The putative hormone islet amyloid polypeptide (IAPP) induces impaired glucose tolerance in cats

K. H. Johnson, T. D. O'Brien, K. Jordan, C. Betsholtz, P. Westermark

Research output: Contribution to journalArticle

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Abstract

Islet amyloid polypeptide (IAPP) has been implicated by in vitro studies as an inhibitor of insulin-stimulated glucose utilization by skeletal muscle cells and also as an inhibitor of insulin-stimulated insulin secretion by beta cells. Increased expression and production of IAPP by beta cells, as has been suggested to occur in cats with impaired glucose tolerance, could thus contribute substantially to the development of the insulin resistance and impaired insulin release which are the hallmarks of Type 2 diabetes mellitus. The effects of IAPP with respect to glucose metabolism in living animals, however, have not been previously reported. In the present in vivo study we show that synthetic amidated IAPP induced impaired glucose tolerance in each of the 3 cats studied, with dramatic impairment (increases in glucose to T 1 2 values of 124% and 234%) in 2 of the 3 cats. Impaired insulin responses were also evident in the 2 cats with the most dramatic states of glucose intolerance. These results provide the most direct evidence to-date that IAPP may have an important role in the development of Type 2 diabetes mellitus.

Original languageEnglish (US)
Pages (from-to)507-513
Number of pages7
JournalBiochemical and Biophysical Research Communications
Volume167
Issue number2
DOIs
StatePublished - Mar 16 1990

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Islet Amyloid Polypeptide
Glucose Intolerance
Cats
Hormones
Insulin
Glucose
Type 2 Diabetes Mellitus
Medical problems
Muscle Cells
Insulin Resistance
Skeletal Muscle
Metabolism
Muscle
Animals
Cells

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The putative hormone islet amyloid polypeptide (IAPP) induces impaired glucose tolerance in cats. / Johnson, K. H.; O'Brien, T. D.; Jordan, K.; Betsholtz, C.; Westermark, P.

In: Biochemical and Biophysical Research Communications, Vol. 167, No. 2, 16.03.1990, p. 507-513.

Research output: Contribution to journalArticle

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