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Investigators at Fujian Medical University Discuss Findings in Hyperglycemia (Metformin Alleviates Hyperglycemia-induced Apoptosis and Differentiation Suppression In Osteoblasts Through Inhibiting the Tlr4 Signaling Pathway)

NewsRx Diabetes Daily

06-11-19

2019 JUN 10 (NewsRx) -- By a News Reporter-Staff News Editor at NewsRx Diabetes Daily -- Research findings on Nutritional and Metabolic Diseases and Conditions - Hyperglycemia are discussed in a new report. According to news reporting originating in Fuzhou, People’s Republic of China, by NewsRx journalists, research stated, “Metformin was found to protect against hyperglycemia-induced injury in osteoblasts, but the cellular mechanisms involved remain unclear. Therefore, the aim of this study was to determine the effect of metformin on hyperglycemia-induced apoptosis and differentiation suppression in osteoblasts and to explore its relationships with the TLR4 signaling pathway.”

Financial supporters for this research include Natural Science Foundation of Fujian Province, Science and Technology Innovation Joint Fund Project, Fujian Province, National Natural Science Foundation of China.

The news reporters obtained a quote from the research from Fujian Medical University, “Main methods: A mouse osteoblast cell line, MC3T3-E1, and a diabetic rat model were used to survey the protective effects of metformin on hyperglycemia-induced injury. TLR4 expression was altered using small interfering (si) RNA and lentivirus-mediated TLR4 overexpression. LPS was used as a specific TLR4 activator, and CLI095 was used as a TLR4 inhibitor. Metformin improved osteoblast differentiation, reduced apoptosis in hyperglycemic osteoblasts, and inhibited TLR4, MyD88 and NF-kappa B expression in a dose-dependent manner. Down-regulating the expression or inhibiting the activity of TLR4 enhanced these protective effects of metformin on osteoblast differentiation, cell viability and cell apoptosis in hyperglycemic conditions, whereas up-regulating the expression or activating the activity of TLR4 had the opposite effects. Activating NF-kappa B suppressed the protective effects of metformin, while inhibiting NF-kappa B activity had the opposite effects. Metformin increased ALP and OCN secretion, enhanced BMP-2 expression, improved bone mineral density (BMD), and decreased TLR4, MyD88 and NF-kappa B levels in the femur tissues of diabetic rats.”

According to the news reporters, the research concluded: “Taken together our experimentation support the hypothesis that metformin may alleviate hyperglycemia-induced apoptosis and differentiation suppression in osteoblasts by inhibiting the TLR4/MyD88/NF-kappa B signaling pathway.”

For more information on this research see: Metformin Alleviates Hyperglycemia-induced Apoptosis and Differentiation Suppression In Osteoblasts Through Inhibiting the Tlr4 Signaling Pathway. Life Sciences, 2019;216():29-38. Life Sciences can be contacted at: Pergamon-Elsevier Science Ltd, The Boulevard, Langford Lane, Kidlington, Oxford OX5 1GB, England. (Elsevier - www.elsevier.com; Life Sciences - http://www.journals.elsevier.com/life-sciences/)

Our news correspondents report that additional information may be obtained by contacting S.J. Yan, Fujian Medical University, First Affiliated Hospital, Dept. of Endocrinology, Fuzhou 350005, Fujian, People’s Republic of China. Additional authors for this research include L.F. Zheng, J.J. Ye, Y. Xie and X.M. Shen.

The direct object identifier (DOI) for that additional information is: https://doi.org/10.1016/j.lfs.2018.11.008. This DOI is a link to an online electronic document that is either free or for purchase, and can be your direct source for a journal article and its citation.

(Our reports deliver fact-based news of research and discoveries from around the world.)

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