{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T08:42:04Z","timestamp":1790412124244,"version":"4.1.0"},"reference-count":46,"publisher":"Oxford University Press (OUP)","issue":"5","license":[{"start":{"date-parts":[[2001,5,1]],"date-time":"2001-05-01T00:00:00Z","timestamp":988675200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2001,5,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Amylin (AMY) is a 37 amino acid peptide cosecreted with insulin (INS) by pancreatic \u03b2-cells and absent in type 1 diabetes, a condition frequently associated with osteopenia. AMY binds to calcitonin receptors, lowers plasma calcium concentration, inhibits osteoclast activity, and stimulates osteoblasts. In the present study, we examined the effects of AMY replacement on bone loss in a streptozotocin (STZ)-induced rodent model type 1 diabetes. Of 50 male Wistar rats studied, 40 were made diabetic with intraperitoneal STZ (50 mg\/kg; plasma glucose concentrations &amp;gt;11 mM within 5 days). Ten nondiabetic control (CONT) rats received citrate buffer without STZ. Diabetic rats were divided into four groups (n = 10\/group) and injected subcutaneously with rat AMY (45 mg\/kg), INS (12 U\/kg), both (same doses), or saline (STZ; diabetic controls) once per day. After 40 days of treatment and five 24-h periods of urine collection for deoxypyridinoline (DPD), the animals were killed, blood was sampled, and femurs were removed. The left femur was tested for mechanical resistance (three-point bending). The right femur was tested for total, diaphyseal (cortical bone), and metaphyseal (trabecular bone) bone densities using dual-energy X-ray absorptiometry (DXA). Bone was ashed to determine total bone mineral (calcium) content. None of the treatments had any significant effect on femoral length and diameter. Untreated diabetic rats (STZ; 145 \u00b1 7N) had lower bone strength than did nondiabetic CONT (164 \u00b1 38; p &amp;lt; 0.05). Total bone mineral density (BMD; g\/cm2) was significantly lower in STZ (0. 2523 \u00b1 0. 0076) than in CONT (0.2826 \u00b1 0.0055), as were metaphyseal and diaphyseal densities. Diabetic rats treated with AMY, INS, or both had bone strengths and bone densities that were indistinguishable from those in nondiabetic CONT. Changes in bone mineral content paralleled those for total BMD (T-BMD). Plasma osteocalcin (OC) concentration, a marker for osteoblastic activity, was markedly lower in untreated diabetic rats (7. 6 \u00b1 0. 9 ng\/ml); p &amp;lt; 0. 05) than in nondiabetic CONT (29. 8 \u00b1 1. 7; p &amp;lt; 0. 05) or than in AMY (20. 1 \u00b1 0. 7; p &amp;lt; 0. 05). Urinary DPD excretion, a marker for bone resorption, was similar in untreated and AMY-treated diabetic rats (35.0 \u00b1 3.1 vs. 35.1 \u00b1 4.4 nmol\/mmol creatinine), intermediate in rats treated with INS (49.9 \u00b1 2.7), and normalized in diabetic rats treated with both agents (58.8 \u00b1 8.9 vs. 63.2 \u00b1 4.5 in CONT). Thus, in our STZ rat model of diabetic osteopenia, addition of AMY improved bone indices apparently by both inhibiting resorption and stimulating bone formation.<\/jats:p>","DOI":"10.1359\/jbmr.2001.16.5.958","type":"journal-article","created":{"date-parts":[[2006,4,26]],"date-time":"2006-04-26T20:48:22Z","timestamp":1146084502000},"page":"958-965","source":"Crossref","is-referenced-by-count":96,"title":["Amylin and Bone Metabolism in Streptozotocin-Induced Diabetic Rats"],"prefix":"10.1093","volume":"16","author":[{"given":"Marie-No\u00eblle","family":"Horcajada-Molteni","sequence":"first","affiliation":[{"name":"M\u00e9tabolisme Min\u00e9ral\u2014U3M, Institut National de la Recherche Agronomique, Clermont-Theix, St. Gen\u00ebs Champanelle, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brigitte","family":"Chanteranne","sequence":"additional","affiliation":[{"name":"M\u00e9tabolisme Min\u00e9ral\u2014U3M, Institut National de la Recherche Agronomique, Clermont-Theix, St. Gen\u00ebs Champanelle, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Patrice","family":"Lebecque","sequence":"additional","affiliation":[{"name":"M\u00e9tabolisme Min\u00e9ral\u2014U3M, Institut National de la Recherche Agronomique, Clermont-Theix, St. Gen\u00ebs Champanelle, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marie-Jeanne","family":"Davicco","sequence":"additional","affiliation":[{"name":"M\u00e9tabolisme Min\u00e9ral\u2014U3M, Institut National de la Recherche Agronomique, Clermont-Theix, St. Gen\u00ebs Champanelle, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Veronique","family":"Coxam","sequence":"additional","affiliation":[{"name":"M\u00e9tabolisme Min\u00e9ral\u2014U3M, Institut National de la Recherche Agronomique, Clermont-Theix, St. Gen\u00ebs Champanelle, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrew","family":"Young","sequence":"additional","affiliation":[{"name":"AMY Pharmaceuticals, Inc., San Diego, California, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jean-Pierre","family":"Barlet","sequence":"additional","affiliation":[{"name":"M\u00e9tabolisme Min\u00e9ral\u2014U3M, Institut National de la Recherche Agronomique, Clermont-Theix, St. Gen\u00ebs Champanelle, France"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2009,12,2]]},"reference":[{"key":"2024020714131788200_bib1","doi-asserted-by":"crossref","first-page":"8628","DOI":"10.1073\/pnas.84.23.8628","article-title":"Purification and characterization of a peptide from amyloid-rich pancreases of type 2 diabetic patients","volume":"84","author":"Cooper","year":"1987","journal-title":"Proc Natl Acad Sci 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