Endoplasmic reticulum stress contributes to beta cell apoptosis in type 2 diabetes

By D. R. Laybutt, A. M. Preston, Mia C. Åkerfeldt, J. Kench, A. K. Busch, A. Biankin, Trevor J. Biden. Diabetologia, 2007

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Loss of autophagy diminishes pancreatic beta cell mass and function with resultant hyperglycemia. (2008, background): “…survival, death, insulin secre- tion, and insulin action, or sensitivity, such as mitochondria c. (Petersen et al., 2004; Rodriguez-Enriquez et al., 2006; Maechler and Wollheim, 1999) and ER (Bernales et al., 2007; Laybutt et al., 2007; Ozcan et al., 2006), rely on autophagy for proper function.”
Insulin Resistance: From Mechanisms to Therapeutic Strategies (2021, background): “β-cells in chronic hyperglycemic diabetic humans and mice, and this contributes to the development of T2DM [142,143].”
The impact of the unfolded protein response on human disease (2012, result): “Importantly, an increase in proinsulin synthesis alone is sufficient to initiate a series of events including proinsulin misfolding, insulin granule depletion, loss of glucose-stimulated insulin secretion, and oxidative stress, similar to those observed in type II diabetes (Huang et al., 2007; Laybu”
Islet amyloid polypeptide, islet amyloid, and diabetes mellitus. (2011, background): “An increased production of the ER-stress markers HSPA5, DDIT3, DNAJC3, and BCL2-associated X protein was detected in human pancreas recovered from diabetic subjects (201).”