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We now demonstrate that GIPR agonist administration critically relies on Gipr expression in the hindbrain, while GIPR antagonism relies on hypothalamic Gipr expressionboth are probably neuronal populations, given that we used hSyn-driven Cre-expression for the region-specific knockout studies

In vitro studies using adipocyte cell lines, including 3T3-L1 cells and primary adipocyte cultures, have used this compound to examine lipolytic signalling, triglyceride hydrolysis mechanisms, fatty acid oxidation pathways, and adipokine secretion

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This upregulation disrupts the Beclin 1/Bcl-2 complex, releasing Beclin 1, which then promotes autophagy under hypoxic conditions (96)