David J. Galton | |
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| Born | 2 May 1937 |
| Alma mater | University College London |
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David Jeremy Galton (born 2 May 1937) is a British physician and researcher in molecular genetics and metabolic disease, primarily the hyperlipidemias and diabetes mellitus. [1] He is an authority figure in his field. [2] [3]
David Galton was educated at Highgate School London and graduated from University College London in 1957 with a BSc (first class honours) and MB.BS (with honours in medicine) 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. [1]
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. [1]
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. [1]
He is currently serving as the librarian of the Galton Institute (formerly the British Eugenics Society) having previously served as vice-president. [4] He is no relation of Francis Galton. [5]
His laboratory's main contributions have been to reveal defects of metabolic regulatory elements in common metabolic disease (mainly diabetes mellitus, the lipemias and atherosclerosis) 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. [6] [7] 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. [8] [9] This can affect expression of the resulting phenotype of hypertriglyceridemia.
His laboratory was one of the first to use single nucleotide polymorphisms (SNPs) to reveal susceptibility genes that predispose individuals to develop metabolic disorders, such as hypertriglyceridemia and atherosclerosis. [10] [11] [12] This led eventually to the development of Genome Wide Association Studies (GWAS) where more than 1400 susceptibility loci have now been identified using SNPs and some have led to useful therapeutic agents such as volanesorsen [10]
Low-density lipoprotein (LDL) is one of the five major groups of lipoprotein that transport all fat molecules around the body in extracellular water. These groups, from least dense to most dense, are chylomicrons, very low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), low-density lipoprotein (LDL) and high-density lipoprotein (HDL). LDL delivers fat molecules to cells. LDL is involved in atherosclerosis, a process in which it is oxidized within the walls of arteries.
Hypercholesterolemia, also called high cholesterol, is the presence of high levels of cholesterol in the blood. It is a form of hyperlipidemia, hyperlipoproteinemia, and dyslipidemia.
Dyslipidemia is a metabolic disorder characterized by abnormally high or low amounts of any or all lipids or lipoproteins in the blood. Dyslipidemia is a risk factor for the development of atherosclerotic cardiovascular diseases (ASCVD), which include coronary artery disease, cerebrovascular disease, and peripheral artery disease. Although dyslipidemia is a risk factor for ASCVD, abnormal levels don't mean that lipid lowering agents need to be started. Other factors, such as comorbid conditions and lifestyle in addition to dyslipidemia, is considered in a cardiovascular risk assessment. In developed countries, most dyslipidemias are hyperlipidemias; that is, an elevation of lipids in the blood. This is often due to diet and lifestyle. Prolonged elevation of insulin resistance can also lead to dyslipidemia. Likewise, increased levels of O-GlcNAc transferase (OGT) may cause dyslipidemia.
Apolipoproteins are proteins that bind lipids to form lipoproteins. They transport lipids in blood, cerebrospinal fluid and lymph.
Hyperlipidemia is abnormally high levels of any or all lipids or lipoproteins in the blood. The term hyperlipidemia refers to the laboratory finding itself and is also used as an umbrella term covering any of various acquired or genetic disorders that result in that finding. Hyperlipidemia represents a subset of dyslipidemia and a superset of hypercholesterolemia. Hyperlipidemia is usually chronic and requires ongoing medication to control blood lipid levels.
Genetic association is when one or more genotypes within a population co-occur with a phenotypic trait more often than would be expected by chance occurrence.
Cholesteryl ester transfer protein (CETP), also called plasma lipid transfer protein, is a plasma protein that facilitates the transport of cholesteryl esters and triglycerides between the lipoproteins. It collects triglycerides from very-low-density (VLDL) or Chylomicrons and exchanges them for cholesteryl esters from high-density lipoproteins (HDL), and vice versa. Most of the time, however, CETP does a heteroexchange, trading a triglyceride for a cholesteryl ester or a cholesteryl ester for a triglyceride.
Apolipoprotein E (Apo-E) is a protein involved in the metabolism of fats in the body of mammals. A subtype is implicated in the Alzheimer's disease and cardiovascular diseases. It is encoded in humans by the gene APOE.
Apolipoprotein B (ApoB) is a protein that in humans is encoded by the APOB gene. It is commonly used to detect risk of atherosclerotic cardiovascular disease.
Lipoprotein(a) is a low-density lipoprotein variant containing a protein called apolipoprotein(a). Genetic and epidemiological studies have identified lipoprotein(a) as a risk factor for atherosclerosis and related diseases, such as coronary heart disease and stroke.
Apolipoprotein AI(Apo-AI) is a protein that in humans is encoded by the APOA1 gene. As the major component of HDL particles, it has a specific role in lipid metabolism.
Apolipoprotein C-III also known as apo-CIII, and apolipoprotein C3, is a protein that in humans is encoded by the APOC3 gene. Apo-CIII is secreted by the liver as well as the small intestine, and is found on triglyceride-rich lipoproteins such as chylomicrons, very low density lipoprotein (VLDL), and remnant cholesterol.
Apolipoprotein A-V is a protein that in humans is encoded by the APOA5 gene on chromosome 11. It is significantly expressed in liver. The protein encoded by this gene is an apolipoprotein and an important determinant of plasma triglyceride levels, a major risk factor for coronary artery disease. It is a component of several lipoprotein fractions including VLDL, HDL, chylomicrons. It is believed that apoA-V affects lipoprotein metabolism by interacting with LDL-R gene family receptors. Considering its association with lipoprotein levels, APOA5 is implicated in metabolic syndrome. The APOA5 gene also contains one of 27 SNPs associated with increased risk of coronary artery disease.
Apolipoprotein A-II is a protein that in humans is encoded by the APOA2 gene. It is the second most abundant protein of the high density lipoprotein particles. The protein is found in plasma as a monomer, homodimer, or heterodimer with apolipoprotein D. ApoA-II regulates many steps in HDL metabolism, and its role in coronary heart disease is unclear. Remarkably, defects in this gene may result in apolipoprotein A-II deficiency or hypercholesterolemia.
Lipidology is the scientific study of lipids. Lipids are a group of biological macromolecules that have a multitude of functions in the body. Clinical studies on lipid metabolism in the body have led to developments in therapeutic lipidology for disorders such as cardiovascular disease.
Harry Harris FRS, FCRP, was a British-born biochemist. His work showed that human genetic variation was not rare and disease-causing but instead was common and usually harmless. He was the first to demonstrate, with biochemical tests, that with the exception of identical twins we are all different at the genetic level. This work paved the way for many well-known genetic concepts and procedures such as DNA fingerprinting, the prenatal diagnosis of disorders using genetic markers, the extensive heterogeneity of inherited diseases, and the mapping of human genes to chromosomes
Wolfgang Patsch is an Austrian physician, specialized in internal medicine/laboratory medicine and a professor in the Department of Pharmacology and Toxicology at the Paracelsus Private Medical University of Salzburg. He is known for his work in the fields of atherosclerosis, common metabolic disorders such as obesity, insulin resistance and type-2 diabetes and neurodegenerative disorders.
Apabetalone is an orally available small molecule created by Resverlogix Corp. that is being evaluated in clinical trials for the treatment of atherosclerosis and associated cardiovascular disease (CVD). In the phase II clinical trial ASSURE in patients with angiographic coronary disease and low high-density lipoprotein cholesterol (HDL-C) levels, apabetalone showed no greater increase in HDL-cholesterol (HDL-c) and apolipoprotein A-I (ApoA-I) levels or incremental regression of atherosclerosis than administration of placebo, while causing a statistically significant greater incidence of elevated liver enzymes. However, pooled analysis of the effect of apabetalone in three phase II clinical trials ASSERT, ASSURE, and SUSTAIN demonstrated increases in HDL-cholesterol (HDL-c) and apolipoprotein A-I (ApoA-I) levels, as well as decreases in the incidence of major adverse cardiac events (MACE). Reduction of MACE was more profound in patients with diabetes mellitus. In a short-term study in prediabetics, favorable changes in glucose metabolism were observed in patients receiving apabetalone. An international, multicenter phase III trial, “Effect of RVX000222 on Time to Major Adverse Cardiovascular Events in High-Risk Type 2 Diabetes Mellitus Subjects with Coronary Artery Disease” (BETonMACE) commenced in October 2015. The trial is designed to determine whether apabetalone in combination with statins can decrease cardiac events compared to treatment with statins alone.
Jasvinder K Gambhir is an Indian doctor, researcher and professor in the fields of clinical biochemistry, diabetology and cardiology. Dr Gambhir completed her master's in biochemistry in 1972 from Punjab University and PhD from Post Graduate Institute of Medical Education and Research She has an experience in the field of over 40 years. She is Senior professor and Head of Department, Biochemistry at University College of Medical Sciences, New Delhi and Senior Professor at School of Medical Sciences and Research Noida. Dr. Gambhir is also a member of American Association of Clinical Chemistry (AACC).
Dr. Robert S. Rosenson is a Professor of Medicine and also lending his services as the Director of cardio metabolic disorders at the Icahn School of Medicine at Mount Sinai.
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