Epidermal growth factor binding is altered in pancreatic acini from diabetic rats

Murray Korc; Lynn M. Matrisian; Rieko Nakamura; Bruce E. Magun

doi:10.1016/0024-3205(84)90562-9

Epidermal growth factor binding is altered in pancreatic acini from diabetic rats

Murray Korc, Lynn M. Matrisian, Rieko Nakamura, Bruce E. Magun

Research output: Contribution to journal › Article › peer-review

20 Scopus citations

Abstract

The effects of streptozotocin-induced diabetes on ¹²⁵I-labeled epidermal growth factor (EGF) binding were studied in rat pancreatic acini. ¹²⁵I-EGF binding was one-half maximal at 20 min, and maximal at 90 min. Saturation data revealed a decreased binding capacity in diabetic acini when compared with normal acini. Insulin, in vivo, normalized the decreased binding capacity. ¹²⁵I-EGF internalization was also decreased in diabetic rat acini. Further, the inhibitory effect of cholecystokinin-octapeptide (CCK₈) on cell-associated ¹²⁵I-EGF radioactivity was significantly greater in diabetic than in normal rat acini. These findings suggest that insulin deficiency may lead to defective regulation of the exocrine pancreas by EGF.

Original language	English (US)
Pages (from-to)	2049-2055
Number of pages	7
Journal	Life Sciences
Volume	35
Issue number	20
DOIs	https://doi.org/10.1016/0024-3205(84)90562-9
State	Published - Nov 12 1984
Externally published	Yes

ASJC Scopus subject areas

General Pharmacology, Toxicology and Pharmaceutics
General Biochemistry, Genetics and Molecular Biology

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10.1016/0024-3205(84)90562-9

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@article{1a9190b6266f468cb607e15cf6c84221,

title = "Epidermal growth factor binding is altered in pancreatic acini from diabetic rats",

abstract = "The effects of streptozotocin-induced diabetes on 125I-labeled epidermal growth factor (EGF) binding were studied in rat pancreatic acini. 125I-EGF binding was one-half maximal at 20 min, and maximal at 90 min. Saturation data revealed a decreased binding capacity in diabetic acini when compared with normal acini. Insulin, in vivo, normalized the decreased binding capacity. 125I-EGF internalization was also decreased in diabetic rat acini. Further, the inhibitory effect of cholecystokinin-octapeptide (CCK8) on cell-associated 125I-EGF radioactivity was significantly greater in diabetic than in normal rat acini. These findings suggest that insulin deficiency may lead to defective regulation of the exocrine pancreas by EGF.",

author = "Murray Korc and Matrisian, {Lynn M.} and Rieko Nakamura and Magun, {Bruce E.}",

note = "Funding Information: i. This study was supported by NIH grant AM-32561 to M.K., NCI grant CA-29290 to B.E.M., and by an award from the KROC Foundation to M.K.",

year = "1984",

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doi = "10.1016/0024-3205(84)90562-9",

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T1 - Epidermal growth factor binding is altered in pancreatic acini from diabetic rats

AU - Korc, Murray

AU - Matrisian, Lynn M.

AU - Nakamura, Rieko

AU - Magun, Bruce E.

N1 - Funding Information: i. This study was supported by NIH grant AM-32561 to M.K., NCI grant CA-29290 to B.E.M., and by an award from the KROC Foundation to M.K.

PY - 1984/11/12

Y1 - 1984/11/12

N2 - The effects of streptozotocin-induced diabetes on 125I-labeled epidermal growth factor (EGF) binding were studied in rat pancreatic acini. 125I-EGF binding was one-half maximal at 20 min, and maximal at 90 min. Saturation data revealed a decreased binding capacity in diabetic acini when compared with normal acini. Insulin, in vivo, normalized the decreased binding capacity. 125I-EGF internalization was also decreased in diabetic rat acini. Further, the inhibitory effect of cholecystokinin-octapeptide (CCK8) on cell-associated 125I-EGF radioactivity was significantly greater in diabetic than in normal rat acini. These findings suggest that insulin deficiency may lead to defective regulation of the exocrine pancreas by EGF.

AB - The effects of streptozotocin-induced diabetes on 125I-labeled epidermal growth factor (EGF) binding were studied in rat pancreatic acini. 125I-EGF binding was one-half maximal at 20 min, and maximal at 90 min. Saturation data revealed a decreased binding capacity in diabetic acini when compared with normal acini. Insulin, in vivo, normalized the decreased binding capacity. 125I-EGF internalization was also decreased in diabetic rat acini. Further, the inhibitory effect of cholecystokinin-octapeptide (CCK8) on cell-associated 125I-EGF radioactivity was significantly greater in diabetic than in normal rat acini. These findings suggest that insulin deficiency may lead to defective regulation of the exocrine pancreas by EGF.

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Epidermal growth factor binding is altered in pancreatic acini from diabetic rats

Abstract

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