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Basal fatty acid oxidation increases after recurrent low glucose in human primary astrocytes – published online 06/10/2018

Fig from Weightman-Potter paper

Paul G. Weightman Potter, Julia M. Vlachaki Walker, Josephine L. Robb, John K. Chilton, Ritchie Williamson, Andrew D Randall, Kate L. J. Ellacott, Craig Beall

Hypoglycaemia is a major limiting factor for good glycaemic control in diabetes. Brain glucose-sensing mechanisms are incompletely understood and the contribution of glia, such as astrocytes, to hypoglycaemia detection and defective glucose counter-regulation requires more study. In this issue, Weightman Potter et al (https://doi.org/10.1007/s00125-018-4744-6) characterise the intrinsic mechanisms by which human primary astrocyte function is altered by acute and recurrent low glucose (RLG) exposure in vitro. They report that astrocytic AMP-activated protein kinase (AMPK) is activated by physiologically relevant reductions in glucose concentration. In addition, they found that basal fatty acid oxidation rates were increased by RLG, as were markers of mitochondrial dysfunction. Glycolytic rates were enhanced after RLG exposure, but this was not due to increased glucose uptake, nor did this lead to increased glycogen content. Moreover, following a recovery period, aspects of mitochondrial function were restored. These novel observations demonstrate that human primary astrocytes adapt to RLG to successfully maintain intracellular nucleotide levels. These data suggest the potential involvement of glial mitochondrial adaptations in defective glucose counterregulation or protection against hypoglycaemia. Studies are needed to further elucidate interactions between neurons and glial cells during and after recurrent hypoglycaemia.

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