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Baza natječaja

Stipendijski program iz područja molekularne biologije

Rok za prijavu: 31.12.2008.

Kontakt institucija: Biotechnology and Biological Sciences Research Council
Razina studija: diplomski studij
Područje studija: prirodne znanosti, biomedicina i zdravstvo
Mjesto studija: Ujedinjeno Kraljevstvo


UK: PhD Studentship in Epigenetics and Fetal Origins of Adult Diseases, a Mechanistic Link?

The fetal origins of adult disease hypothesis proposes that late onset disorders such as heart disease and type 2 diabetes maybe a consequence of metabolic programming in response to poor nutrition in utero. Accordingly, it has been suggested that the baby receives from their mother a forecast of the nutritional environment they will receive after birth and modify its metabolism, whole body physiology and growth trajectory appropriately to maximize its chances of survival postnatally. However, these adaptations become detrimental if the postnatal conditions differ from those experienced during fetal life and thus lead to increased disease susceptibility. This hypothesis has been supported by numerous epidemiological studies, which have shown an association between low birth weight and the subsequent development of type 2 diabetes, insulin resistance and the metabolic syndrome, and also by a number of animal studies. However, very few studies have addressed the molecular mechanisms by which a phenomenon that occurs in utero has a phenotypic consequence many years later.

This studentship will aim at providing first experimental evidence that epigenetics plays an important role in this fascinating biological phenomena. Epigenetics refers to covalent modifications of DNA and core histones which are heritable and affect genome function without altering the nucleotide sequence of DNA. It is an attractive candidate mechanism for fetal programming because it confers and maintains cellular "memory" for many cell divisions.

The student will use an integrated approach combining whole animal nutritional programming, gene-specific candidate approaches and functional epigenomics using DNA arrays to detect alterations in the epigenome associated with nutritional programming. These studies will be performed on a defined cell type of key importance in the pathogenesis of type 2 diabetes, the pancreatic beta cell, in the well established maternal protein restriction animal model of fetal programming. Subsequent work will focus on targeting DNA methylation to key metabolic genes to induce gene expression and metabolic changes in vitro.

This studentship may lead to the identification of novel causes and biomarkers of type 2 diabetes (a disease that affects 150 million worldwide). This work is done in close collaboration with the fetal programming group of Dr. Susan Ozanne at the Department of Clinical Biochemistry, University of Cambridge.


Dr Miguel Constancia
Email: Miguel.constancia@bbsrc.ac.uk  
Tel: 01223 496496





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