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Published in: Osteoporosis International 3/2004

01-03-2004 | Original Article

Amylin fasting plasma levels are decreased in patients with osteoporosis

Authors: J. Bronský, R. Průša

Published in: Osteoporosis International | Issue 3/2004

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Abstract

Amylin is a polypeptide hormone produced in pancreatic beta-cells that belongs to the family of calcitonin gene-related peptides. There is a 20% sequence homology between amylin and calcitonin and 44% homology with calcitonin gene-related peptide. Amylin and its fragments stimulate the proliferation of osteoblasts, inhibit bone resorption, and increase bone density and the amount of bone mass. We measured amylin total and unreduced amylin fasting plasma levels in patients with osteoporosis (n=28; 3 men, 25 women; mean age 65 years), type 2 diabetes mellitus (n=10; 5 men, 5 women; 64 years), and in the control group (n=24; 11 men, 13 women; 53 years) using an ELISA kit with immunofluorescent detection (Linco). Amylin total plasma levels in patients with osteoporosis were 3.33±0.46 pmol/l (mean±SEM), in patients with type 2 diabetes 6.29±1.47 pmol/l (mean±SEM), and in the control group 8.48±3.12 pmol/l (mean±SEM). Mean plasma levels were lower in patients with osteoporosis than in patients with type 2 diabetes and in the control group. Unreduced amylin plasma levels in patients with osteoporosis (n=28) were 2.51±0.87 pmol/l (mean±SEM), in patients with type 2 diabetes (n=10) 4.15±0.95 pmol/l (mean±SEM) and in the control group (n=5) 13.50±3.94 pmol/l (mean±SEM). Plasma levels were significantly lower in patients with osteoporosis than in patients with type 2 diabetes (P<0.01) and in the control group (P<0.001). Amylin plasma levels are decreased in patients with osteoporosis. Amylin deficiency in these patients may contribute to the development of osteoporosis. Amylin should be investigated in relation to the pharmacological treatment of osteoporosis.
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Metadata
Title
Amylin fasting plasma levels are decreased in patients with osteoporosis
Authors
J. Bronský
R. Průša
Publication date
01-03-2004
Publisher
Springer-Verlag
Published in
Osteoporosis International / Issue 3/2004
Print ISSN: 0937-941X
Electronic ISSN: 1433-2965
DOI
https://doi.org/10.1007/s00198-003-1538-5

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