Cooney
While diet is one major factor in fat accumulation and affects our chances of developing type 2 diabetes, it has become clear in recent years that energy expenditure is important too. When we exercise, we burn off fat. However, regulating muscle energy expenditure is more complex than simply increasing activity. This fact is exemplified by our recent studies in genetically engineered mice missing the c-Cbl gene. These animals eat more and have less fat because their energy expenditure is revved up. We are focusing on the molecular reason for this change and believe the answer will provide major clues for the control of insulin resistance. When fat enters a muscle cell from blood there are two choices. It is either stored as an intracellular lipid or it is channelled into the mitochondria, where it is burned. In c-Cbl knock out mice, we see evidence of the second choice, resulting in constant fat burning and reduced fat storage. Recent evidence suggests that, as humans age, their mitochondrial function deteriorates, and this is possibly associated with reduced mitochondrial burning. This work could help to explain the increased incidence of type 2 diabetes as people age. We are also interested in the daily circadian rhythms that affect metabolism and therefore fat storage.
Staff
 Senior Research OfficerDr Nigel Turner |
 Research OfficerDr Michael Swarbrick |
 Research AssistantElaine Preston |
 Research OfficerDr Lowenna Holt |
 Research AssistantSimon Leslie |
 Research
AssistantLauren Wright |
 PhD StudentJane Reznick |
Visiting Students Samuel Hess Matthew Sloper |
