Carbonic anhydrase VIII regulates glucose-induced insulin secretion and hepatic glucose production via IP3R1-mediated Ca2+ release

ABSTRACT: Intracellular Ca2+ dynamics represent a key mechanism in glucose-induced insulin secretion (GIIS) and hepatic glucose production (HGP). In this study, we demonstrated that Car8wdl mice, a global carbonic anhydrase VIII (CA8)-deficient model, had increased GIIS and moderate HGP elevation in vivo and ex vivo. These phenotypes were mediated by the enhancement of inositol-3-phosphate receptor 1 (IP3R1)-facilitated Ca2+ release attributable to the absence of CA8. In the isolated CA8-deficient hepatocytes, increased gluconeogenic gene expression was detected, and the enhancement of HGP was not attenuated by PKA and PLC inhibitor treatment. In ob/ob mice, CA8 expression was increased in pancreatic islets but decreased in hepatocytes, whereas hepatic CA8 overexpression reduced glucagon-induced HGP

INSTRUMENT(S): Illumina HiSeq 1000

ORGANISM(S): Mus musculus

SUBMITTER: Muhammad Fauzi 

PROVIDER: E-MTAB-15682 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress