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Related Experiment Videos

Accelerated bone resorption in senescence-accelerated mouse (SAM-P/6).

M Kawase1, M Tsuda, T Matsuo

  • 1Biology Research Laboratories, Takeda Chemical Industries, Ltd., Osaka, Japan.

Journal of Bone and Mineral Research : the Official Journal of the American Society for Bone and Mineral Research
|June 1, 1989
PubMed
Summary

Senescence-accelerated mouse P/6 (SAM-P/6) exhibit low bone mass due to accelerated bone resorption. This is linked to a potential hyperparathyroid state, indicated by elevated urinary cyclic AMP (cAMP) and serum tartrate-resistant acid phosphatase (TRAP).

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Area of Science:

  • Bone biology
  • Gerontology
  • Mouse models of aging

Background:

  • Senescence-accelerated mouse (SAM) substrains exhibit distinct aging phenotypes.
  • SAM-P/6 mice are characterized by accelerated aging and potential bone density deficits.

Purpose of the Study:

  • To investigate the underlying mechanisms of low bone mass in SAM-P/6 mice.
  • To analyze age-associated changes in bone and biochemical markers in SAM-P/6 compared to normal SAM-R/1 mice.

Main Methods:

  • Comparative analysis of femoral bone composition and urinary/serum markers between SAM-P/6 and SAM-R/1 mice.
  • Measurement of hydroxyproline, calcium, phosphorus, cyclic AMP (cAMP), alkaline phosphatase, and tartrate-resistant acid phosphatase (TRAP).
  • In vitro assessment of SAM-P/6 serum's effect on calcium release from fetal rat ulna.

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Main Results:

  • SAM-P/6 mice showed lower femoral hydroxyproline and higher urinary excretion of cAMP, calcium, hydroxyproline, and phosphorus.
  • Elevated serum calcium and inorganic phosphorus were observed in SAM-P/6 mice.
  • Increased serum alkaline phosphatase and TRAP activities in SAM-P/6 mice, with serum stimulating calcium release in vitro.

Conclusions:

  • Accelerated bone resorption in SAM-P/6 mice contributes to decreased bone mass.
  • A possible hyperparathyroid state, suggested by elevated urinary cAMP and serum TRAP, drives this bone resorption.
  • These findings highlight a specific mechanism for age-related bone loss in this mouse model.