Meiling Tong
Nanjing Medical University
42 Papers
249 Citations
Meiling Tong is an academic researcher from Nanjing Medical University. The author has contributed to research in topics: Medicine & Biology. The author has an hindex of 12, co-authored 34 publications.
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Papers
Mitochondrial dysfunction is induced by high levels of glucose and free fatty acids in 3T3-L1 adipocytes.
Chun-Lin Gao,Chun Zhu,Ya-Ping Zhao,Xiao-Hui Chen,Chenbo Ji,Chun-Mei Zhang,Jin-Gai Zhu,Zhengkun Xia,Meiling Tong,Xirong Guo +9 more
TL;DR: It was found that high glucose, high FFAs, or high glucose+high FFAs reduced insulin-stimulated glucose uptake in differentiated 3T3-L1 adipocytes and the mitochondria became smaller and more compact.
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miR-148a is Associated with Obesity and Modulates Adipocyte Differentiation of Mesenchymal Stem Cells through Wnt Signaling
Chunmei Shi,Min Zhang,Meiling Tong,Lei Yang,Lingxia Pang,Ling Chen,Guangfeng Xu,Xia Chi,Qin Hong,Yuhui Ni,Chen-Bo Ji,Xirong Guo +11 more
TL;DR: The results suggest that miR-148a is a biomarker of obesity in human subjects and mouse model, which represents a CREB-modulated miRNA that acts to repress Wnt1, thereby promoting adipocyte differentiation.
TNF-α induces mitochondrial dysfunction in 3T3-L1 adipocytes
Xiao-Hui Chen,Ya-Ping Zhao,Mei Xue,Chen-Bo Ji,Chun-Lin Gao,Jin-Gai Zhu,Da-Ni Qin,Chun-Zhao Kou,Xiao-Hong Qin,Meiling Tong,Xirong Guo +10 more
TL;DR: Investigating whether mitochondrial dysfunction is involved in pathogenesis of TNF-alpha-mediated insulin resistance found it to be a potential target for the treatment of insulin resistance.
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Over-expression of NYGGF4 inhibits glucose transport in 3T3-L1 adipocytes via attenuated phosphorylation of IRS-1 and Akt.
Chun-Mei Zhang,Xiao-Hui Chen,Bin Wang,Feng Liu,Xia Chi,Meiling Tong,Yuhui Ni,Rong-hua Chen,Xirong Guo +8 more
TL;DR: The potential role of NYGGF4 in glucose homeostasis and possibly in the pathogenesis of obesity is highlighted, as it reduces glucose uptake in response to insulin and impaired insulin-stimulated GLUT4 translocation.
Over-expression of NYGGF4 (PID1) inhibits glucose transport in skeletal myotubes by blocking the IRS1/PI3K/AKT insulin pathway
TL;DR: Over-expression of NYGGF4 inhibits glucose transport in skeletal myotubes by blocking the IRS1/PI3K/AKT insulin pathway and highlights the potential role of NY GGF4 in glucose homeostasis and the development of insulin resistance in obesity.
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