Professor of Molecular Genetics & Metabolism
- Wellcome Trust Senior Fellow in Basic Biomedical Science
Anna Gloyn is based jointly at the Oxford Centre for Diabetes Endocrinology and Metabolism and the Wellcome Trust Centre for Human Genetics (WTCHG) at the University of Oxford.
Anna completed her DPhil at the University of Oxford under the supervision of the late Professor Robert Turner. Her post-doctoral training was carried out at the University of Exeter under the mentorship of Professors Andrew Hattersley & Sian Ellard and at the University of Pennsylvania in Philadelphia under the mentorship of Professor Franz Matschinsky.
Anna’s research is focused on using naturally occurring mutations in humans as tools to identity critical regulatory pathways and insights into normal physiology. Anna’s early post-doctoral research led to the identification a new genetic aetiology for permanent and transient neonatal diabetes due to KCNJ11 mutations and resulted in one of the first examples of the determination of the molecular genetic aetiology leading to improved treatment options for patients. Whilst in Oxford, Anna's team discovered a novel genetic cause of constitutive insulin sensitivity in humans due to mutations in the PTEN gene highlighting the complex interplay between pathways involved in cell-growth and metabolism.
Anna's current research projects are focused on the translation of genetic association signals for type 2 diabetes and glycaemic traits mechanisms for beta-cell dysfunction and diabetes. Her group uses a variety of complementary approaches, including human genetics, genomics, physiology and islet-biology to dissect out the molecular mechanisms driving disease pathogenesis.
Anna is an active member of multiple internal genetic discovery efforts including: NIH/Pharma funded Accelerated Medicines Partnership, DIAGRAM (Diabetes Genetics Replication and Meta-analysis), MAGIC (Meta-analysis of Glucose and Insulin traits Consortium), Type 2 Diabetes Genetic Exploration by Next-generation sequencing in multi-Ethnic Samples (T2D-GENES) and the Genetics of Type 2 Diabetes (GoT2D). She is also involved in the IMI funded STEMBANCC project which is working to deliver human IPS cell derived beta-cell models for drug discovery efforts.
Anna’s work has been recognized both nationally and internationally as she is a recipient of a European Association for the Study of Diabetes (EASD) Rising Star Award (2005), the RD Lawrence Named Lecturer (Diabetes UK Annual Professional Conference 2009), the GB Morgagni Silver Medal (2014) and the EASD Minkowski Prize (2014).
The Gloyn group currently consists of a multidisciplinary team of clinical and basic scientists.
Transcript Expression Data from Human Islets Links Regulatory Signals from Genome-Wide Association Studies for Type 2 Diabetes and Glycemic Traits to Their Downstream Effectors.
van de Bunt M. et al, (2015), Plos genet, 11
Genetic fine mapping and genomic annotation defines causal mechanisms at type 2 diabetes susceptibility loci.
Gaulton KJ. et al, (2015), Nat genet, 47, 1415 - 1425
Author Correction: Regulatory variants at KLF14 influence type 2 diabetes risk via a female-specific effect on adipocyte size and body composition.
Small KS. et al, (2018), Nat genet, 50
Patterns of differential gene expression in a cellular model of human islet development, and relationship to type 2 diabetes predisposition.
Perez-Alcantara M. et al, (2018), Diabetologia, 61, 1614 - 1622
Maturity onset diabetes of the young due to HNF1A variants in Croatia.
Pavić T. et al, (2018), Biochem med (zagreb), 28
NKX6.1 induced pluripotent stem cell reporter lines for isolation and analysis of functionally relevant neuronal and pancreas populations.
Gupta SK. et al, (2018), Stem cell res, 29, 220 - 231
Regulatory variants at KLF14 influence type 2 diabetes risk via a female-specific effect on adipocyte size and body composition.
Small KS. et al, (2018), Nat genet, 50, 572 - 580