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  3. Glycolipid toxicity induces osteogenic dysfunction via the TLR4/S100B pathway

Glycolipid toxicity induces osteogenic dysfunction via the TLR4/S100B pathway

  • Int Immunopharmacol. 2021 Aug;97:107792. doi: 10.1016/j.intimp.2021.107792.
Bo Liang 1,  Ximei Shen 2,  Chao Lan 3,  Youfen Lin 3,  Chuanchuan Li 3,  Shuai Zhong 3,  Sunjie Yan 4
Affiliations

Affiliations

  • 1 Department of Endocrinology, M.D. Candidate, The First Affiliated Hospital of Fujian Medical University, China; Department of Endocrinology, The Second Affiliated Hospital of Fujian Medical University, China.
  • 2 Department of Endocrinology, M.D. Candidate, The First Affiliated Hospital of Fujian Medical University, China; Diabetes Research Institute of Fujian Province, Fuzhou, Fujian, China.
  • 3 Department of Endocrinology, M.D. Candidate, The First Affiliated Hospital of Fujian Medical University, China.
  • 4 Department of Endocrinology, M.D. Candidate, The First Affiliated Hospital of Fujian Medical University, China; Diabetes Research Institute of Fujian Province, Fuzhou, Fujian, China. Electronic address: fjyansunjie@163.com.
PMID: 34051593 DOI: 10.1016/j.intimp.2021.107792
Abstract

Diabetes can cause bone metabolism disorders and osteoporosis. The occurrence of both diabetes mellitus and osteoporosis increases the disability and mortality of elderly individuals due to pathological fracture. Abnormal metabolism of nutrientsis considered to be one of the important mechanisms of diabetes mellitus-induced osteoporosis. This study preliminarily explored the roles of TLR4 (Toll-like Receptor 4) and S100B in osteogenic dysfunction induced by glycolipid toxicity. In this study, a diabetic rat model and TLR4-knockdown diabetic rat model were used in vivo. MC3T3-E1 cells in a high glucose and palmitic acid environment were used as glycolipid toxicity cell models in vitro. We investigated the effects of TLR4 and S100B on osteogenesis by overexpression or inhibition of TLR4 and S100B in vitro. We found that when TLR4 or S100B was inhibited, ALP and OCN were significantly up-regulated and p-ERK was significantly down regulated in the glycolipid model. These results suggest that TLR4/S100B may play a role in reducing glycolipid toxicity by regulating ERK phosphorylation.

Keywords

Glycolipid toxicity; Osteogenic dysfunction; TLR4/S100B.

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