Heat-shock treatment of mouse pancreatic islets results in a partial loss of islet cells but no remaining functional impairment among the surviving beta cells.
To elucidate the role of thermal stress on the function of pancreatic beta cells, isolated mouse pancreatic islets were incubated for 30 min at 42 degrees C. This resulted in decreased glucose-stimulated insulin secretion, inhibited total protein and pro-insulin synthesis and the induction of heat-shock proteins with molecular weights of 64 and 88 kDa. Six days later, the islets exposed to heat shock showed a lower DNA content, indicating islet cell death. However, the insulin secretory response and rates of oxygen consumption in the presence of glucose were normal. It is suggested that the induction of heat-shock proteins does not permanently impair beta-cell function, but rather protects these cells from lasting damage.
Welsh
M
M
Department of Medical Cell Biology, Uppsala University, Sweden.
Eizirik
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DL
Strandell
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D000818:Animals; D002470:Cell Survival; D004247:DNA / Q000032:analysis / Q000378:metabolism; D005947:Glucose / Q000494:pharmacology; D006360:Heat-Shock Proteins / Q000378:metabolism / Q000502:physiology; D006358:Hot Temperature / Q000009:adverse effects*; D007328:Insulin / Q000032:analysis / Q000378:metabolism; D007515:Islets of Langerhans / Q000166:cytology* / Q000378:metabolism / Q000502:physiology; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D010100:Oxygen / Q000493:pharmacokinetics
D006360:Heat-Shock Proteins; D007328:Insulin; D004247:DNA; D005947:Glucose; D010100:Oxygen