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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):
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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Short-term and long-term effects of caesarean section on the health of women and children
Sandall, J., Tribe, R. M. & Taylor, P. D., 13 Oct 2018, In: The Lancet. 392, p. 1349-1357Research output: Contribution to journal › Article › peer-review
718 Citations (Scopus) -
Maternal obesity and the developmental programming of hypertension: a role for leptin
Taylor, P. D., Samuelsson, A.-M. & Poston, L., Mar 2014, In: Acta Physiologica. 210, 3, p. 508-23Research output: Contribution to journal › Review article › peer-review
86 Citations (Scopus) -
Developmental origins of obesity and the metabolic syndrome: the role of maternal obesity
Armitage, J. A., Poston, L. & Taylor, P. D., 2008, In: FRONTIERS OF HORMONE RESEARCH. 36, p. 73-84 12 p.Research output: Contribution to journal › Review article › peer-review
204 Citations (Scopus) -
Diet-induced obesity in female mice leads to offspring hyperphagia, adiposity, hypertension, and insulin resistance: a novel murine model of developmental programming
Samuelsson, A.-M., Matthews, P. A., Argenton, M., Christie, M. R., McConnell, J. M., Jansen, E. H. J. M., Piersma, A. H., Ozanne, S. E., Twinn, D. F., Remacle, C., Rowlerson, A., Poston, L. & Taylor, P. D., Feb 2008, In: Hypertension. 51, 2, p. 383-392 10 p.Research output: Contribution to journal › Article › peer-review
743 Citations (Scopus) -
Dietary soy isoflavone-induced increases in antioxidant and eNOS gene expression lead to improved endothelial function and reduced blood pressure in vivo
Mahn, K., Borras, C., Knock, G. A., Taylor, P., Khan, I. Y., Sugden, D., Poston, L., Ward, J. P., Sharpe, R. M., Vina, J., Aaronson, P. I. & Mann, G. E., Oct 2005, In: Faseb Journal. 19, 10, p. 1755 - 1757 3 p.Research output: Contribution to journal › Article › peer-review
175 Citations (Scopus)