Title:	Loss of BIM increases mitochondrial oxygen consumption and lipid oxidation, reduces adiposity and improves insulin sensitivity in mice
Authors:	Wali, JA Galic, S Tan, CYR Gurzov, EN Frazier, AE Connor, T Ge, JJ Pappas, EG Stroud, D Varanasi, LC Selck, C Ryan, MT Thorburn, DR Kemp, BE Krishnamurthy, B Kay, TWH Thomas, HE
Issue Year:	2018
Publisher	NATURE PUBLISHING GROUP
Series	Cell Death Differ.:
Abstract	BCL-2 proteins are known to engage each other to determine the fate of a cell after a death stimulus. However, their evolutionary conservation and the many other reported binding partners suggest an additional function not directly linked to apoptosis regulation. To identify such a function, we studied mice lacking the BH3-only protein BIM. BIM-/- cells had a higher mitochondrial oxygen consumption rate that was associated with higher mitochondrial complex IV activity. The consequences of increased oxygen consumption in BIM-/- mice were significantly lower body weights, reduced adiposity and lower hepatic lipid content. Consistent with reduced adiposity, BIM-/- mice had lower fasting blood glucose, improved insulin sensitivity and hepatic insulin signalling. Lipid oxidation was increased in BIM-/- mice, suggesting a mechanism for their metabolic phenotype. Our data suggest a role for BIM in regulating mitochondrial bioenergetics and metabolism and support the idea that regulation of metabolism and cell death are connected.
URI:	https://publications.svi.edu.au/publications/4717
Other Identifiers	10.1038/cdd.2017.168
Publication type	Article