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Related Experiment Videos

Amylin increases bone volume but cannot ameliorate diabetic osteopenia

D F Romero1, H P Bryer, B Rucinski

  • 1Department of Medicine, Albert Einstein Medical Center, Philadelphia, Pennsylvania 19141, USA.

Calcified Tissue International
|January 1, 1995
PubMed
Summary

Amylin, a hormone co-secreted with insulin, may not prevent diabetic osteopenia. Studies in rats suggest amylin does not improve bone mineral metabolism in diabetes, despite its bone-conserving properties in non-diabetic states.

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Area of Science:

  • Endocrinology
  • Bone Metabolism
  • Diabetes Research

Background:

  • Amylin, co-secreted with insulin by pancreatic beta-cells, has demonstrated bone-conserving properties.
  • Type 1 diabetes is associated with low amylin and osteopenia, while Type 2 diabetes shows less bone loss with high amylin levels.

Purpose of the Study:

  • To investigate the effects of amylin on bone mineral metabolism in normal and streptozotocin-induced diabetic rats.
  • To determine if amylin administration can mitigate streptozotocin-induced diabetic osteopenia.

Main Methods:

  • Ten-week-old male Sprague-Dawley rats were divided into four groups: control, amylin-treated, diabetic, and diabetic amylin-treated.
  • Amylin (100 pmol/100 g b.w.) was administered daily via subcutaneous injection for 19 days.

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  • Histomorphometric analysis of double calcein-labeled tibiae was performed.

    • Main Results:

    • Blood glucose levels in diabetic rats remained high (>600 mg/dl) and were unaffected by amylin.
    • Serum levels of osteocalcin, IGF-1, PTH, and 1,25(OH)2D were significantly lower in diabetic rats compared to controls.
    • Amylin transiently increased serum osteocalcin in non-diabetic rats but had no effect in diabetic rats.

    Conclusions:

    • Amylin does not appear to modify streptozotocin-induced diabetic osteopenia in rats.
    • The bone-protective effects of amylin may be diminished or absent in the context of diabetes-induced metabolic changes.