4.3 Article

Hypercholesterolemia accelerates bone loss in postmenopausal women

Journal

CLIMACTERIC
Volume 14, Issue 1, Pages 105-111

Publisher

INFORMA HEALTHCARE
DOI: 10.3109/13697137.2010.507888

Keywords

OSTEO-SONO-ASSESSMENT INDEX; LIPID PROFILE; CHOLESTEROL; POSTMENOPAUSE; BONE LOSS

Funding

  1. Japan Menopause Society
  2. Bayer Schering Pharma

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Objectives To clarify the effect of lipid profiles on postmenopausal bone loss using a longitudinal method and to determine whether cytokines are involved in bone loss. Methods The subjects were Japanese residents participating in the Iwaki Health Promotion Projects. Women with one or more of the following factors were excluded: a history of surgical menopause, current or past users of bisphosphonates or current user of other drugs known to influence bone and lipid metabolism, and current medication for diabetes or hypertension. Consequently, 99 postmenopausal women (61.2 +/- 7.7 years old) and 85 premenopausal women (41.2 +/- 8.6 years old) were selected for this study. The osteo-sono-assessment index (OSI) of the left calcaneal bone was obtained twice at 1-year intervals and the annual percentage change in OSI was calculated. Serum total cholesterol, high and low density lipoprotein cholesterol, triglycerides, homocysteine and cytokines such as adipocytokines, interleukins and tumor necrosis factor-alpha were measured. Postmenopausal women were grouped into three groups according to their basal cholesterol level, and the relationship between basal cholesterol level and annual change in OSI was studied. Results The annual percentage change in OSI in postmenopausal women with a serum total cholesterol level >= 240 mg/dl was significantly higher compared to those with a normal total cholesterol level, suggesting that hypercholesterolemia accelerates postmenopausal bone loss. No significant differences were seen in any of the cytokines that presumably cause bone resorption. Conclusion These results showed that hypercholesterolemia has an inverse effect on bone loss independent of cytokines presumed to mediate bone loss.

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