Palmitate-induced impairment of glucose-stimulated insulin secretion by pancreatic beta cells is disconnected from concomitant mitochondrial respiratory defects
Year: 2015
Type: conference-paper
Abstract: Background and aims: Pancreatic beta cell mitochondria couple the oxidative breakdown of glucose to the synthesis of ATP and are essential for glucose-stimulated insulin secretion (GSIS).Indeed, mitochondrial respiratory activity might prove a good indicator of functional beta cell integrity, and insight in islet respiration may thus benefit transplantation protocols.With this study we aimed to clarify the connection between mitochondrial function and GSIS in pancreatic beta cells subjected to glucolipotoxic conditions. Materials and methods:Islets isolated from C57BL/6 mice and INS-1E insulinoma cells were exposed for 24 or 48 hr to BSA-conjugated palmitate (free concentration 20-40 nM) in the presence of 11 mM glucose.Glucose sensitivity of oxidative phosphorylation was derived from absolute oxygen uptake rates measured in a Seahorse XF24, and insulin was quantified by ELISA.Respiratory activity and insulin secretion were normalised to islet DNA or INS-1E cell number determined from PicoGreen and DAPI fluorescence, respectively.Significance of palmitate effects was evaluated with Student's t-tests.
Source: PEARL (University of Plymouth)
Language: English
Subfield: Endocrinology, Diabetes and Metabolism
Field: Medicine
Domain: Health Sciences
Open Access status: green
OpenAlex ID: W2260025843