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Amylin inhibits ovariectomy-induced bone loss in rats

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Amylin (AMY), a peptide co-secreted with insulin by pancreatic beta-cells, inhibits bone resorption and stimulates osteoblastic activity. The ovariectomized (OVX) rat is an established animal model for human osteoporosis. Thus, the present experiment was performed to study the effects of AMY on estrogen deficiency-induced bone loss in rats. Thirty-one 6-month-old Wistar rats were randomized by body weight (BW) into two groups. The first underwent surgical OVX (n=21). The second was sham-operated (SH; n=10). Sixty days after surgery, 11 OVX rats were s.c. injected with rat AMY (3 microg/100 g BW/day, for 30 days; OVX+AMY), and 10 with solvent alone in the same way (0.15 ml/100 g BW; OVX). Each rat, housed in an individual cage, was fed daily the mean quantity of diet consumed the day before by SH rats. This diet contained 0.24% calcium and 0. 16% phosphorus. The 31 animals were killed on day 90. No difference in daily weight gain and BW was observed between groups. Neither AMY treatment nor OVX had any significant effect upon femoral morphology, femoral failure load, diaphyseal femoral density (representative of cortical bone) and total femoral calcium content. Nevertheless, both distal metaphyseal (representative of cancellous bone) and total femoral bone densities were higher in SH and OVX+AMY than in OVX rats. The highest plasma osteocalcin concentration was measured in OVX+AMY rats. Simultaneously, urinary deoxypyridinoline excretion was lower in OVX+AMY than in OVX rats. These results indicate that in OVX rats, AMY treatment inhibited trabecular bone loss both by inhibiting resorption and by stimulating osteoblastic activity.
Title: Amylin inhibits ovariectomy-induced bone loss in rats
Description:
Amylin (AMY), a peptide co-secreted with insulin by pancreatic beta-cells, inhibits bone resorption and stimulates osteoblastic activity.
The ovariectomized (OVX) rat is an established animal model for human osteoporosis.
Thus, the present experiment was performed to study the effects of AMY on estrogen deficiency-induced bone loss in rats.
Thirty-one 6-month-old Wistar rats were randomized by body weight (BW) into two groups.
The first underwent surgical OVX (n=21).
The second was sham-operated (SH; n=10).
Sixty days after surgery, 11 OVX rats were s.
c.
injected with rat AMY (3 microg/100 g BW/day, for 30 days; OVX+AMY), and 10 with solvent alone in the same way (0.
15 ml/100 g BW; OVX).
Each rat, housed in an individual cage, was fed daily the mean quantity of diet consumed the day before by SH rats.
This diet contained 0.
24% calcium and 0.
16% phosphorus.
The 31 animals were killed on day 90.
No difference in daily weight gain and BW was observed between groups.
Neither AMY treatment nor OVX had any significant effect upon femoral morphology, femoral failure load, diaphyseal femoral density (representative of cortical bone) and total femoral calcium content.
Nevertheless, both distal metaphyseal (representative of cancellous bone) and total femoral bone densities were higher in SH and OVX+AMY than in OVX rats.
The highest plasma osteocalcin concentration was measured in OVX+AMY rats.
Simultaneously, urinary deoxypyridinoline excretion was lower in OVX+AMY than in OVX rats.
These results indicate that in OVX rats, AMY treatment inhibited trabecular bone loss both by inhibiting resorption and by stimulating osteoblastic activity.

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