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Xiaojing Wei Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Xi’an Jiaotong University Health Science Center, Xi’an, China
Key Laboratory of Environment and Genes Related to Diseases, Ministry of Education of China, Xi’an Jiaotong University, Xi’an, China
Institute of Neuroscience, Translational Medicine Institute, Xi’an Jiaotong University Health Science Center, Xi’an, China

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Yutian Tan Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Xi’an Jiaotong University Health Science Center, Xi’an, China
Key Laboratory of Environment and Genes Related to Diseases, Ministry of Education of China, Xi’an Jiaotong University, Xi’an, China
Institute of Neuroscience, Translational Medicine Institute, Xi’an Jiaotong University Health Science Center, Xi’an, China

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Jiaqi Huang Institute of Basic Medicine, School of Medicine, Tsinghua University, Beijing, China

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Ximing Dong Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Xi’an Jiaotong University Health Science Center, Xi’an, China
Key Laboratory of Environment and Genes Related to Diseases, Ministry of Education of China, Xi’an Jiaotong University, Xi’an, China
Institute of Neuroscience, Translational Medicine Institute, Xi’an Jiaotong University Health Science Center, Xi’an, China

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Weijie Feng Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Xi’an Jiaotong University Health Science Center, Xi’an, China
Key Laboratory of Environment and Genes Related to Diseases, Ministry of Education of China, Xi’an Jiaotong University, Xi’an, China
Institute of Neuroscience, Translational Medicine Institute, Xi’an Jiaotong University Health Science Center, Xi’an, China

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Tanglin Liu Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Xi’an Jiaotong University Health Science Center, Xi’an, China
Key Laboratory of Environment and Genes Related to Diseases, Ministry of Education of China, Xi’an Jiaotong University, Xi’an, China
Institute of Neuroscience, Translational Medicine Institute, Xi’an Jiaotong University Health Science Center, Xi’an, China

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Zhao Yang Department of Obstetrics and Gynecology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China

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Guiying Yang Department of Obstetrics and Gynecology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China

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Xiao Luo Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Xi’an Jiaotong University Health Science Center, Xi’an, China
Key Laboratory of Environment and Genes Related to Diseases, Ministry of Education of China, Xi’an Jiaotong University, Xi’an, China
Institute of Neuroscience, Translational Medicine Institute, Xi’an Jiaotong University Health Science Center, Xi’an, China

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N1-methylnicotinamide (MNAM), a product of methylation of nicotinamide through nicotinamide N-methyltransferase, displays antidiabetic effects in male rodents. This study aimed to evaluate the ameliorative potential of MNAM on glucose metabolism in a gestational diabetes mellitus (GDM) model. C57BL/6N mice were fed with a high-fat diet (HFD) for 6 weeks before pregnancy and throughout gestation to establish the GDM model. Pregnant mice were treated with 0.3% or 1% MNAM during gestation. MNAM supplementation in CHOW diet and HFD both impaired glucose tolerance at gestational day 14.5 without changes in insulin tolerance. However, MNAM supplementation reduced hepatic lipid accumulation as well as mass and inflammation in visceral adipose tissue. MNAM treatment decreased GLUT4 mRNA and protein expression in skeletal muscle, where NAD+ salvage synthesis and antioxidant defenses were dampened. The NAD+/sirtuin system was enhanced in liver, which subsequently boosted hepatic gluconeogenesis. GLUT1 protein was diminished in placenta by MNAM. In addition, weight of placenta, fetus weight, and litter size were not affected by MNAM treatment. The decreased GLUT4 in skeletal muscle, boosted hepatic gluconeogenesis and dampened GLUT1 in placenta jointly contribute to the impairment of glucose tolerance tests by MNAM. Our data provide evidence for the careful usage of MNAM in treatment of GDM.

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Xiaopan Yang Beijing Institute of Biotechnology, Academy of Military Medical Sciences, Beijing, China

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Xiaojing Fan Department of Endocrinology, Fifth Medical Center of Chinese PLA General Hospital, Beijing, China

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Jiangyue Feng Beijing Sungen Biomedical Technology Co. Ltd., Beijing, China

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

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Jingfei Li Beijing Institute of Biotechnology, Academy of Military Medical Sciences, Beijing, China
Institute of Physical Science and Information Technology, Anhui University, Hefei, China

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

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

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

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

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

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

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Qi Gao Beijing Sungen Biomedical Technology Co. Ltd., Beijing, China

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Fei Zheng Beijing Sungen Biomedical Technology Co. Ltd., Beijing, China

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Lei Xu Beijing Sungen Biomedical Technology Co. Ltd., Beijing, China

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

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Dandan Zhang Department of Laboratory, the Third Medical Center of Chinese PLA General Hospital, Beijing, China
Department of Laboratory, General Hospital of Armed Police Forces, Anhui Medical University, Hefei, China

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Hongbin Song Department of Laboratory, the Third Medical Center of Chinese PLA General Hospital, Beijing, China
Department of Laboratory, General Hospital of Armed Police Forces, Anhui Medical University, Hefei, China

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Yufei Wang Department of Laboratory, the Third Medical Center of Chinese PLA General Hospital, Beijing, China
Department of Laboratory, General Hospital of Armed Police Forces, Anhui Medical University, Hefei, China

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Xueping Ma Department of Laboratory, the Third Medical Center of Chinese PLA General Hospital, Beijing, China
Department of Laboratory, General Hospital of Armed Police Forces, Anhui Medical University, Hefei, China

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Zhiwei Sun Beijing Sungen Biomedical Technology Co. Ltd., Beijing, China

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Cheng Cao Beijing Institute of Biotechnology, Academy of Military Medical Sciences, Beijing, China

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Xiaoli Yang Department of Laboratory, the Third Medical Center of Chinese PLA General Hospital, Beijing, China
Department of Laboratory, General Hospital of Armed Police Forces, Anhui Medical University, Hefei, China

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Hui Zhong Beijing Institute of Biotechnology, Academy of Military Medical Sciences, Beijing, China

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Yi Fang Beijing Institute of Biotechnology, Academy of Military Medical Sciences, Beijing, China
Department of Endocrinology, Fifth Medical Center of Chinese PLA General Hospital, Beijing, China

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

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Golgi protein 73 (GP73), also called Golgi membrane protein 1 (GOLM1), 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. Notably, the aberrantly upregulated GP73 levels were indispensable for the enhanced protein kinase A signaling pathway associated with diabetes. In diet-induced obese 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 streptozotocin (STZ) and high-fat diet/STZ-induced diabetic mice. We thus concluded that GP73 was a feasible therapeutic target for the treatment of diabetes.

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