Hepatic glucose sensing is required to preserve cell glucose competence
Because BAs increase β cell glucose competence , we propose that their glucose -dependent production may form the basis for a liver/pancreatic islet axis to control β cell glucose competence . Results Suppressed glucose uptake but normal glucose production after hepatic Glut2 inactivation.
We showed that chronic BAs or farnesoid X receptor (FXR) agonist treatment of primary islets increases glucose -stimulated insulin secretion, an effect not seen in islets from Fxr-/- mice. Collectively, our data show that glucose sensing by the liver controls β cell glucose competence and suggest BAs as a potential mechanistic link ...
Hepatic glucose sensing is required to preserve cell glucose competence
Feeding, energy expenditure, and insulin sensitivity were identical in LG2KO and control mice. Glucose tolerance was initially normal after Glut2 inactivation, but LG2KO mice exhibited progressive impairment of glucose -stimulated insulin secretion even though β cell mass and insulin content remained normal.
Such details provide a deeper understanding and appreciation for Cell Glucose Competence.
We showed that chronic BAs or farnesoid X receptor (FXR) agonist treatment of primary islets increases glucose -stimulated insulin secretion, an effect not seen in islets from Fxr -/- mice. Collectively, our data show that glucose sensing by the liver controls β cell glucose competence and suggest BAs as a potential mechanistic link.
PDF Hepatic glucose sensing is required to preserve cell glucose competence
on β cell glucose competence that is observed only in long-term studies. Thus, much more work will be required to fully elucidat the role of BAs on diverse aspects of the control of glucose homeostasis. Finally, since cholesterol is the precursor of other biologically active substances, such as isoprenoid, dolichol, or steroids, it may be that o
Collectively, our data show that glucose sensing by the liver controls beta- cell glucose competence , through a mechanism that likely depends on bile acid production and action on beta- cells .
Hepatic glucose sensing is required to preserve P cell glucose competence
Key Details About Cell Glucose Competence
Gluco-incretin hormones increase the glucose competence of pancreatic beta- cells by incompletely characterized mechanisms. We searched for genes that were differentially expressed in islets from control and Glp1r−/−; Gipr−/− (dKO) mice, which show ...
We report that intra-islet glucagon secreted from α- cells signals through β- cell glucagon and GLP-1 receptors (GcgR and GLP-1R), thereby conferring to rat islets their competence to exhibit first-phase glucose -stimulated insulin secretion (GSIS).
More Context About Cell Glucose Competence
Glucose Uptake Process Diagram Illustrating Cellular Mechanisms Stock. This note connects the source idea with the visuals in a simple, reader-friendly way.
Figure 1 from Intra-islet glucagon confers β-cell glucose competence. It works as a short bridge between the article summary and the gallery section.
Activation of the glucose receptor Glut-4 by insulin. | BioRender. It works as a short bridge between the article summary and the gallery section.
