GP73 blockade alleviates abnormal glucose homeostasis in diabetic mice

in Journal of Molecular Endocrinology
Authors:
Xiaopan YangX Yang, Beijing Institute of Biotechnology, Academy of Military Medical Sciences, Beijing, China

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Xiaojing FanX Fan, Department of Endocrinology, 5th Medical Center of Chinese PLA General Hospital, Beijing, China

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Jiangyue FengJ Feng, Beijing Institute of Biotechnology, Academy of Military Medical Sciences, Beijing, China

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Tinghui FanT Fan, Beijing Institute of Biotechnology, Academy of Military Medical Sciences, Beijing, China

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Jingfei LiJ Li, Institute of Physical Science and Information Technology, Anhui University, Hefei, China

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Linfei HuangL Huang, Beijing Institute of Biotechnology, Academy of Military Medical Sciences, Beijing, China

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Luming WanL Wan, Beijing Institute of Biotechnology, Academy of Military Medical Sciences, Beijing, China

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Huan YangH Yang, Beijing Institute of Biotechnology, Academy of Military Medical Sciences, Beijing, China

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Huilong LiH Li, Beijing Institute of Biotechnology, Academy of Military Medical Sciences, Beijing, China

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Jing GongJ Gong, Beijing Institute of Biotechnology, Academy of Military Medical Sciences, Beijing, China

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Yanhong ZhangY Zhang, Beijing Institute of Biotechnology, Academy of Military Medical Sciences, Beijing, China

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Qi GaoQ Gao, none, Beijing Sungen Biomedical Technology Co. Ltd., Beijing, China

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Fei ZhengF Zheng, none, Beijing Sungen Biomedical Technology Co. Ltd, Beijing, China

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Lei XuL Xu, none, Beijing Sungen Biomedical Technology Co. Ltd., Beijing, China

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Haotian LinH Lin, Beijing Institute of Biotechnology, Academy of Military Medical Sciences, Beijing, China

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Dandan ZhangD Zhang, Department of Clinical Laboratory, 3rd Medical Center of Chinese PLA General Hospital, Beijing, China

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Hongbin SongH Song, Department of Clinical Laboratory, 3rd Medical Center of Chinese PLA General Hospital, Beijing, China

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Yufei WangY Wang, Department of Clinical Laboratory, 3rd Medical Center of Chinese PLA General Hospital, Beijing, China

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Xueping MaX Ma, Department of Clinical Laboratory, 3rd Medical Center of Chinese PLA General Hospital, Beijing, China

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Zhiwei SunZ Sun, Beijing Institute of Biotechnology, Academy of Military Medical Sciences, Beijing, China

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Cheng CaoC Cao, Department of Genetic Engineering, Beijing Institute of Biotechnology, Academy of Military Medical Sciences, Beijing, China

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Xiaoli YangX Yang, Department of Clinical Laboratory,, 3rd Medical Center of Chinese PLA General Hospital, Beijing, China

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Hui ZhongH Zhong, Department of Genetic Engineering, Academy of Military Medical Sciences, Beijing Institute of Biotechnology, Beijing, China

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Yi FangY Fang, Department of Endocrinology, 5th Medical Center of Chinese PLA General Hospital, Beijing, China

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Congwen WeiC Wei, Beijing Institute of Biotechnology, Academy of Military Medical Sciences, Beijing, China

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Correspondence: Congwen Wei, Email: weicongwen@aliyun.com
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Golgi protein 73 (GP73) is a resident Golgi type II transmembrane protein and is considered as a serum marker for the detection of a variety of cancers. A recent work revealed the role of the secreted GP73 in stimulating liver glucose production and systemic glucose homeostasis. Since exaggerated hepatic glucose production plays a key role in the pathogenesis of type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM), GP73 may thus represent a potential therapeutic target for treating diabetic patients with pathologically elevated levels. Here in this study, we found that the circulating GP73 levels were significantly elevated in T2DM and positively correlated with hemoglobin A1C (HbA1c). Notably, the aberrantly up-regulated GP73 levels were indispensable for the enhanced PKA signaling pathway associated with diabetes. In diet-induced obese (DIO) mouse model, GP73 siRNA primarily targeting liver tissue was potently effective in alleviating abnormal glucose metabolism. Ablation of GP73 from whole animals also exerted a profound glucose-lowering effect. Importantly, neutralizing circulating GP73 improved glucose metabolism in STZ and HFD/STZ-induced diabetic mice. We thus concluded that GP73 was a feasible therapeutic target for the treatment of diabetes.

 

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