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作 者:Changhong Li Yi Zhang Li Chen Xiaoying Li
机构地区:[1]Nanjing AscendRare and Hua Medicine,Nanjing,Jiangsu 210000,China [2]Hua Medicine,Shanghai 201203,China [3]Department of Endocrinology and Metabolism,Zhongshan Hospital,Fudan University,Shanghai 200032,China
出 处:《Life Metabolism》2023年第5期12-16,共5页生命(代谢(英文)
基 金:supported by the grant from the National Natural Science Foundation of China(No.32241011).
摘 要:Glucokinase (GK) plays a pivotal role in glucose homeostasis as the glucose sensor in the pancreas and liver. Loss of function of GK results in hyperglycemia, and gain of function causes congenital hyperinsulinemic hypoglycemia. We speculate that the progressive loss of GK at both messenger RNA (mRNA) and protein levels in the islets and liver would be the key mechanism for Type 2 diabetes (T2D) pathogenesis. The development of GK activator (GKA) as an anti-diabetic drug has been endeavored for several decades. The failure of the early development of GKAs is due to the limitation of understanding the mode of GKA action. The success of dorzagliatin in the treatment of T2D has brought new hope for GK in setting a good model for repairing the underlying defects in the pancreatic islets and liver of T2D patients.
关 键 词:glucokinases glucokinase activator Type 2 diabetes pancreaticβcells LIVER glucose homeostasis
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