Allsopp, Sherry-Ann2022-11-012022-11-012022-01-28https://hdl.handle.net/2139/54430Medicinal cannabis and cannabinoid-based products are becoming more accessible as policies continue to globally change towards the status of Cannabis sativa. It is likely that patients with type-2 diabetes (T2D) might opt to use these products as a means of controlling this debilitating disease. Moreover, others might use them in an attempt to relieve neuropathic pain associated with complications of T2D while still actively taking their medication. Incretin mimetics or glucagon-like peptide 1 receptor (GLP-1R) agonists represent a class of medication prescribed for the control of glucose in T2D. By activating the GLP-1R, a G-protein coupled receptor located on the pancreatic beta cell, these molecules augment glucose-stimulated insulin secretion, and improve whole-body glucose homeostasis. Cannabinoids exert their activity via two classical cannabinoid receptors, cannabinoid-1 and 2 (CB1R and CB2R, respectively), which are also G-protein coupled receptors located in several parts of the body including the pancreatic beta cell. Recently, it has been shown that CB1R blockade resulted in an increase in GLP-1R-mediated insulin secretion. However, global blockade of CB1R results in unfavourable psychological effects. To date, no investigations have been conducted on the impact of CB2R on the GLP-1R mediated insulin secretion. By using a Chinese hamster ovary cell line stably and transiently transfected with both GLP-1R and CB2R respectively, as well as utilizing agonists and antagonists of these receptors, I will investigate whether modulation of the CB2R has an impact on GLP-1R-mediated insulin secretion by assessing cyclic adenosine monophosphate (cAMP) accumulation and the underlying signalling pathway.enMedicinal CannabiscannabinoidreceptorsOther