Alaa Shaheen
Kafr El-Sharakwa Medical Centre, Egypt
Posters-Accepted Abstracts: J Diabetes Metab
There is a debate on the function of mitochondrial uncoupling protein-2 in beta cells and its involvement in palmitate-induced impairment of glucose-stimulated insulin secretion. Some investigators suggested that uncoupling protein-2 is involved in this impairment while others denied its involvement. Based on the results of their studies, this controversy can be solved by hypothesizing that palmitate-induced impairment of glucose-stimulated insulin secretion occurs in two stages, early stage and late stage, depending on the integrity of electron supply and transport system through electron transport chain after palmitate treatment. Prolonged exposure of beta cells to palmitate can impair this system. Early stage impairment occurs due to uncoupling by uncoupling protein-2 when this system is still intact. When this system becomes impaired, late stage impairment occurs due to reduced ATP production independent of uncoupling by uncoupling protein-2. The change in glucose-stimulated oxygen uptake after palmitate treatment reflects the integrity of this system and can be used to differentiate between the two stages. Some beta-cell lines appear to be more resistant to palmitate-induced impairment of electron supply and transport system than others and therefore, early stage is prominent in the more resistant cell lines and less prominent in the less resistant cell lines.
Email: alaa-shaheen@outlook.com
