Polar bears (Ursus maritimus), the most evolutionary advanced hibernators, avoid significant bone loss during hibernation.
Some hibernating animals are known to reduce muscle and bone loss associated with mechanical unloading during prolonged immobilisation,compared to humans. However, here we show that wild pregnant polar bears (Ursus maritimus) are the first known animals to avoid significant bone loss altogether, despite six months of continuous hibernation. Using serum biochemical markers of bone turnover, we showed that concentrations for bone resorption are not significantly increased as a consequence of hibernation in wild polar bears. This is in sharp contrast to previous studies on other hibernating species, where for example, black bears (Ursus americanus), show a 3-4 fold increase in serum bone resorption concentrations posthibernation,and must compensate for this loss through rapid bone recovery on remobilisation, to avoid the risk of fracture. In further contrast to black bears, serum concentrations of bone formation markers were highly significantly increased in pregnant female polar bears compared to non-pregnant,thus non-hibernating females both prior to and after hibernation. However, bone formation concentrations in new mothers were significantly reduced compared to pre-hibernation concentrations. The de-coupling of bone turnover in favour of bone formation prior to hibernation, suggests that wild polar bears may posses a unique physiological mechanism for building bone in protective preparation against expected osteopenia associated with disuse,starvation, and hormonal drives to mobilise calcium for reproduction, during hibernation. Understanding this physiological mechanism could have profound implications for a natural solution for the prevention of osteoporosis in animals subjected to captivity with inadequate space for exercise,humans subjected to prolonged bed rest while recovering from illness, or astronauts exposed to antigravity during spaceflight.© 2008 Elsevier Inc. All rights reserved.
Lennox
Alanda R
AR
Veterinary Basic Sciences, Royal Veterinary College, Hawkshead lane, North Mymms, Hertfordshire, AL9 7TA, United KingdomInstitute of Orthopaedics and Musculoskeletal Science, University College London, Royal National Orthopaedic Hospital, Stanmore, HA7 4LP, United Kingdom. alennox@rvc.ac.uk
Goodship
Allen E
AE
D000220:Adaptation, Biological / Q000502:physiology*; D000818:Animals; D005075:Biological Evolution; D018488:Bone Demineralization, Pathologic / Q000097:blood / Q000453:epidemiology / Q000662:veterinary*; D001862:Bone Resorption / Q000097:blood / Q000453:epidemiology / Q000662:veterinary; D024042:Collagen Type I / Q000097:blood; D005260:Female; D006605:Hibernation / Q000502:physiology*; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D010446:Peptide Fragments / Q000097:blood; D010455:Peptides / Q000097:blood; D011247:Pregnancy; D011347:Procollagen / Q000097:blood; D001503:Ursidae / Q000097:blood / Q000502:physiology*
D024042:Collagen Type I; D010446:Peptide Fragments; D010455:Peptides; D011347:Procollagen; C052929:collagen type I trimeric cross-linked peptide; C042813:procollagen type I carboxy terminal peptide; D007334:Insulin-Like Growth Factor I