PMID- 24373234
OWN - NLM
STAT- MEDLINE
DCOM- 20140710
LR  - 20220410
IS  - 1878-0814 (Electronic)
IS  - 1877-1173 (Print)
IS  - 1877-1173 (Linking)
VI  - 121
DP  - 2014
TI  - Regulation of glucose homeostasis by GLP-1.
PG  - 23-65
LID - B978-0-12-800101-1.00002-8 [pii]
LID - 10.1016/B978-0-12-800101-1.00002-8 [doi]
AB  - Glucagon-like peptide-1(7-36)amide (GLP-1) is a secreted peptide that acts as a 
      key determinant of blood glucose homeostasis by virtue of its abilities to slow 
      gastric emptying, to enhance pancreatic insulin secretion, and to suppress 
      pancreatic glucagon secretion. GLP-1 is secreted from L cells of the 
      gastrointestinal mucosa in response to a meal, and the blood glucose-lowering 
      action of GLP-1 is terminated due to its enzymatic degradation by 
      dipeptidyl-peptidase-IV (DPP-IV). Released GLP-1 activates enteric and autonomic 
      reflexes while also circulating as an incretin hormone to control endocrine 
      pancreas function. The GLP-1 receptor (GLP-1R) is a G protein-coupled receptor 
      that is activated directly or indirectly by blood glucose-lowering agents 
      currently in use for the treatment of type 2 diabetes mellitus (T2DM). These 
      therapeutic agents include GLP-1R agonists (exenatide, liraglutide, lixisenatide, 
      albiglutide, dulaglutide, and langlenatide) and DPP-IV inhibitors (sitagliptin, 
      vildagliptin, saxagliptin, linagliptin, and alogliptin). Investigational agents 
      for use in the treatment of T2DM include GPR119 and GPR40 receptor agonists that 
      stimulate the release of GLP-1 from L cells. Summarized here is the role of GLP-1 
      to control blood glucose homeostasis, with special emphasis on the advantages and 
      limitations of GLP-1-based therapeutics.
CI  - (c) 2014 Elsevier Inc. All rights reserved.
FAU - Nadkarni, Prashant
AU  - Nadkarni P
AD  - Department of Medicine, State University of New York (SUNY), Upstate Medical 
      University, Syracuse, New York, USA; Joslin Diabetes Center, State University of 
      New York (SUNY), Upstate Medical University, Syracuse, New York, USA.
FAU - Chepurny, Oleg G
AU  - Chepurny OG
AD  - Department of Medicine, State University of New York (SUNY), Upstate Medical 
      University, Syracuse, New York, USA.
FAU - Holz, George G
AU  - Holz GG
AD  - Department of Medicine, State University of New York (SUNY), Upstate Medical 
      University, Syracuse, New York, USA; Department of Pharmacology, State University 
      of New York (SUNY), Upstate Medical University, Syracuse, New York, USA. 
      Electronic address: holzg@upstate.edu.
LA  - eng
GR  - R01 DK045817/DK/NIDDK NIH HHS/United States
GR  - R01 DK069575/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - Netherlands
TA  - Prog Mol Biol Transl Sci
JT  - Progress in molecular biology and translational science
JID - 101498165
RN  - 0 (GLP1R protein, human)
RN  - 0 (Glucagon-Like Peptide-1 Receptor)
RN  - 0 (Receptors, Glucagon)
RN  - 89750-14-1 (Glucagon-Like Peptide 1)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Animals
MH  - Diabetes Mellitus, Type 2/drug therapy/metabolism
MH  - Glucagon-Like Peptide 1/biosynthesis/*metabolism
MH  - Glucagon-Like Peptide-1 Receptor
MH  - Glucose/*metabolism
MH  - *Homeostasis
MH  - Humans
MH  - Insulin-Secreting Cells/metabolism
MH  - Receptors, Glucagon/agonists/metabolism
PMC - PMC4159612
MID - NIHMS616869
OTO - NOTNLM
OT  - Diabetes
OT  - GLP-1
OT  - Glucagon
OT  - Glucose
OT  - Hyperglycemia
OT  - Incretin hormone
OT  - Insulin
COIS- All authors declare no conflict of interest concerning any of the concepts 
      addressed in this review of the literature.
EDAT- 2014/01/01 06:00
MHDA- 2014/07/11 06:00
PMCR- 2014/09/10
CRDT- 2013/12/31 06:00
PHST- 2013/12/31 06:00 [entrez]
PHST- 2014/01/01 06:00 [pubmed]
PHST- 2014/07/11 06:00 [medline]
PHST- 2014/09/10 00:00 [pmc-release]
AID - B978-0-12-800101-1.00002-8 [pii]
AID - 10.1016/B978-0-12-800101-1.00002-8 [doi]
PST - ppublish
SO  - Prog Mol Biol Transl Sci. 2014;121:23-65. doi: 
      10.1016/B978-0-12-800101-1.00002-8.