English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Tools annual

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Presents the access of premium content as premium feature

Premium Content

Global: Zendy Plus annual

Global: Zendy Free Plan

The glucose-dependency of cholecystokinin-8 (CCK-8)-stimulated insulin release was investigated at high (11.1 and 16.7 mM) glucose concentrations in rat pancreas perfusion and islet perifusion using glucose analogues, pseudo-alpha-D-glucose and 2-deoxy-D-glucose. In perfused pancreas, both glucose analogues (22.4 mM) inhibited high glucose (16.7 mM)-induced insulin release, but not normal glucose (5.6 mM)-induced insulin release, with or without CCK-8 (1 nM). In perifused islets, the same level of either of the glucose analogues inhibited high glucose (11.1 mM)-induced insulin release, with or without CCK-8 (100 nM). These results demonstrate that CCK-8-stimulated insulin release only at high glucose level is glucose-dependent.

Dependence of Cholecystokinin-8-Stimulated Insulin Release on High Glucose Levels Is Evidenced by Pseudo-.ALPHA.-D-Glucose in Rat Pancreas and Islets.