Paul Taylor

Paul Taylor

Dr

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    Biographical details

    Paul Taylor is Senior Lecturer in Developmental Programming at King’s College London. Dr Taylor is a cardiovascular physiologist by training, with an interest in the early life origins of cardiovascular and metabolic disease. In 1994 he obtained a PhD in Physiology from United Medical & Dental Schools, London University investigating the mechanisms underlying the vascular complications of diabetes. This was followed by postdoctoral training in the Vascular Biology Unit, Boston University USA, and Department Clinical Pharmacology, St George’s Hospital Medical School, London.  A further post-doctoral position in 2000 at King’s College London combined interests in nutrition and cardiovascular disease with the emerging field of developmental programming. In 2005, he was appointed Lecturer in Developmental Programming at Kings and established his laboratory within the Maternal & Fetal research Unit, Division of Reproduction & Endocrinology. He was made Senior Lecturer in 2008.

    Dr Taylor’s research interests include the ‘developmental programming’ effects of maternal nutrition and the hormonal environment in obese and diabetic pregnancy on the offspring’s future cardiovascular and metabolic health. Specifically, the group aim to investigate the physiological processes and the cellular and molecular mechanisms whereby a baby’s exposure to an aberrant hormonal environment in pregnancy and lactation gives rise to increased risk of obesity and cardiovascular disorders in later life. Recent publications in the journals Hypertension and PLoS One provide evidence for the early life origins of hypertension and hyperphagia secondary to maternal obesity in pregnancy.

    Research interests

    Developmental origins of obesity and the metabolic syndrome
    Maternal obesity increases all the common complications of pregnancy, however increasing evidence suggests that there is also a long lasting effect in terms of offspring metabolic and cardiovascular health. We have developed a number of models of human pregnancy which allow detailed investigation of the mechanisms whereby maternal obesity predisposes adult offspring to hyperphagia (increased appetite) and hyperadiposity (obesity), hypertension (high blood pressure) insulin resistance (type 2 diabetes) dyslipidaemia (abnormal blood lipids) and other metabolic disorders of the pancreas and liver (NAFPD and  NAFLD ). 

     
    Developmental Origins of Hypertension and Cardiac Dysfunction
    We have recently reported that maternal obesity can induce a permanent leptin resistant state of hyperphagia together with sympathetically mediated hypertension in juvenile offspring.  We are currently exploring the mechanisms in the developing brain involved in blood pressure regulation and the potential for intervention in the obese mother or in neonatal life. Clinical studies will determine if children of obese mothers are similarly affected.

    Hypothalamic mechanisms underlying neonatal programming of appetite and energy balance
    We will investigate the signals and processes underlying the ontogeny of hyperphagia secondary to maternal obesity. Central to our objectives is the physiological and pathophysiological regulation of neonatal leptin and its subsequent effects on leptin-signalling and peptidergic pathways intrinsic to the hypothalamus.

    Expertise related to UN Sustainable Development Goals

    In 2015, UN member states agreed to 17 global Sustainable Development Goals (SDGs) to end poverty, protect the planet and ensure prosperity for all. This person’s work contributes towards the following SDG(s):

    • SDG 3 - Good Health and Well-being

    Education/Academic qualification

    Doctor of Philosophy, Resistance artery function in the streptozotocin diabetic rat, University of London

    Award Date: 1 Jan 1994

    Bachelor of Science, Kingston University

    Award Date: 1 Jan 1989

    Keywords

    • QP Physiology
    • Pregnancy
    • Developmental Programming
    • Obesity
    • Hypertension
    • Diabetes
    • NAFLD

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