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- W32611442 abstract "Insulin regulates the energy homeostasis of the human body. This is synthesized in the endoplasmic reticulum (ER) of pancreatic beta cells from proinsulin. Chronic hyperglycemia increases considerably the proinsulin secretion, overcrowding the ER. Recent experimental evidence demonstrates that such states favor the proinsulin denaturation. The biophysical mechanism of this cellular dysfunction remains largely unknown. We use basic molecular principles and numerical simulations of time-dependent crowding conditions in the ER to show that crowding effects enhance the propensity of proinsulin molecules to (mis)fold in compressed, nonnative structures. Present results suggest: i) misfolding events and toxic accumulations increase dramatically if the proinsulin load exceeds 50% of the available space and ii) insufficient lag time for the relaxation of the ER between consecutive proinsulin uploads can cause irreversible alterations of folding capabilities. Present study may prove useful in generating new testable statements on circumstances leading to the development of diabetes." @default.
- W32611442 created "2016-06-24" @default.
- W32611442 creator A5031618666 @default.
- W32611442 date "2009-03-01" @default.
- W32611442 modified "2023-09-27" @default.
- W32611442 title "Dilation of the endoplasmic reticulum in beta cells due to molecular overcrowding?" @default.
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- W32611442 doi "https://doi.org/10.1016/j.bpc.2008.12.003" @default.
- W32611442 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/19121888" @default.
- W32611442 hasPublicationYear "2009" @default.
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