PMID- 19672815
OWN - NLM
STAT- MEDLINE
DCOM- 20100114
LR  - 20131121
IS  - 1439-4286 (Electronic)
IS  - 0018-5043 (Linking)
VI  - 41
IP  - 11
DP  - 2009 Nov
TI  - Glucose, metformin, and AICAR regulate the expression of G protein-coupled 
      receptor members in INS-1 beta cell.
PG  - 799-804
LID - 10.1055/s-0029-1234043 [doi]
AB  - Glucagon-like peptide-1 receptor (GLP-1R), glucose-dependent insulinotropic 
      polypeptide receptor (GIPR), and G protein-coupled receptor 40 (GPR40) are 
      members of G protein-coupled receptors (GPCR) family. They are abundantly 
      expressed in islet beta cells, and mediate effects of incretins and fatty acids 
      in beta cells. Glucose and 5-AMP-activated protein kinase (AMPK) are known to be 
      involved in the regulation of beta cell function. Metformin and the potential 
      therapeutic drug for type 2 diabetes, 5-amino-4-imidazolecarboxamide riboside 
      (AICAR), are both known activators of AMPK. Here we studied the effects of 
      glucose, metformin, and AICAR on the expression of GPCR in INS-1 beta cell. INS-1 
      beta cells were supplemented with different concentrations of glucose, metformin, 
      or AICAR. The expressions of GLP-1R, GIPR, GPR40, and a nuclear transcription 
      factor - peroxisome-proliferator activated receptor alpha (PPARalpha) - were 
      analyzed by real-time RT-PCR and immunoblotting. The time-course of the mRNA 
      degradation of these receptors was also monitored by applying actinomycin D to 
      cells. We demonstrated that the expressions of GLP-1R, GIPR, and PPARalpha were 
      downregulated when INS-1beta cells were treated with glucose, while their 
      expressions were upregulated when treated with metformin or AICAR. Glucose, 
      metformin, or AICAR treatment had no obvious effect on the expression of GPR40. 
      These results indicate that glucose, metformin, and AICAR regulated the 
      expressions of incretin receptors and PPARalpha, but not GPR40 in beta cells. 
      Whether AMPK is a key regulator of these factors mediated receptor regulation 
      remains to be investigated further.
FAU - Pan, Q R
AU  - Pan QR
AD  - Department of Endocrinology and Metabolism, Peking Union Medical College 
      Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, 
      Suaifuyuan Wangfujing Beijing, P. R. China.
FAU - Li, W H
AU  - Li WH
FAU - Wang, H
AU  - Wang H
FAU - Sun, Q
AU  - Sun Q
FAU - Xiao, X H
AU  - Xiao XH
FAU - Brock, B
AU  - Brock B
FAU - Schmitz, O
AU  - Schmitz O
LA  - eng
PT  - Journal Article
DEP - 20090811
PL  - Germany
TA  - Horm Metab Res
JT  - Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et 
      metabolisme
JID - 0177722
RN  - 0 (G-protein-coupled receptor 40, rat)
RN  - 0 (Receptors, G-Protein-Coupled)
RN  - 0 (Ribonucleotides)
RN  - 360-97-4 (Aminoimidazole Carboxamide)
RN  - 9100L32L2N (Metformin)
RN  - F0X88YW0YK (AICA ribonucleotide)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Aminoimidazole Carboxamide/*analogs & derivatives/pharmacology
MH  - Animals
MH  - Cell Line, Tumor
MH  - Gene Expression Regulation/*drug effects
MH  - Glucose/*metabolism
MH  - Insulin-Secreting Cells/*drug effects/metabolism
MH  - Metformin/*pharmacology
MH  - Rats
MH  - Receptors, G-Protein-Coupled/*genetics/*metabolism
MH  - Ribonucleotides/*pharmacology
EDAT- 2009/08/13 09:00
MHDA- 2010/01/15 06:00
CRDT- 2009/08/13 09:00
PHST- 2009/08/13 09:00 [entrez]
PHST- 2009/08/13 09:00 [pubmed]
PHST- 2010/01/15 06:00 [medline]
AID - 10.1055/s-0029-1234043 [doi]
PST - ppublish
SO  - Horm Metab Res. 2009 Nov;41(11):799-804. doi: 10.1055/s-0029-1234043. Epub 2009 
      Aug 11.