4.5 Article

Glucagon-like peptide-1 attenuates diabetes-associated osteoporosis in ZDF rat, possibly through the RAGE pathway

期刊

BMC MUSCULOSKELETAL DISORDERS
卷 23, 期 1, 页码 -

出版社

BMC
DOI: 10.1186/s12891-022-05396-5

关键词

Glucagon-like peptide-1; Advanced glycation endproducts; Diabetes; Osteoporosis; Liraglutide

资金

  1. National Natural Science Foundation of China [81500679]
  2. Natural Science Foundation of Guangdong Province, China [2017A030313519]
  3. Science and Technology Plan of Guangdong Province [2017A020215045]
  4. Science and Technology Plan of Guangzhou [202102020165]
  5. Guangdong Basic and Applied Basic Research Foundation [2020A1515010288, 2021A1515220101]

向作者/读者索取更多资源

GLP-1 receptor agonist liraglutide can have a beneficial effect on bone in diabetes by ameliorating the accumulation of advanced glycation endproducts (AGEs). It prevents deterioration of trabecular microarchitecture and enhances bone strength. In vitro experiments also show that GLP-1 attenuates AGEs-mediated damage in osteogenic proliferation and differentiation.
Background Diabetes-associated osteoporosis are partly caused by accumulation of advanced glycation endproducts (AGEs). Glucagon-like peptide-1 (GLP-1) has been shown to regulate bone turnover. Here we explore whether GLP-1 receptor agonist (GLP1RA) can have a beneficial effect on bone in diabetes by ameliorating AGEs. Methods In the present study, we evaluated the effects of the GLP-1 receptor agonist liraglutide, insulin and dipeptidyl peptidase-4 inhibitor saxagliptin on Zucker diabetic fatty rats. Meanwhile, we observed the effect of GLP-1 on AGEs-mediated osteoblast proliferation and differentiation and the signal pathway. Results Liraglutide prevented the deterioration of trabecular microarchitecture and enhanced bone strength. Moreover, it increased serum Alpl, Ocn and P1NP levels and decreased serum CTX. In vitro we confirmed that GLP-1 could attenuate AGEs-mediated damage in osteogenic proliferation and differentiation. Besides, GLP-1 down-regulated the ROS that caused by AGEs and the mRNA and protein expression of Rage . Conclusions Altogether, our findings suggest that GLP-1 receptor agonist promotes osteoblastogenesis and suppresses bone resorption on obese type 2 diabetic rats to a certain degree. The mechanism of these effects may be partly mediated by AGEs-RAGE-ROS pathway via the interaction with GLP-1 receptor.

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