Back to Search
Start Over
Role of histamine H 3 receptor in glucagon‐secreting αTC1.6 cells
- Source :
- FEBS Open Bio, FEBS Open Bio, Vol 5, Iss 1, Pp 36-41 (2015)
- Publication Year :
- 2014
- Publisher :
- Wiley, 2014.
-
Abstract
- Highlights • Histamine H3 receptor is expressed in pancreatic α-cells. • Histamine H3 receptor negatively regulates glucagon secretion from αTC1.6 cells. • Immepip, a selective H3 receptor agonist, decreases serum glucagon concentration in rats.<br />Pancreatic α-cells secrete glucagon to maintain energy homeostasis. Although histamine has an important role in energy homeostasis, the expression and function of histamine receptors in pancreatic α-cells remains unknown. We found that the histamine H3 receptor (H3R) was expressed in mouse pancreatic α-cells and αTC1.6 cells, a mouse pancreatic α-cell line. H3R inhibited glucagon secretion from αTC1.6 cells by inhibiting an increase in intracellular Ca2+ concentration. We also found that immepip, a selective H3R agonist, decreased serum glucagon concentration in rats. These results suggest that H3R modulates glucagon secretion from pancreatic α-cells.
- Subjects :
- endocrine system
Pancreatic α-cells
medicine.medical_specialty
QH301-705.5
Histamine H1 receptor
H3KO, histamine H3 receptor-gene knockout
Biology
CNS, central nervous system
Article
General Biochemistry, Genetics and Molecular Biology
Histamine H3 receptor
Histamine receptor
chemistry.chemical_compound
H3R, histamine H3 receptor
Histamine H2 receptor
Internal medicine
medicine
Histamine H4 receptor
Biology (General)
VDCCs, voltage-dependent Ca2+ channels
Glucagon secretion
GLP, glucagon-like peptide
αTC1.6 cells
Immepip
Endocrinology
chemistry
KRB, Krebs–Ringer bicarbonate buffer
Glucagon receptor family
hormones, hormone substitutes, and hormone antagonists
Subjects
Details
- ISSN :
- 22115463
- Volume :
- 5
- Database :
- OpenAIRE
- Journal :
- FEBS Open Bio
- Accession number :
- edsair.doi.dedup.....02a91ed8a3e7953b287bc0aaa5c98eb6
- Full Text :
- https://doi.org/10.1016/j.fob.2014.12.001