2017
DOI: 10.1016/j.bbrc.2016.12.125
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Adipose-derived mesenchymal stem cells ameliorate hyperglycemia through regulating hepatic glucose metabolism in type 2 diabetic rats

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Cited by 47 publications
(42 citation statements)
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“…A recent study indicated a novel mechanism by which MSCs alleviated insulin resistance, which involved the regulation of M2 macrophage polarization and promotion of interleukin-6 production in adipose tissue (33). Another study indicated that MSCs improved hyperglycemia by regulating hepatic glucose metabolism in an AMP-activated protein kinase signaling pathway-dependent manner (17). However, in the peripheral insulin target tissues, skeletal muscle accounts for ~70-90% of insulin-stimulated glucose disposal, which serves an important role in the modulation of insulin resistance (23).…”
Section: Discussionmentioning
confidence: 99%
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“…A recent study indicated a novel mechanism by which MSCs alleviated insulin resistance, which involved the regulation of M2 macrophage polarization and promotion of interleukin-6 production in adipose tissue (33). Another study indicated that MSCs improved hyperglycemia by regulating hepatic glucose metabolism in an AMP-activated protein kinase signaling pathway-dependent manner (17). However, in the peripheral insulin target tissues, skeletal muscle accounts for ~70-90% of insulin-stimulated glucose disposal, which serves an important role in the modulation of insulin resistance (23).…”
Section: Discussionmentioning
confidence: 99%
“…Adipose-derived MSC isolation, culture and identification. Adipose-derived MSCs were isolated and purified from immature rats as described previously (17,19). Briefly, rats were anesthetized with pentobarbital sodium intraperitoneally (60 mg/kg) and sacrificed by cervical dislocation; adipose tissue isolated from the groin was digested using 0.05% trypsin and 0.1% collagen I.…”
Section: Animalsmentioning
confidence: 99%
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“…比例, 而通过小干扰RNA抑制MSCs中IL-6表达, 显著 抑制脂肪组织中M2型巨噬细胞极化, 从而很大程度上 抑制MSCs减轻脂肪组织胰岛素抵抗的效应. 脂肪来源 间充质干细胞(adipose stromal cells, ASCs)通过激 活AMPK磷酸化促进肝脏肝糖原合成并抑制肝糖输 出而改善肝脏胰岛素抵抗 [17] ; 此外UC-MSCs还可通 过下调2型糖尿病大鼠肝脏和脂肪组织中慢性炎症 小体NLRP3的表达, 改善肝脏和脂肪组织的慢性炎 症, 激活PI3K-AKT的表达, 改善大鼠的胰岛素抵抗 [18] . 上述研究结果为干细胞治疗糖尿病奠定了新的理论 基础.…”
Section: 实Uc-mscs输注增加了脂肪组织中m2型巨噬细胞的unclassified