Martin Brand, Ph.D.,
Understanding the function of mitochondria within cells
Dr Brand has a B.Sc. in Biochemistry from the University of Manchester Institute of Science and Technology and a Ph.D. in Biochemistry, University of Bristol (with Professor Brian Chappell) and did his postdoctoral fellowship at Johns Hopkins University. In addition, Dr. Brand is the Group Leader for the MRC Dunn Human Nutrition Unit, a fellow of the Academy of Medical Sciences and currently contributing to these editorial Boards: Biochimica et Biophysica Acta; Cell Metabolism; Physiological and Biochemical Zoology. The driving force behind Dr. Brand’s research is the understanding of how the function of mitochondria within cells is regulated to give the exquisite control of nutrient use and energy turnover that is characteristic of healthy cells. Mitochondria oxidize nutrients to release energy, and capture that energy to make ATP. The Brand lab is particularly fascinated by variations in the efficiency of this process.
This leads naturally into study of the efficiency, of how its regulation and its effects on cells and organisms can be described quantitatively, of its mechanism and its functions, and of how we might be able to alter it to affect conditions such as obesity, degenerative diseases and normal ageing. The inefficiency is caused by leaks of protons across the mitochondrial inner membrane. The Brand lab is investigating basal proton leak catalysed by non-specific processes and inducible proton leak catalysed by specific uncoupling proteins (UCP1, UCP2 and UCP3). The Brand lab team are interested in the mechanism of proton transport by these proteins, and how they are regulated by nucleotides, fatty acids, free radicals and other molecules to produce relevant responses to physiological signals. The Brand lab wants to understand their proton leak functions in different cells, and their involvement in thermogenesis, endocrine function (such as insulin secretion in pancreatic beta cells), immune function, inflammation, free radical-mediated signalling, oxidative damage and ageing. These proteins provide potential targets for new pharmaceuticals aimed at treating obesity and protecting against free radical-related mitochondrial damage and degeneration. For example, when human UCP3 is expressed in mouse muscle, the mitochondria make ATP less efficiently, so the mice eat more but gain less weight than normal.
