David J. Galton


David Jeremy Galton was a British physician and researcher in molecular genetics and metabolic disease, primarily the hyperlipidemias and diabetes mellitus.
He is not related to Francis Galton the Victorian-era polymath and eugenicist.

Early life and education

David Galton was educated at Highgate School London and graduated from University College London in 1957 with a BSc and MB.BS in 1960. After house-staff training he went to the National Institutes of Health, Bethesda Maryland, USA to study with Robert Scow and Martin Rodbell.

Career

On returning to the UK he obtained a Fellowship at the Hammersmith Hospital to work with Russell Fraser and later elected to the consultant staff at St Bartholomew's Hospital London. He was then elected to a Professorship, Department of Medicine, London University and is now an Emeritus Professor at London University.
Galton was elected Chairman of Clinical Science from 1978 to 1980. He served on the scientific grants committee of Diabetes UK from 1984 to 1987 and again from 1989 to 1991. He was elected secretary of the European Atherosclerosis Society from 1988 to 1993 and Chairman of HEART UK from 1999 to 2001. He has been a Consultant Physician to St. Bartholomew's and Moorfield's Eye Hospitals.
He served as the librarian of the Galton Institute having previously served as vice-president.

Research

His laboratory's main contributions have been to reveal defects of metabolic regulatory elements in common metabolic disease at both phenotype and genotype levels:
His group identified the earliest loss of an allosteric regulation of a rate-determining enzyme, phosphofructokinase by citrate in minimal deviation tumours, lipomata. Many more such defects have subsequently come to light particularly to deregulate pathways in early neoplasia.
Abnormalities in the covalent modification of peptide regulators were found to have effects on enzyme activity. Thus one extra sialyl residue on apolipoprotein C3 impairs its action on lipoprotein lipase. This can affect expression of the resulting phenotype of hypertriglyceridemia.
His laboratory was one of the first to use single nucleotide polymorphisms to reveal susceptibility genes that predispose individuals to develop metabolic disorders, such as hypertriglyceridemia and atherosclerosis. This led eventually to the development of Genome Wide Association Studies where more than 1400 susceptibility loci have now been identified using SNPs and some have led to useful therapeutic agents such as volanesorsen

Awards