Antonio Vidal-Puig | Associate Faculty

Vidal-Puig, Antonio

I am a Professor of Molecular Nutrition and Metabolism at Cambridge University. My main activity is to do research as a Principal Investigator at the Medical Research Council Metabolic Disease Unit (MRC MDU Unit) and at the Wellcome trust Sanger Institute. I serve as Scientific Director of the Cambridge Phenomics Center, a state-of-the-art center that applies multidisciplinary approaches to murine metabolic phenotyping. I also see patients as an Honorary Consultant in Metabolic Medicine at Addenbrooke’s Hospital.

The research of my laboratory, the TVPLab (TVPLab, focuses on elucidating the molecular mechanisms linking obesity with insulin resistance, diabetes and cardiometabolic complications and on the development of related therapeutic strategies.

The Vision of the group is to lead the discovery of “the new biological concepts/molecular mechanism s that are going to transform the treatment of obesity and diabetes”.

Our Mission is to unravel the mechanisms controlling energy homeostasis and understand how they fail and cause obesity and diabetes. Our mission is not to find specific drugs. The reason for our existence is to identify the biochemical paths that these drugs should target.

The group is well known by its creativity reflected in the “adipose tissue expandability hypothesis” and the concept of “lipotoxicity” to explain the association between obesity and insulin resistance. We are also leaders in the field of thermogenesis and brown adipose tissue. Here at the Sanger Institute we will be working on a project related to Brown adipose tissue and human iPs cells, funded by an ERC advanced award and will also contribute to the characterization of animal models related to obesity and diabetes modelling human and systems biology derived data.

Our research strategies include a combination of hypothesis driven and non-biased systems approaches that make use of purposely genetically modified animal models, stem cell biology, human biological samples (including induced pluripotent stem cells), and sophisticated omics technologies and bioinformatics integration of large datasets.

Besides doing research I am also interested in management of talent in research intensive institutions. Over the years I have become fascinated by the highly talented PhD students and post docs I came across and on many occasions how their talent was wasted. So I believe a major problem in academic science is the poor management of this great talent to realise its value. Thus I am interested in better understanding and developing innovative approaches to talent management in academic research-intensive institutions. How it is best to manage the talent of academic scientists is an area under researched. However I am confident that some of the insights I have gained from current business management practices may be transferable and contribute to obtain the full value of science.


  • Hypophagia and metabolic adaptations in mice with defective ATGL-mediated lipolysis cause resistance to HFD-induced obesity.

    Schreiber R, Hofer P, Taschler U, Voshol PJ, Rechberger GN et al.

    Proceedings of the National Academy of Sciences of the United States of America 2015;112;45;13850-5

  • Regulation of mitochondrial morphology and function by stearoylation of TFR1.

    Senyilmaz D, Virtue S, Xu X, Tan CY, Griffin JL et al.

    Nature 2015;525;7567;124-8

  • Prostaglandin profiling reveals a role for haematopoietic prostaglandin D synthase in adipose tissue macrophage polarisation in mice and humans.

    Virtue S, Masoodi M, de Weijer BA, van Eijk M, Mok CY et al.

    International journal of obesity (2005) 2015;39;7;1151-60

  • Hematopoietic IKBKE limits the chronicity of inflammasome priming and metaflammation.

    Patel MN, Bernard WG, Milev NB, Cawthorn WP, Figg N et al.

    Proceedings of the National Academy of Sciences of the United States of America 2015;112;2;506-11

  • A Selective Sweep on a Deleterious Mutation in CPT1A in Arctic Populations.

    Clemente FJ, Cardona A, Inchley CE, Peter BM, Jacobs G et al.

    American journal of human genetics 2014;95;5;584-589

  • Increased dihydroceramide/ceramide ratio mediated by defective expression of degs1 impairs adipocyte differentiation and function.

    Barbarroja N, Rodriguez-Cuenca S, Nygren H, Camargo A, Pirraco A et al.

    Diabetes 2015;64;4;1180-92

  • Adaptive changes of the Insig1/SREBP1/SCD1 set point help adipose tissue to cope with increased storage demands of obesity.

    Carobbio S, Hagen RM, Lelliott CJ, Slawik M, Medina-Gomez G et al.

    Diabetes 2013;62;11;3697-708

  • Below thermoneutrality, changes in activity do not drive changes in total daily energy expenditure between groups of mice.

    Virtue S, Even P and Vidal-Puig A

    Cell metabolism 2012;16;5;665-71

  • BMP8B increases brown adipose tissue thermogenesis through both central and peripheral actions.

    Whittle AJ, Carobbio S, Martins L, Slawik M, Hondares E et al.

    Cell 2012;149;4;871-85

  • Differential lipid partitioning between adipocytes and tissue macrophages modulates macrophage lipotoxicity and M2/M1 polarization in obese mice.

    Prieur X, Mok CY, Velagapudi VR, Núñez V, Fuentes L et al.

    Diabetes 2011;60;3;797-809

  • Hypothalamic AMPK and fatty acid metabolism mediate thyroid regulation of energy balance.

    López M, Varela L, Vázquez MJ, Rodríguez-Cuenca S, González CR et al.

    Nature medicine 2010;16;9;1001-8

  • Coordination of PGC-1beta and iron uptake in mitochondrial biogenesis and osteoclast activation.

    Ishii KA, Fumoto T, Iwai K, Takeshita S, Ito M et al.

    Nature medicine 2009;15;3;259-66

  • Hypothalamic fatty acid metabolism mediates the orexigenic action of ghrelin.

    López M, Lage R, Saha AK, Pérez-Tilve D, Vázquez MJ et al.

    Cell metabolism 2008;7;5;389-99

  • PPAR gamma 2 prevents lipotoxicity by controlling adipose tissue expandability and peripheral lipid metabolism.

    Medina-Gomez G, Gray SL, Yetukuri L, Shimomura K, Virtue S et al.

    PLoS genetics 2007;3;4;e64

  • Ablation of PGC-1beta results in defective mitochondrial activity, thermogenesis, hepatic function, and cardiac performance.

    Lelliott CJ, Medina-Gomez G, Petrovic N, Kis A, Feldmann HM et al.

    PLoS biology 2006;4;11;e369

  • The link between nutritional status and insulin sensitivity is dependent on the adipocyte-specific peroxisome proliferator-activated receptor-gamma2 isoform.

    Medina-Gomez G, Virtue S, Lelliott C, Boiani R, Campbell M et al.

    Diabetes 2005;54;6;1706-16