Upregulation Of Renal GLUT2 And SGLT2 Is Involved In High-Fat Diet-Induced Gestational Diabetes In Mice

Yong-Kuan Jiang,1,* Kai-Yue Xin,2,3,* Hong-Wei Ge,4 Fei-Juan Kong,5,6 Gang Zhao2,7 1Department of Anesthesiology, Ningbo No.6 Hospital, Ningbo, Zhejiang, People’s Republic of China; 2Department of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan Universi...

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Autores principales: Jiang YK, Xin KY, Ge HW, Kong FJ, Zhao G
Formato: article
Lenguaje:EN
Publicado: Dove Medical Press 2019
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Acceso en línea:https://doaj.org/article/1f9fce15c97c4d7f9492a87736ad9a78
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id oai:doaj.org-article:1f9fce15c97c4d7f9492a87736ad9a78
record_format dspace
institution DOAJ
collection DOAJ
language EN
topic Gestational diabetes mellitus
Insulin resistance
Renal threshold for glucose
GLUT2
SGLT2
Specialties of internal medicine
RC581-951
spellingShingle Gestational diabetes mellitus
Insulin resistance
Renal threshold for glucose
GLUT2
SGLT2
Specialties of internal medicine
RC581-951
Jiang YK
Xin KY
Ge HW
Kong FJ
Zhao G
Upregulation Of Renal GLUT2 And SGLT2 Is Involved In High-Fat Diet-Induced Gestational Diabetes In Mice
description Yong-Kuan Jiang,1,* Kai-Yue Xin,2,3,* Hong-Wei Ge,4 Fei-Juan Kong,5,6 Gang Zhao2,7 1Department of Anesthesiology, Ningbo No.6 Hospital, Ningbo, Zhejiang, People’s Republic of China; 2Department of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, People’s Republic of China; 3Department of Cardiology, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, People’s Republic of China; 4Department of Urology, Affiliated Hangzhou First People’s Hospital, Zhejiang University School of Medicine, Hangzhou, People’s Republic of China; 5Department of Endocrinology and Metabolism, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People’s Republic of China; 6Department of Endocrinology and Metabolism, Xuhui District Central Hospital of Shanghai, Shanghai, People’s Republic of China; 7Department of Cardiology, Kashgar Prefecture Second People’s Hospital, Kashi, Xinjiang, People’s Republic of China*These authors contributed equally to this workCorrespondence: Fei-Juan KongDepartment of Endocrinology and Metabolism, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, No. 100 Haining Road, Hongkou District, Shanghai 200080, People’s Republic of ChinaTel +86-21-63240090Fax +86-21-63240090Email kongfeijuan@163.comGang ZhaoDepartment of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, No. 180 Fenglin Road, Xuhui District, Shanghai 200032, People’s Republic of ChinaTel +86-21-64041990 ext. 2745Fax +86-21-64223006Email gangzhao2012@outlook.comIntroduction: Gestational diabetes mellitus (GDM) is a metabolic disorder during mid- to late-pregnancy characterized by hyperglycemia, insulin resistance and fetal mal-development. Glucose transporter type 2 (GLUT2) and sodium-coupled glucose cotransporters 2 (SGLT2) in the proximal tubules play a critical role in the reabsorption of glucose and have been linked to the occurrence of type 2 diabetes mellitus (T2DM). Our study was designed to investigate the role of GLUT2 and SGLT2 in the pathogenesis of GDM, which is considered a forerunner of T2DM, and investigate the related molecular mechanism.Methods: High-fat diet (HFD) was utilized to build a GDM mouse model that closely induces metabolic abnormalities similar to human GDM. Body weight, blood glucose and serum insulin were recorded in the experimental process. Glucose tolerance was determined by the use of an intraperitoneal glucose tolerance test (IPGTT). In addition, levels of GLUT2 and SGLT2 were evaluated to further explore the underlying mechanism of GDM.Results: HFD feeding induced abnormal glucose metabolism as manifested by increased levels of blood glucose and insulin and prominent glucose intolerance. Additionally, fetal mice from mother feed on HFD showed higher mean body weight. Furthermore, HFD feeding led to an increase in the number of positive cells of GLUT2 and SGLT2 in the renal proximal tubule and the expressions of renal GLUT2 and SGLT2 mRNA and proteins in mice. However, no obvious change was observed in renal morphology.Conclusion: Our study demonstrates a potential involvement of renal GLUT2 and SGLT2 in GDM pathology in an HFD-induced GDM mouse model, which further supports the role of renal GLUT2 and SGLT2 not only in T1DM and T2DM but also in GDM.Keywords: gestational diabetes mellitus, insulin resistance, renal threshold for glucose, GLUT2, SGLT2
format article
author Jiang YK
Xin KY
Ge HW
Kong FJ
Zhao G
author_facet Jiang YK
Xin KY
Ge HW
Kong FJ
Zhao G
author_sort Jiang YK
title Upregulation Of Renal GLUT2 And SGLT2 Is Involved In High-Fat Diet-Induced Gestational Diabetes In Mice
title_short Upregulation Of Renal GLUT2 And SGLT2 Is Involved In High-Fat Diet-Induced Gestational Diabetes In Mice
title_full Upregulation Of Renal GLUT2 And SGLT2 Is Involved In High-Fat Diet-Induced Gestational Diabetes In Mice
title_fullStr Upregulation Of Renal GLUT2 And SGLT2 Is Involved In High-Fat Diet-Induced Gestational Diabetes In Mice
title_full_unstemmed Upregulation Of Renal GLUT2 And SGLT2 Is Involved In High-Fat Diet-Induced Gestational Diabetes In Mice
title_sort upregulation of renal glut2 and sglt2 is involved in high-fat diet-induced gestational diabetes in mice
publisher Dove Medical Press
publishDate 2019
url https://doaj.org/article/1f9fce15c97c4d7f9492a87736ad9a78
work_keys_str_mv AT jiangyk upregulationofrenalglut2andsglt2isinvolvedinhighfatdietinducedgestationaldiabetesinmice
AT xinky upregulationofrenalglut2andsglt2isinvolvedinhighfatdietinducedgestationaldiabetesinmice
AT gehw upregulationofrenalglut2andsglt2isinvolvedinhighfatdietinducedgestationaldiabetesinmice
AT kongfj upregulationofrenalglut2andsglt2isinvolvedinhighfatdietinducedgestationaldiabetesinmice
AT zhaog upregulationofrenalglut2andsglt2isinvolvedinhighfatdietinducedgestationaldiabetesinmice
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spelling oai:doaj.org-article:1f9fce15c97c4d7f9492a87736ad9a782021-12-02T06:12:41ZUpregulation Of Renal GLUT2 And SGLT2 Is Involved In High-Fat Diet-Induced Gestational Diabetes In Mice1178-7007https://doaj.org/article/1f9fce15c97c4d7f9492a87736ad9a782019-10-01T00:00:00Zhttps://www.dovepress.com/upregulation-of-renal-glut2-and-sglt2-is-involved-in-high-fat-diet-ind-peer-reviewed-article-DMSOhttps://doaj.org/toc/1178-7007Yong-Kuan Jiang,1,* Kai-Yue Xin,2,3,* Hong-Wei Ge,4 Fei-Juan Kong,5,6 Gang Zhao2,7 1Department of Anesthesiology, Ningbo No.6 Hospital, Ningbo, Zhejiang, People’s Republic of China; 2Department of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, People’s Republic of China; 3Department of Cardiology, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, People’s Republic of China; 4Department of Urology, Affiliated Hangzhou First People’s Hospital, Zhejiang University School of Medicine, Hangzhou, People’s Republic of China; 5Department of Endocrinology and Metabolism, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People’s Republic of China; 6Department of Endocrinology and Metabolism, Xuhui District Central Hospital of Shanghai, Shanghai, People’s Republic of China; 7Department of Cardiology, Kashgar Prefecture Second People’s Hospital, Kashi, Xinjiang, People’s Republic of China*These authors contributed equally to this workCorrespondence: Fei-Juan KongDepartment of Endocrinology and Metabolism, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, No. 100 Haining Road, Hongkou District, Shanghai 200080, People’s Republic of ChinaTel +86-21-63240090Fax +86-21-63240090Email kongfeijuan@163.comGang ZhaoDepartment of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, No. 180 Fenglin Road, Xuhui District, Shanghai 200032, People’s Republic of ChinaTel +86-21-64041990 ext. 2745Fax +86-21-64223006Email gangzhao2012@outlook.comIntroduction: Gestational diabetes mellitus (GDM) is a metabolic disorder during mid- to late-pregnancy characterized by hyperglycemia, insulin resistance and fetal mal-development. Glucose transporter type 2 (GLUT2) and sodium-coupled glucose cotransporters 2 (SGLT2) in the proximal tubules play a critical role in the reabsorption of glucose and have been linked to the occurrence of type 2 diabetes mellitus (T2DM). Our study was designed to investigate the role of GLUT2 and SGLT2 in the pathogenesis of GDM, which is considered a forerunner of T2DM, and investigate the related molecular mechanism.Methods: High-fat diet (HFD) was utilized to build a GDM mouse model that closely induces metabolic abnormalities similar to human GDM. Body weight, blood glucose and serum insulin were recorded in the experimental process. Glucose tolerance was determined by the use of an intraperitoneal glucose tolerance test (IPGTT). In addition, levels of GLUT2 and SGLT2 were evaluated to further explore the underlying mechanism of GDM.Results: HFD feeding induced abnormal glucose metabolism as manifested by increased levels of blood glucose and insulin and prominent glucose intolerance. Additionally, fetal mice from mother feed on HFD showed higher mean body weight. Furthermore, HFD feeding led to an increase in the number of positive cells of GLUT2 and SGLT2 in the renal proximal tubule and the expressions of renal GLUT2 and SGLT2 mRNA and proteins in mice. However, no obvious change was observed in renal morphology.Conclusion: Our study demonstrates a potential involvement of renal GLUT2 and SGLT2 in GDM pathology in an HFD-induced GDM mouse model, which further supports the role of renal GLUT2 and SGLT2 not only in T1DM and T2DM but also in GDM.Keywords: gestational diabetes mellitus, insulin resistance, renal threshold for glucose, GLUT2, SGLT2Jiang YKXin KYGe HWKong FJZhao GDove Medical PressarticleGestational diabetes mellitusInsulin resistanceRenal threshold for glucoseGLUT2SGLT2Specialties of internal medicineRC581-951ENDiabetes, Metabolic Syndrome and Obesity: Targets and Therapy, Vol Volume 12, Pp 2095-2105 (2019)