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Pancreatic β-cell mass is regulated by autophagy.Stimulation of autophagy by GLP-1 promotes β-cell survival.GLP-1 impacts on autophagy in other cell types.Uncovers a potential therapeutic pathway to modulate β-cell mass.Autophagy is a highly conserved intracellular recycling pathway that serves to recycle damaged organelles/proteins or superfluous nutrients during times of nutritional stress to provide energy to maintain intracellular homeostasis and sustain core metabolic functions. Under these conditions, autophagy functions as a cell survival mechanism but impairment of this pathway can lead to pro-death stimuli. Due to their role in synthesising and secreting insulin, pancreatic β-cells have a high requirement for robust degradation pathways. Recent research suggests that functional autophagy is required to maintain β-cell survival and function in response to high fat diet suggesting a pro-survival role. However, a role for autophagy has also been implicated in the pathogenesis of type 2 diabetes. Thus, the pro-survival vs pro-death role of autophagy in regulating β-cell mass requires discussion. Emerging evidence suggests that Glucagon-Like Peptide-1 (GLP-1) may exert beneficial effects on glucose homeostasis via autophagy-dependent pathways both in pancreatic β-cells and in other cell types. The aim of the current review is to: i) summarise the literature surrounding β-cell autophagy and its pro-death vs pro-survival role in regulating β-cell mass; ii) review the literature describing the impact of GLP-1 on β-cell autophagy and in other cell types; iii) discuss the potential underlying mechanisms.