Abstract
One of the mysteries in understanding the pathogenesis of diabetes is how glucagon-producing alpha cells in the pancreas remain relatively protected from the toxic environment created by metabolic stress, while insulin-producing beta cells are not protected and die by apoptosis. Metabolic stress refers to conditions of hyperglycemia, or chronically high levels of plasma glucose, and hyperlipidemia that includes increased levels of saturated fatty acids of which palmitate is the most abundant in human plasma. It is believed to be an important cause of beta cell apoptosis in type 2 diabetes. Marroqui and co-workers have made inroads into discovering how alpha cells survive metabolic stress by showing they express higher amounts of survival factors than beta cells (Marroqui et al., 2015).
Highlights
The evidence for a role for beta cell ER stress in type 2 diabetes comes from electron microscopy of ER appearance, as well as protein and mRNA expression studies in pancreas sections and islets of organ donors with type 2 diabetes (Butler et al, 2003; Laybutt et al, 2007)
Others have suggested that sick beta cells dedifferentiate and degranulate in type 2 diabetes and this could be a major mechanism of beta cell failure
The authors of the current study did not comment on whether they saw any apoptotic insulin-negative beta cells. This is an important question because it is not clear if the sick beta cells prolong their survival by de-differentiation, or if this is a step preceding apoptosis
Summary
The evidence for a role for beta cell ER stress in type 2 diabetes comes from electron microscopy of ER appearance, as well as protein and mRNA expression studies in pancreas sections and islets of organ donors with type 2 diabetes (Butler et al, 2003; Laybutt et al, 2007). The authors of the current study did not comment on whether they saw any apoptotic insulin-negative beta cells. The authors went on to study the mechanism of protection of alpha cells from ER stress-induced apoptosis. The Bcl-2-regulated pathway of apoptosis is activated by cellular stresses.
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