Alteraciones metabólicas en ratas diabéticas eSS

STELLA MARIS DANIELE; GUSTAVO ROBERTO COINTRY; RICARDO FRANCISCO CAPOZZA; STELLA MARIS MARTINEZ; LIDA MORISOLI; JOSÉ LUIS FERRETTI

Rosario

Congreso; XXIII Reunión de la Asociación Argentina de Osteología y Metabolismo Mineral; 2006

Asociación Argentina de Osteología y Metabolismo Mineral

   Tomographic (pQCT) and mechanical data of femurs and metabolic data from 9 type-II diabetic eSS rats and 10 unaffected e controls weighing 390-440g were obtained to define their pathogenetic relationships.    eSS rats showed a. excessive cortical tissue vBMD and stiffness (vCtD, E) and diaphyseal stiffness, with low resilience and toughness (resistance to crack generation and progress), b. impaired bone mass-geometry indicators (BMC, cortical area, moment of inertia -MI-) with respect to body weight, and c. low diaphyseal strength (fracture load), with respect to controls (ANOVA, always p<0.001). A Bone Strength Index (BSI=MI.vCtD) which disregards mineralization-unrelated microstructural factors, underestimated the actual bone strength. eSS rats were hypercalciuric, and serum PTH varied directly with blood glucose, fructosamine and P and inversely with Ca. Despite their generally low values in eSS, bone mass-geometry indicators improved as a function of blood PTH, glucose and fructosamine (not Ca or P). Bone “material” or strength indicators did not vary with metabolic indicators in eSS but they did when analyzed together with controls.    Data shows that eSS rats have 1. delayed bone growth; 2. bone matrix hypermineralization and altered microstructural properties; 3. excessive stiffness of bone tissue and bones with impaired resilience and toughness (after 2); 4. inadequate bone geometry because the reduced bone strain by customary usage reduced bone mechanostat stimulation (after 3), and 5. bone weakness (after 3-4). An enhanced PTH activity, secondary either or both to hypercalciuria or to the diabetic condition, would be anabolic on bone formation but not enough to compensate for the primary delay of bone growth.