PMID- 38322335
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20240210
IS  - 2211-3835 (Print)
IS  - 2211-3843 (Electronic)
IS  - 2211-3835 (Linking)
VI  - 14
IP  - 2
DP  - 2024 Feb
TI  - Metabolic basis of solute carrier transporters in treatment of type 2 diabetes 
      mellitus.
PG  - 437-454
LID - 10.1016/j.apsb.2023.09.004 [doi]
AB  - Solute carriers (SLCs) constitute the largest superfamily of membrane transporter 
      proteins. These transporters, present in various SLC families, play a vital role 
      in energy metabolism by facilitating the transport of diverse substances, 
      including glucose, fatty acids, amino acids, nucleotides, and ions. They actively 
      participate in the regulation of glucose metabolism at various steps, such as 
      glucose uptake (e.g., SLC2A4/GLUT4), glucose reabsorption (e.g., SLC5A2/SGLT2), 
      thermogenesis (e.g., SLC25A7/UCP-1), and ATP production (e.g., SLC25A4/ANT1 and 
      SLC25A5/ANT2). The activities of these transporters contribute to the 
      pathogenesis of type 2 diabetes mellitus (T2DM). Notably, SLC5A2 has emerged as a 
      valid drug target for T2DM due to its role in renal glucose reabsorption, leading 
      to groundbreaking advancements in diabetes drug discovery. Alongside SLC5A2, 
      multiple families of SLC transporters involved in the regulation of glucose 
      homeostasis hold potential applications for T2DM therapy. SLCs also impact drug 
      metabolism of diabetic medicines through gene polymorphisms, such as 
      rosiglitazone (SLCO1B1/OATP1B1) and metformin (SLC22A1-3/OCT1-3 and SLC47A1, 
      2/MATE1, 2). By consolidating insights into the biological activities and 
      clinical relevance of SLC transporters in T2DM, this review offers a 
      comprehensive update on their roles in controlling glucose metabolism as 
      potential drug targets.
CI  - (c) 2024 The Authors.
FAU - Le, Jiamei
AU  - Le J
AD  - Shanghai Key Laboratory of Molecular Imaging, Zhoupu Hospital, Shanghai 
      University of Medicine and Health Sciences, Shanghai 201318, China.
AD  - School of Health Science and Engineering, University of Shanghai for Science and 
      Technology, Shanghai 200093, China.
FAU - Chen, Yilong
AU  - Chen Y
AD  - School of Health Science and Engineering, University of Shanghai for Science and 
      Technology, Shanghai 200093, China.
FAU - Yang, Wei
AU  - Yang W
AD  - Metabolic Disease Research Center, Zhengzhou Central Hospital Affiliated to 
      Zhengzhou University, Zhengzhou 450007, China.
FAU - Chen, Ligong
AU  - Chen L
AD  - School of Pharmaceutical Sciences, Tsinghua University, Beijing 100084, China.
FAU - Ye, Jianping
AU  - Ye J
AD  - Metabolic Disease Research Center, Zhengzhou Central Hospital Affiliated to 
      Zhengzhou University, Zhengzhou 450007, China.
AD  - Research Center for Basic Medicine, Academy of Medical Sciences, Zhengzhou 
      University, Zhengzhou 450052, China.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20230915
PL  - Netherlands
TA  - Acta Pharm Sin B
JT  - Acta pharmaceutica Sinica. B
JID - 101600560
PMC - PMC10840401
OTO - NOTNLM
OT  - ATP production
OT  - Energy metabolism
OT  - Glucose homeostasis
OT  - Polymorphisms
OT  - Solute carriers (SLCs)
OT  - Type 2 diabetes mellitus (T2DM)
EDAT- 2024/02/07 06:42
MHDA- 2024/02/07 06:43
PMCR- 2023/09/15
CRDT- 2024/02/07 03:59
PHST- 2023/05/26 00:00 [received]
PHST- 2023/07/10 00:00 [revised]
PHST- 2023/08/09 00:00 [accepted]
PHST- 2024/02/07 06:43 [medline]
PHST- 2024/02/07 06:42 [pubmed]
PHST- 2024/02/07 03:59 [entrez]
PHST- 2023/09/15 00:00 [pmc-release]
AID - S2211-3835(23)00357-X [pii]
AID - 10.1016/j.apsb.2023.09.004 [doi]
PST - ppublish
SO  - Acta Pharm Sin B. 2024 Feb;14(2):437-454. doi: 10.1016/j.apsb.2023.09.004. Epub 
      2023 Sep 15.