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Loss of BIM increases mitochondrial oxygen consumption and lipid oxidation, reduces adiposity and improves insulin sensitivity in mice.
- Source :
-
Cell death and differentiation [Cell Death Differ] 2018 Jan; Vol. 25 (1), pp. 217-225. Date of Electronic Publication: 2017 Oct 20. - Publication Year :
- 2018
-
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 <superscript>-/-</superscript> 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 <superscript>-/-</superscript> mice were significantly lower body weights, reduced adiposity and lower hepatic lipid content. Consistent with reduced adiposity, BIM <superscript>-/-</superscript> mice had lower fasting blood glucose, improved insulin sensitivity and hepatic insulin signalling. Lipid oxidation was increased in BIM <superscript>-/-</superscript> 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.
- Subjects :
- Animals
Bcl-2-Like Protein 11 genetics
Electron Transport Complex IV metabolism
Energy Metabolism
Glucose metabolism
Hepatocytes metabolism
Insulin Resistance
Liver metabolism
Membrane Potential, Mitochondrial
Mice
Oxidation-Reduction
Oxygen Consumption
Weight Loss
Adiposity
Bcl-2-Like Protein 11 physiology
Lipid Metabolism
Mitochondria metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 1476-5403
- Volume :
- 25
- Issue :
- 1
- Database :
- MEDLINE
- Journal :
- Cell death and differentiation
- Publication Type :
- Academic Journal
- Accession number :
- 29053141
- Full Text :
- https://doi.org/10.1038/cdd.2017.168