| First Author | Wali JA | Year | 2018 |
| Journal | Cell Death Differ | Volume | 25 |
| Issue | 1 | Pages | 217-225 |
| PubMed ID | 29053141 | Mgi Jnum | J:271923 |
| Mgi Id | MGI:6282310 | Doi | 10.1038/cdd.2017.168 |
| Citation | Wali JA, et al. (2018) Loss of BIM increases mitochondrial oxygen consumption and lipid oxidation, reduces adiposity and improves insulin sensitivity in mice. Cell Death Differ 25(1):217-225 |
| abstractText | 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. |
