Author:
Tiyasatkulkovit Wacharaporn,Aksornthong Sirion,Adulyaritthikul Punyanuch,Upanan Pornpailin,Wongdee Kannikar,Aeimlapa Ratchaneevan,Teerapornpuntakit Jarinthorn,Rojviriya Catleya,Panupinthu Nattapon,Charoenphandhu Narattaphol
Abstract
AbstractExcessive salt intake has been associated with the development of non-communicable diseases, including hypertension with several cardiovascular consequences. Although the detrimental effects of high salt on the skeleton have been reported, longitudinal assessment of calcium balance together with changes in bone microarchitecture and strength under salt loading has not been fully demonstrated. To address these unanswered issues, male Sprague–Dawley rats were fed normal salt diet (NSD; 0.8% NaCl) or high salt diet (HSD; 8% NaCl) for 5 months. Elevation of blood pressure, cardiac hypertrophy and glomerular deterioration were observed in HSD, thus validating the model. The balance studies were performed to monitor calcium input and output upon HSD challenge. The HSD-induced increase in calcium losses in urine and feces together with reduced fractional calcium absorption led to a decrease in calcium retention. With these calcium imbalances, we therefore examined microstructural changes of long bones of the hind limbs. Using the synchrotron radiation x-ray tomographic microscopy, we showed that trabecular structure of tibia and femur of HSD displayed a marked increase in porosity. Consistently, the volumetric micro-computed tomography also demonstrated a significant decrease in trabecular bone mineral density with expansion of endosteal perimeter in the tibia. Interestingly, bone histomorphometric analyses indicated that salt loading caused an increase in osteoclast number together with decreases in osteoblast number and osteoid volume. This uncoupling process of bone remodeling in HSD might underlie an accelerated bone loss and bone structural changes. In conclusion, long-term excessive salt consumption leads to impairment of skeletal mass and integrity possibly through negative calcium balance.
Funder
National Research Council of Thailand and Mahidol University
Chulalongkorn University
Post-doctoral fellowship grant awarded by Mahidol University
Thailand Research Fund (TRF)-Royal Golden Jubilee Ph.D. Program
Faculty of Allied Health Sciences, Burapha University
Thailand Research Fund (TRF) through International Research Network Program
Mahidol University–Multidisciplinary Research Cluster (MU–MRC) grant
Central Instrumental Facility (CIF/CNI), Faculty of Science Mahidol University
Thailand Toray Science Foundation
Mahidol University
The Medical Association of Thailand–Prasert Prasarttong-Osoth Initiative
Publisher
Springer Science and Business Media LLC
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