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Diabetes, Vol 39, Issue 6 752-756, Copyright © 1990 by American Diabetes Association
Effects of meal ingestion on plasma amylin concentration in NIDDM and nondiabetic humans
PC Butler, J Chou, WB Carter, YN Wang, BH Bu, D Chang, JK Chang and RA Rizza
Department of Medicine, Mayo Medical School, Rochester, Minnesota 55905.
Recent interest has focused on the potential role of amylin in the
pathogenesis of non-insulin-dependent diabetes mellitus (NIDDM). This
37-amino acid peptide is found in extracellular amyloid deposits in
approximately 50% of pancreatic islets of patients with NIDDM and has been
shown to inhibit skeletal muscle glycogen synthesis in vitro.
Immunocytochemical studies have colocalized amylin and insulin within
beta-cell secretory granules in nondiabetic humans, provoking the following
questions. Is amylin cosecreted with insulin? Are circulating amylin
concentrations higher in patients with NIDDM either before or after food
ingestion? To answer these questions, we developed a sensitive and specific
immunoassay to measure plasma concentrations of amylin in humans. Use of
this assay indicated that, in lean nondiabetic subjects, glucose ingestion
resulted in an increase (P less than 0.001) in the plasma concentration of
amylin (from 2.03 +/- 0.22 to 3.78 +/- 0.39 pM) and insulin (from 48.3 +/-
3.1 to 265 +/- 44 pM). There was a significant correlation between the
concentrations of insulin and amylin (r = 0.74, P less than 0.001) and the
increase in insulin and amylin concentration (r = 0.65, P less than 0.005).
Fasting concentrations of amylin did not differ in diabetic and
weight-matched nondiabetic subjects and showed a similar pattern of change
after ingestion of a mixed meal. We conclude that amylin is secreted in
response to ingestion of either glucose or a mixed meal and circulates at
concentrations that do not differ in patients with NIDDM and nondiabetic
subjects. It remains to be determined whether amylin at physiological
concentrations influences carbohydrate metabolism and if so whether its
effects differ in diabetic and nondiabetic humans.

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Copyright © 1990 by the American Diabetes Association.
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