PMID- 7820779
OWN - NLM
STAT- MEDLINE
DCOM- 19950216
LR  - 20190830
IS  - 0171-967X (Print)
IS  - 0171-967X (Linking)
VI  - 55
IP  - 4
DP  - 1994 Oct
TI  - Surgically induced uremia in rats. II: Osseous PTH-susceptible signaling systems 
      as predictors of bone resorption.
PG  - 281-7
AB  - Predicting the course of parathormone (PTH)-elicited bone turnover in both humans 
      and experimental rat models with moderate chronic uremia, using only standard 
      clinical chemistry analyses, is often difficult. Consequently, rat bone from 1 + 
      2/3 nephrectomized animals, after 230 days of progressive renal failure, was 
      examined for PTH-stimulated adenylate cyclase (AC) and phospholipase C (PL-C) 
      activities. Correlations to biological parameters related to the function of bone 
      and kidney were made. Reduced renal function was demonstrated by increased serum 
      creatinine; circulating 1,25 dihydroxyvitamin D3 below detection level; 
      diminished renal PTH-elicited AC activity; and decreased urinary cAMP excretion. 
      PTH-activated renal PL-C was also reduced. However, no significant differences 
      were seen in urine creatinine, calcium, phosphate, and hydroxyproline, nor in 
      serum PTH, alkaline phosphatase, calcium, and phosphate. Notwithstanding, renal 
      osteodystrophy developed as estimated by increased plasticity of the long bones, 
      as well as reduction of the diaphyseal (Dd) and inner femoral mid-shaft (Di) 
      diameters. Femoral cancellous bone exhibited a substantial elevation of both 
      eroded surface (ES) and osteoid surface (OS) as well as a marked reduction in 
      trabecular bone volume (TBV). Calvarial PTH-activated AC was enhanced, whereas 
      corresponding PL-C was markedly reduced. PTH-enhanced AC correlated positively 
      with ES and negatively with Di, respectively. PTH-enhanced PL-C, however, 
      correlated positively with bone calcium content and negatively with ES. Our 
      results indicate that bone modeling and remodeling are to a large extent related 
      to PTH-elicited signaling systems, and cannot easily be predicted by standard 
      clinical chemistry analyses.
FAU - Jablonski, G
AU  - Jablonski G
AD  - Institute of Medical Biochemistry, University of Oslo, Norway.
FAU - Danielsen, C C
AU  - Danielsen CC
FAU - Mosekilde, L
AU  - Mosekilde L
FAU - Gordeladze, J O
AU  - Gordeladze JO
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Calcif Tissue Int
JT  - Calcified tissue international
JID - 7905481
RN  - 0 (Parathyroid Hormone)
RN  - EC 3.1.4.- (Type C Phospholipases)
RN  - EC 4.6.1.1 (Adenylyl Cyclases)
SB  - IM
MH  - Adenylyl Cyclases/metabolism
MH  - Animals
MH  - Bone Remodeling/physiology
MH  - Bone Resorption/*etiology/physiopathology
MH  - Bone and Bones/physiology
MH  - Chronic Kidney Disease-Mineral and Bone Disorder/etiology/physiopathology
MH  - Female
MH  - Hyperparathyroidism, Secondary/etiology/physiopathology
MH  - Kidney/physiology
MH  - Nephrectomy
MH  - Parathyroid Hormone/*physiology
MH  - Rats
MH  - Rats, Wistar
MH  - Signal Transduction/physiology
MH  - Type C Phospholipases/metabolism
MH  - Uremia/complications/etiology/*physiopathology
EDAT- 1994/10/01 00:00
MHDA- 1994/10/01 00:01
CRDT- 1994/10/01 00:00
PHST- 1994/10/01 00:00 [pubmed]
PHST- 1994/10/01 00:01 [medline]
PHST- 1994/10/01 00:00 [entrez]
AID - 10.1007/BF00310407 [doi]
PST - ppublish
SO  - Calcif Tissue Int. 1994 Oct;55(4):281-7. doi: 10.1007/BF00310407.