Constantinos Christodoulides
MBChB, MRCP, PhD
University Research Lecturer
- British Heart Foundation Intermediate Clinical Research Fellow
Cell and Molecular Biology
My work focuses on understanding how obesity leads to the development of diabetes and cardiovascular disease. In particular, my research aims to understand how a family of growth factors, known as Wnts regulates adipocyte number (adipose tissue 'expandability') and distribution within the body; two key determinants of susceptibility to obesity-associated cardiometabolic disease. In order to achieve this we employ human genetic and physiological approaches, accompanied by functional studies in human fat depot-specific cellular models. Recently we identified a key Wnt receptor, LRP5, as a novel human fat distribution gene.
Of interest LRP5 is a current drug target for the treatment of osteoporosis illustrating the translational potential of the research. In the longer term we hope to exploit our findings to develop novel therapies for obesity and cardiometabolic diseases.
I am currently a BHF Intermediate Clinical Research Fellow and Honorary Consultant in Endocrinology and Diabetes. Prior to this I competed my PhD at the University of Cambridge before taking up an Academic Clinical Lecturer post at the University of Oxford.
Recent publications
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Bidirectional Mendelian randomization highlights causal relationships between circulating INHBC and multiple cardiometabolic diseases and traits.
Journal article
Loh NY. et al, (2024), Diabetes
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Investigating the impact of metabolic syndrome traits on telomere length: a Mendelian randomization study.
Journal article
Loh NY. et al, (2023), Obesity (Silver Spring)
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Metabolic Syndrome traits and telomere length: a Mendelian Randomization study.
Journal article
LOH N. et al, (2023), Obesity
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Obesity, Fat Distribution and Risk of Cancer in Women and Men: A Mendelian Randomisation Study.
Journal article
CHRISTODOULIDES C. et al, (2022), Nutrients
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TCF7L2 plays a complex role in human adipose progenitor biology, which might contribute to genetic susceptibility to type 2 diabetes.
Journal article
Verma M. et al, (2022), Metabolism, 133