Craig Beall

Mgl2+ cDC2 triggering of fungal allergic inflammation depends on a spore induced glycolytic shift fuelled by local availability of glucose

This study shows that Mgl2+ cDC2s trigger fungal allergic inflammation through a glycolytic shift driven by glucose availability after spore uptake.

Validation of a refined protocol for mouse oral glucose tolerance testing without gavage

This paper validates a refined, non-invasive method for mouse oral glucose tolerance testing that avoids gavage, showing reduced stress and improved consistency in glucose tolerance measurements.

Regulation of astrocyte metabolism by mitochondrial translocator protein 18kDa

This study investigates the role of TSPO in astrocyte metabolism and inflammation, finding that TSPO deficiency alters metabolic flexibility but not the inflammatory response to LPS.

Astrocytes in the dorsal vagal complex are not activated by systemic glucoprivation and their chemogenetic activation does not elicit homeostatic glucoregulatory responses in mice

This study shows DVC astrocytes do not respond to systemic glucoprivation and their activation does not restore blood glucose in mice.

Analysis of the transcriptome and DNA methylome in response to acute and recurrent low glucose in human primary astrocytes

This study examines gene expression and DNA methylation changes in human astrocytes exposed to acute and recurrent low glucose, identifying UPR-related gene activation and methylation patterns.

Regulation of food intake by astrocytes in the brainstem dorsal vagal complex

This study shows that astrocytes in the brainstem dorsal vagal complex regulate food intake by inhibiting appetite through a circuit without causing aversion.

Brain permeable AMPK activator R481 raises glycemia by autonomic nervous system activation and amplifies the counterregulatory response to hypoglycemia in rats

The paper shows that R481, a brain-permeable AMPK activator, raises blood glucose and enhances counterregulatory responses to hypoglycemia in rats without affecting insulin sensitivity.

Human primary astrocytes increase basal fatty acid oxidation following recurrent low glucose to maintain intracellular nucleotide levels

This study shows that human astrocytes increase fatty acid oxidation under recurrent low glucose to maintain nucleotide levels, indicating mitochondrial dysfunction in hypoglycemia response.