PMID- 31686881
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220411
IS  - 1178-7007 (Print)
IS  - 1178-7007 (Electronic)
IS  - 1178-7007 (Linking)
VI  - 12
DP  - 2019
TI  - Upregulation Of Renal GLUT2 And SGLT2 Is Involved In High-Fat Diet-Induced 
      Gestational Diabetes In Mice.
PG  - 2095-2105
LID - 10.2147/DMSO.S221396 [doi]
AB  - INTRODUCTION: 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.
CI  - (c) 2019 Jiang et al.
FAU - Jiang, Yong-Kuan
AU  - Jiang YK
AD  - Department of Anesthesiology, Ningbo No.6 Hospital, Ningbo, Zhejiang, People's 
      Republic of China.
FAU - Xin, Kai-Yue
AU  - Xin KY
AD  - Department of Cardiology, Shanghai Institute of Cardiovascular Diseases, 
      Zhongshan Hospital, Fudan University, Shanghai, People's Republic of China.
AD  - Department of Cardiology, Cheeloo College of Medicine, Shandong University, 
      Jinan, Shandong, People's Republic of China.
FAU - Ge, Hong-Wei
AU  - Ge HW
AD  - Department of Urology, Affiliated Hangzhou First People's Hospital, Zhejiang 
      University School of Medicine, Hangzhou, People's Republic of China.
FAU - Kong, Fei-Juan
AU  - Kong FJ
AD  - Department of Endocrinology and Metabolism, Shanghai General Hospital, Shanghai 
      Jiao Tong University School of Medicine, Shanghai, People's Republic of China.
AD  - Department of Endocrinology and Metabolism, Xuhui District Central Hospital of 
      Shanghai, Shanghai, People's Republic of China.
FAU - Zhao, Gang
AU  - Zhao G
AD  - Department of Cardiology, Shanghai Institute of Cardiovascular Diseases, 
      Zhongshan Hospital, Fudan University, Shanghai, People's Republic of China.
AD  - Department of Cardiology, Kashgar Prefecture Second People's Hospital, Kashi, 
      Xinjiang, People's Republic of China.
LA  - eng
PT  - Journal Article
DEP - 20191014
PL  - New Zealand
TA  - Diabetes Metab Syndr Obes
JT  - Diabetes, metabolic syndrome and obesity : targets and therapy
JID - 101515585
PMC - PMC6800457
OTO - NOTNLM
OT  - GLUT2
OT  - SGLT2
OT  - gestational diabetes mellitus
OT  - insulin resistance
OT  - renal threshold for glucose
COIS- The authors declare no conflicts of interest, financial or otherwise in this 
      work.
EDAT- 2019/11/07 06:00
MHDA- 2019/11/07 06:01
PMCR- 2019/10/14
CRDT- 2019/11/06 06:00
PHST- 2019/06/30 00:00 [received]
PHST- 2019/09/13 00:00 [accepted]
PHST- 2019/11/06 06:00 [entrez]
PHST- 2019/11/07 06:00 [pubmed]
PHST- 2019/11/07 06:01 [medline]
PHST- 2019/10/14 00:00 [pmc-release]
AID - 221396 [pii]
AID - 10.2147/DMSO.S221396 [doi]
PST - epublish
SO  - Diabetes Metab Syndr Obes. 2019 Oct 14;12:2095-2105. doi: 10.2147/DMSO.S221396. 
      eCollection 2019.