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Cholesterol extraction from pancreatic beta cells has previously been shown to disrupt the internalisation, clustering and cAMP responses of the glucagon-like peptide-1 receptor (GLP-1R), a class B1 GPCR with key roles in the control of blood glucose levels via the potentiation of insulin secretion in beta cells and weight reduction via the modulation of brain appetite control centres

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Protein kinase C and fatty acid transport protein 4 (FATP4) [144] play an important role in the increase of GLP-1 secretion and improvement in glycemic tolerance caused by oleic acid (OA), both in vivo and in vitro [145]