Publication: Lactobacillus paracasei HII01, xylooligosaccharide and synbiotics improve tibial microarchitecture in obese-insulin resistant rats
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Issued Date
2019-08-01
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17564646
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2-s2.0-85067066253
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Mahidol University
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SCOPUS
Bibliographic Citation
Journal of Functional Foods. Vol.59, (2019), 371-379
Suggested Citation
Sathima Eaimworawuthikul, Wannipa Tunapong, Titikorn Chunchai, Panan Suntornsaratoon, Narattaphol Charoenphandhu, Parameth Thiennimitr, Nipon Chattipakorn, Siriporn C. Chattipakorn Lactobacillus paracasei HII01, xylooligosaccharide and synbiotics improve tibial microarchitecture in obese-insulin resistant rats. Journal of Functional Foods. Vol.59, (2019), 371-379. doi:10.1016/j.jff.2019.06.004 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/49748
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Title
Lactobacillus paracasei HII01, xylooligosaccharide and synbiotics improve tibial microarchitecture in obese-insulin resistant rats
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Abstract
© 2019 Elsevier Ltd High-fat diet (HFD)-induced obese-insulin resistance negatively affects bone via gut microbiota dysbiosis-triggered systemic inflammation. The biotic treatment can improve metabolic status in HFD-fed rats. However, the microarchitectural analysis by bone histomorphometry of the tibia have not been determined. Forty-eight male Wistar rats were fed with normal diet or HFD for 24 weeks. At week13, rats were received either a vehicle, Lactobacillus paracasei HII01, xylooligosaccharides, or synbiotics. Blood analyses and tibial histomorphometry were performed. We found that L. paracasei HII01, xylooligosaccharides, and synbiotics improved obese-insulin resistance and systemic inflammation in HFD-fed rats. These biotics equally increased bone volume fraction and trabecular thickness, reduced osteoclast surface and active erosion surface, increased the double labeled surface, mineralizing surface, mineral apposition rate and bone formation rate of HFD-fed rats. In conclusion, these biotic therapies exerted an enhancement of bone microarchitecture in HFD-fed rats possibly by mitigating osteoclast-mediated bone resorption and promoting osteoblast-induced bone formation.