QUICK SEARCH:   [advanced] Author: Keyword(s):
Home     Help     Feedback     Subscriptions     Archive     Search     Table of Contents

First published online April 18, 2006
Journal of Experimental Biology 209, 1630-1638 (2006)
Published by The Company of Biologists 2006
doi: 10.1242/jeb.02185

This Article Summary Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Donahue, S. W. Articles by McGee, M. E. Search for Related Content PubMed PubMed Citation Articles by Donahue, S. W. Articles by McGee, M. E.

Parathyroid hormone may maintain bone formation in hibernating black bears (Ursus americanus) to prevent disuse osteoporosis

Seth W. Donahue^1,*, Sarah A. Galley¹, Michael R. Vaughan², Patricia Patterson-Buckendahl³, Laurence M. Demers⁴, Josef L. Vance¹ and Meghan E. McGee¹

¹ Michigan Technological University, 1400 Townsend Drive, Houghton, MI 49931, USA
² Virginia Polytechnic Institute and State University, Blacksburg, VA, USA
³ Rutgers University, Piscataway, NJ, USA
⁴ The Pennsylvania State University, Hershey, PA, USA

View larger version (16K): [in a new window]   Fig. 1. Normalized serum resorption (ICTP) and formation (PICP and osteocalcin) marker concentrations during the 3-month hibernation period. Each data point is the mean value from five bears. Serum was collected every 10 days; the first sample was taken December 31, the last was March 31. The resorption marker increased immediately after the onset of hibernation. After 10–20 days, the formation markers increased and appeared to remain coupled to the increased resorption for the duration of hibernation. The PICP and ICTP concentration values for the entire study period (i.e. pre-hibernation, hibernation and post-hibernation seasons) have previously been published (Donahue et al., 2003a).

View larger version (11K): [in a new window]   Fig. 2. Serum osteocalcin levels were significantly correlated with serum PTH levels for pre-hibernation, hibernation and post-hibernation. Samples were pooled (N=27).

View larger version (11K): [in a new window]   Fig. 3. The amount of PGE2 released by osteoblastic cells was greatest when the cells were treated with serum collected in the post-hibernation period (N=9). P-values are for comparisons with the post-hibernation value. Pre-hibernation (N=8) and hibernation (N=7) values were not different from each other (P=0.48). Values are means ± s.e.m.

View larger version (20K): [in a new window]   Fig. 4. Proposed differences in bone remodeling and calcium metabolism between human bedrest (Shackelford et al., 2004), spinal cord injury (SCI) (Maimoun et al., 2005; Modlesky et al., 2005), hyperparathyroidism (HPT) (Brockstedt et al., 1995; Monchik and Gorgun, 2004) and hibernating bears. There is increased remodeling activity in all four conditions; however, bone resorption (Resorb) and formation (Form) appear to be balanced in hibernating bears whereas they are unbalanced in the other three conditions. This imbalance leads to increased cortical porosity and decreased bone mineral density (BMD) and cortical thickness in humans. However, cortical porosity decreases and cortical cross-sectional area and mineral content are unchanged in hibernating bears (McGee et al., 2006). As in human inactivity, resorption increases and formation decreases in hibernating bats and hamsters, leading to increased cortical porosity and decreased cortical thickness (Kwiecinski et al., 1987; Steinberg et al., 1979; Steinberg et al., 1981; Steinberg et al., 1986). In the human conditions, calcium liberated by bone resorption is excreted in urine and increases total (tCa) and ionized (iCa) serum calcium concentration. Bears, however, do not urinate during hibernation and thus it is likely that the calcium liberated by bone resorption is recycled back into bone, which is possibly facilitated by PTH increasing renal reabsorption of calcium.