CA8 links pancreatic insulin secretion and liver glucose production in mouse models
A mouse study reports that CA8 regulates both pancreatic insulin secretion and liver glucose production. Opposite changes occurred in the two organs in obesity and type-two-diabetes models; the result does not demonstrate treatment effects in people.

CA8 changes in opposite directions in islets and liver cells
A research group reported that CA8 regulates the strength of IP3R1-dependent intracellular calcium signaling and thereby coordinates post-meal insulin secretion and fasting hepatic glucose production. In mice lacking CA8, both measures increased. In an obesity/type 2 diabetes model, CA8 reportedly increased in pancreatic islets but decreased in liver cells.
The supplied research summary does not provide a directly comparable prior measurement or intervention result for this study.
In the reported mouse experiments, restoring CA8 in the liver suppressed excessive glucose production and fasting blood glucose. The findings also describe opposite CA8 changes in pancreatic islets and liver cells in an obesity/type 2 diabetes model.
The reported result places insulin secretion and hepatic glucose production within a shared regulatory mechanism rather than treating them only as separate abnormalities. It does not establish a treatment effect or clinical application in people.
Sources
- 京都大学 研究成果膵臓と肝臓をつなぐ血糖調節のしくみを解明―2型糖尿病の複雑な病態から新治療へ―Read source →