School of Biosciences
 

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Simon Welham

Assistant Professor in Nutritional Science, Faculty of Science

Contact

  • workNorth Laboratory
    Sutton Bonington Campus
    Sutton Bonington
    Leicestershire
    LE12 5RD
    UK
  • work0115 951 6129
  • fax0115 951 6122

Research Summary

Iodine nutrition.

Iodine is an element required in trace amounts for the synthesis of thyroid hormone. Chronic under-consumption can lead to hypothyroidism and other thyroid outcomes resulting in disturbed metabolic homeostasis. A low iodine status in pregnancy can have severe to catastrophic impacts on the unborn fetus, increasing the likelyhood of miscarriage and for those babies that survive, there is a significant risk of impaired neural development resulting in cognitive defects, the most severe of which is cretinism.

We have been working for some time on identifying groups at risk of iodine deficiency and attempting to determine effective routes to restoration of dietary iodine intake, as salt iodisation, an effective government driven intervention present across much of the globe, is not in place in the UK. We, along with many others, have shown that low consumption of milk and dairy products can lead to very low iodine intakes and we are now working to facilitate the increased iodisation of alternative milk and dairy replacement products.

Fetal programming.

Exposure to maternal undernutrition in early life directly impacts upon fetal growth and development and permanently alters postnatal physiology. This has been demonstrated to predispose individuals towards cardiovascular disease, diabetes and obesity in adulthood. An important aspect of these phenotypes is that they are both permanent and worsen with age. My current research seeks to examine the role of epigenetic modifications, most notably DNA methylation, brought about by in utero exposure to maternal undernutrition, in programming insulin resistance and how this might be modulated by ageing. In addition, I am also interested in understanding the mechanisms by which fetal growth impairment results in alterations in cellular determination during development.

Renal development.

The processes by which the metanephric, or true kidney is formed are incompletely understood. Many of these processes, if aberrantly impacted upon, result either in inadequate renal development, often leading to a nephron deficit, or more severely, renal malformations for which the only useful treatment is transplant. One of the areas of renal development which we are interested in understanding is the process of cellular migration within the "stem" population of nephron progenitor cells (i.e. those which will go on to form nephrons). By elucidating the mechanisms which control both the rate and direction of migration of these cells, we hope to reveal how the structure of the kidney is established and, importantly, the processes which mediate cessation of renal development.

Recent Publications

School of Biosciences

University of Nottingham
Sutton Bonington Campus
Nr Loughborough
LE12 5RD, UK

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