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While additional research is necessary to explore the potential role of GLP-1Rs expressed outside of the beta cell, including within the enteric and peripheral nervous systems, in enhancing beta cell function through enteral glucose mediation, current evidence indicates that the central nervous system (CNS) GLP-1Rs are not essential for the physiological regulation of blood sugar levels by endogenous GLP-1 or the pharmacological control of glucose homeostasis dependent on GLP-1Rs

19,20 Researchers have shown that the upregulation of disease-promoting transcription factors is one of the major impulsions of disease progression, propelled by deregulated transcriptional programs involving diverse interweaved actions of transcriptional co-activators