Glucose-stimulated insulin secretion is not obligatorily linked to an increase in O2 consumption in betaHC9 cells.
We investigated the effects of glucose on the rates of oxygen consumption (OCR) and insulin secretion (ISR) by betaHC9 cells derived from mouse pancreatic islets with beta-cell hyperplasia. Our results demonstrate that the OCR by betaHC9 cells incubated in nutrient-rich DMEM is unaffected by glucose (0-25 mM), is dissociated from the ISR (which increases with the addition of glucose), and is always higher than that measured in PBS. Glucose (25 mM) increases both the OCR and ISR when added to nutrient-free PBS. On the basis of results presented here, we suggest that, contrary to the current consensus, the observed increases in the OCR by beta-cells upon addition of glucose to nutrient-free buffers may be unrelated to the process of glucose-stimulated insulin secretion (GSIS) and, instead, related to nutrient starvation. We believe that a reevaluation of the implication of changes in OCR upon glucose stimulation in the process of GSIS is warranted and that OCR and ISR measurements should be performed in more physiological media to avoid nutrient starvation artifacts.
Papas
K K
KK
Core Technologies/Analytics and Bio-Nuclear Magnetic Resonance, Novartis Institute for Biomedical Research, Summit, New Jersey 07901-1398, USA.
Jarema
M A
MA
D000818:Animals; D002460:Cell Line; D005947:Glucose / Q000494:pharmacology*; D006965:Hyperplasia; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology*; D051379:Mice; D010101:Oxygen Consumption / Q000502:physiology*
D007328:Insulin; D005947:Glucose