title: Endogenously produced n-3 fatty acids protect against ovariectomy induced bone loss in fat-1 transgenic mice.
abstract: Aging is associated with bone loss, leading to increased risk of fractures. Recently, there is growing interest in identifying nutritional supplements that can prevent bone loss with minimum side effects. There is increasing evidence for the beneficial effects of n-3 fatty acids in the prevention of bone loss. A transgenic mouse model (fat-1) that produces n-3 fatty acids endogenously and its wild type counterpart were used in this study to determine the effects of endogenously produced n-3 fatty acids on serum bone turnover markers, long bones, and lumbar vertebrae. Serum alkaline phosphatase and P1NP levels decreased significantly in wild type mice after ovariectomy. No significant changes were seen in osteocalcin. Cancellous and cortical bone mass were higher in the femur of fat-1 mice. In wild type mice, there was significant loss of bone after ovariectomy in the distal femur, femoral neck, proximal tibia, and fourth lumbar vertebra. However, in fat-1 mice, there was no, or significantly less, bone lost after ovariectomy in all the sites studied. We conclude that endogenously produced n-3 fatty acids can attenuate ovariectomy induced bone loss in the different bone sites studied, mainly as a consequence of decreased bone resorption at the endosteal surface.
authors.affiliation: Department of Medicine, Division of Clinical Immunology and Rheumatology, Medical Research Division, E-RAHC, University of Texas Health Science Center at San Antonio, 1214 W. Schunior, Edinburg, TX 78541, USA. banu@uthscsa.edu
authors.forename: Jameela
authors.initials: J
authors.lastname: Banu
authors.forename: Arunabh
authors.initials: A
authors.lastname: Bhattacharya
authors.forename: Mizanur
authors.initials: M
authors.lastname: Rahman
authors.forename: J X
authors.initials: JX
authors.lastname: Kang
authors.forename: Gabriel
authors.initials: G
authors.lastname: Fernandes
mesh_terms: D000273:Adipose Tissue; D000469:Alkaline Phosphatase / Q000097:blood; D000818:Animals; D001835:Body Weight; D015519:Bone Density; D029742:Caenorhabditis elegans Proteins / Q000235:genetics; D044943:Fatty Acid Desaturases / Q000235:genetics; D015525:Fatty Acids, Omega-3 / Q000378:metabolism*; D005260:Female; D005269:Femur / Q000502:physiology; D005360:Fibula / Q000502:physiology; D008159:Lumbar Vertebrae / Q000502:physiology; D051379:Mice; D008822:Mice, Transgenic; D015675:Osteocalcin / Q000097:blood; D010024:Osteoporosis / Q000209:etiology / Q000517:prevention & control*; D010052:Ovariectomy; D010446:Peptide Fragments / Q000097:blood; D011347:Procollagen / Q000097:blood; D013977:Tibia / Q000502:physiology
chemical_list: D029742:Caenorhabditis elegans Proteins; D015525:Fatty Acids, Omega-3; D010446:Peptide Fragments; D011347:Procollagen; C466741:fat-1 protein, C elegans; C047202:procollagen Type I N-terminal peptide; D015675:Osteocalcin; D044943:Fatty Acid Desaturases; D000469:Alkaline Phosphatase
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