement resulted in any significant changes in the hepatic alkaline phosphatase isoenzyme.
UR - https://www.scopus.com/pages/publications/0019849147
U2 - 10.1016/0026-0495(81)90040-8
DO - 10.1016/0026-0495(81)90040-8
M3 - Article
C2 - 7031417
AN - SCOPUS:0019849147
SN - 0026-0495
VL - 30
SP - 1190
EP - 1194
JO - Metabolism
JF - Metabolism
IS - 12
ER -