title: The effects of low dose parathyroid hormone on lumbar vertebrae in a rat model for chronic alcohol abuse.
abstract: This study evaluated the hypothesis that increased bone marrow adipogenesis is coupled to decreased bone formation in rats consuming alcohol. Parathyroid hormone (PTH) increased bone formation but had no effect on marrow adiposity. We conclude that increased adiposity does not prevent the bone anabolic response to PTH.
  
  
  BACKGROUND
  Alcoholism results in decreased bone formation and increased bone marrow adiposity. The present study tested the hypothesis that these reciprocal changes are coupled by evaluating the effect of intermittent PTH on bone formation and bone marrow adiposity in a rat model for chronic alcohol abuse.
  
  
  METHODS
  Three-month-old male Sprague Dawley rats (n = 10-11/group) were fed the Lieber-DeCarli liquid diet with 35% of the calories derived from ethanol. Control rats were pair-fed an isocaloric alcohol-free diet. The rats were administered low dose PTH (1 µg/kg/day sc, 5 d/week) or vehicle for 6 weeks. Cancellous bone architecture in lumbar vertebrae was evaluated by micro-computed tomography followed by histomorphometric assessment of bone formation and marrow adiposity.
  
  
  RESULTS
  Alcohol increased bone marrow adiposity but reduced bone formation. The latter was due to decreases in mineralizing perimeter/bone perimeter, a surrogate measure of osteoblast number, and mineral apposition rate, a measure of osteoblast activity. PTH increased bone formation by increasing mineralizing perimeter/bone perimeter. In contrast, PTH had no effect on mineral apposition rate or bone marrow adiposity. Interactions between alcohol consumption and PTH treatment were not detected for any endpoints evaluated.
  
  
  CONCLUSIONS
  PTH treatment blunted the decrease in mineralizing perimeter/bone perimeter in alcohol-fed rats but was ineffective in preventing the increase in bone marrow adiposity. These findings suggest that the alcohol-induced increase in adipocytes is not directly responsible for the accompanying reduction in bone formation.
authors.affiliation: Department of Nutrition and Exercise Sciences, Oregon State University, 107d Milam Hall, Corvallis, OR 97331, USA.
authors.forename: K S
authors.initials: KS
authors.lastname: Howe
authors.forename: U T
authors.initials: UT
authors.lastname: Iwaniec
authors.forename: R T
authors.initials: RT
authors.lastname: Turner
mesh_terms: D017667:Adipocytes / Q000187:drug effects; D050154:Adiposity / Q000187:drug effects; D000437:Alcoholism / Q000503:physiopathology*; D000818:Animals; D001853:Bone Marrow / Q000187:drug effects / Q000503:physiopathology; D004195:Disease Models, Animal; D000431:Ethanol / Q000494:pharmacology; D008159:Lumbar Vertebrae / Q000000981:diagnostic imaging / Q000187:drug effects* / Q000503:physiopathology; D008297:Male; D010006:Osteoblasts / Q000187:drug effects; D010012:Osteogenesis / Q000187:drug effects* / Q000502:physiology; D010281:Parathyroid Hormone / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D055114:X-Ray Microtomography / Q000379:methods
chemical_list: D010281:Parathyroid Hormone; D000431:Ethanol