title: Glucocorticosteroid-induced osteoporosis in adult primiparous Göttingen miniature pigs: effects on bone mineral and mineral metabolism.
abstract: Information on the pathophysiology of glucocorticoid-induced osteoporosis (GIO) is limited, since its clinical picture often reflects a combined effect of glucocorticoids (GC) and the treated systemic disease (i.e., inflammation and immobility). In 50 healthy adult (30-mo-old) primiparous Göttingen minipigs, we studied the short-term (8 mo, n = 30) and long-term (15 mo, n = 10) effect of GC on bone and mineral metabolism longitudinally and cross-sectionally compared with a control group (n = 10). All animals on GC treatment received prednisolone orally at a dose of 1.0 mg x kg body wt(-1) x day(-1) for 8 wk and thereafter at 0.5 mg/kg body wt(-1) x day(-1). In the short term, GC reduced bone mineral density (BMD) at the lumbar spine by -47.5 +/- 5.1 mg/cm(3) from baseline (P < 0.001), which was greater (P < 0.05) than the loss [not significant (NS)] in the control group of -11.8 +/- 12.6 mg/cm(3). Calcium absorption decreased from baseline by -2,488 +/- 688 mg/7 days (P < 0.001) compared with -1,380 +/- 1,297 mg/7 days (NS) in the control group. Plasma bone alkaline phosphatase (BAP) decreased from baseline by -17.8 +/- 2.2 U/l (P < 0.000), which was significantly different (P < 0.05) from the value of the control group of -1.43 +/- 4.8 U/l. In the long term, the loss of BMD became more pronounced and bone mineral content (BMC), trabecular thickness, mechanical stability, calcium absorption, 25-hydroxyvitamin D(3), 1,25-dihydroxyvitamin D(3), and parathyroid hormone tended to be lower compared with the control group. There was a negative association between the cumulative dose of GC and BMD, which was associated with impaired osteoblastogenesis. In conclusion, the main outcomes after GC treatment are comparable to symptoms of GC-induced osteoporosis in human subjects. Thus the adult Göttingen miniature pig appears to be a valuable animal model for GC-induced osteoporosis.
authors: Institute of Physiology and Biochemistry of Nutrition, Federal Research Centre for Nutrition and Food-Location Kiel, Hermann-Weigmann-Str. 1, D-24103 Kiel, Germany. katharina.scholz-ahrens@bfel.de
authors: K E
authors: KE
authors: Scholz-Ahrens
authors: G
authors: G
authors: Delling
authors: B
authors: B
authors: Stampa
authors: A
authors: A
authors: Helfenstein
authors: H-J
authors: HJ
authors: Hahne
authors: Y
authors: Y
authors: Açil
authors: W
authors: W
authors: Timm
authors: R
authors: R
authors: Barkmann
authors: J
authors: J
authors: Hassenpflug
authors: J
authors: J
authors: Schrezenmeir
authors: C-C
authors: CC
authors: Glüer
mesh_terms: D000818:Animals; D001835:Body Weight / Q000187:drug effects; D015519:Bone Density / Q000187:drug effects*; D001842:Bone and Bones / Q000187:drug effects / Q000502:physiology; D002118:Calcium / Q000097:blood / Q000652:urine; D019245:Compressive Strength / Q000187:drug effects; D004195:Disease Models, Animal; D005260:Female; D005938:Glucocorticoids; D008903:Minerals / Q000378:metabolism*; D010024:Osteoporosis / Q000139:chemically induced* / Q000378:metabolism; D010298:Parity; D010758:Phosphorus / Q000097:blood / Q000652:urine; D011247:Pregnancy; D013552:Swine; D013997:Time Factors
chemical_list: D005938:Glucocorticoids; D008903:Minerals; D010758:Phosphorus; D002118:Calcium