Vidal-Puig Group | Obesity-associated Metabolic Complications

Vidal-Puig Group | Obesity-associated Metabolic Complications

Vidal-Puig Group

Our Research and Approach

The Vidal-Puig group focuses on obesity and diabetes and more specifically trying to understand why being obese causes cardiometabolic complications. We feel that this link is the accumulation of fat in the heart, muscle or liver and we feel that if we understand this link we may be able to prevent obese people from dying from heart attacks or developing diabetes. For this we study how to prevent the accumulation of lipids in these organs through activation of the brown fat, a type of fat which helps to prevent obesity and diabetes.

We aim to learn why being obese causes metabolic and cardiovascular problems and to provide the rational for mechanistically driven therapeutic approaches to prevent these complications which are the main cause of morbidity amongst obese patients. The projects we will develop at the Sanger Institute includes a focus on human iPS white and brown adipose tissue funded by ERC and phenotyping characterisation of murine models relevant for obesity and metabolic complications.

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People

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Antonio Vidal-Puig
Group Leader

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.

Research Programmes

Publications

  • 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