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
Dr Bronwyn Hegarty |
Dr Nigel Turner |
Elaine Preston |
Susan Beale |
| Hons Student Reg Leones |
Lauren Wright |
Jane Reznick |
Dr Timo Kanzleiter |
