Vitamin E deficiency reduced lumbar bone calcium content in female rats

Research output: Contribution to journalArticle

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Abstract

Vitamin E deficiency has been found to impair bone calcification. This study was done to determine the effects of vitamin E deficiency and supplementation on parathyroid hormone, i.e. the hormone involved in bone regulation. Female Sprague-Dawley rats were divided into 4 groups: 1) normal rat chow (RC), 2) vitamin E deficiency (VED), vitamin E deficient rats supplemented with 3) 60 mg/kg α-tocotrienol (ATT) and 4) 60 mg/kg α-tocopherol (ATF). Treatment was carried out for 3 months. Vitamin E deficiency caused hypocalcaemia during the first month of the treatment period, increased the parathyroid hormone level in the second month and decreased the bone calcium content in the 4th lumbar bone at the end of the treatment. Vitamin E supplementation (ATT and ATF) failed to improve these conditions. The bone formation marker, osteocalcin, and the bone resorption marker, deoxypyridinoline did not change throughout the study period. In conclusion vitamin E deficiency impaired bone calcium homeostasis with subsequent secondary hyperparathyroidism and vertebral bone loss. Replacing the vitamin E with pure ATF or pure ATT alone failed to correct the changes seen.

Original languageEnglish
Pages (from-to)623-630
Number of pages8
JournalMedical Journal of Malaysia
Volume59
Issue number5
Publication statusPublished - 2004

Fingerprint

Vitamin E Deficiency
Calcium
Bone and Bones
Tocopherols
Parathyroid Hormone
Vitamin E
Tocotrienols
Secondary Hyperparathyroidism
Hypocalcemia
Osteocalcin
Bone Resorption
Osteogenesis
Sprague Dawley Rats
Homeostasis
Hormones

Keywords

  • Bone metabolism
  • Female rats
  • Parathyroid hormone
  • Vitamin E deficiency

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Vitamin E deficiency reduced lumbar bone calcium content in female rats. / Mohamed, Norazlina; Chua, C. W.; Soelaiman, Ima Nirwana.

In: Medical Journal of Malaysia, Vol. 59, No. 5, 2004, p. 623-630.

Research output: Contribution to journalArticle

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