I work to understand how thermogenesis in adipose tissue is altered by changes in diet and metabolic health. In the long term I aim to find ways to specifically exploit thermogenic mechanisms to better treat diseases such as obesity, diabetes, cardiovascular disease and anorexia.

I am currently identifying and characterizing the neuronal circuits that respond to metabolic and dietary changes to elicit more or less thermogenesis. At the same time I examine the impact of these changes on the metabolic health of cells, tissues and whole organisms. To achieve this I combine the latest nueuromodulatory techniques such as opto- and chemogenetics with my extensive experience performing detailed in vivo and in vitro metabolic phenotyping.

Honors & Awards

  • Long-Term Fellowship, EMBO (10/01/13 - 09/30/15)
  • Equality Champion, Athena Swan (10/01/10 - 10/01/11)
  • Student Representative, Cambridge University Clinical School Graduate Education Committee (10/01/06 - 10/01/09)
  • Traveling Fellowship, Disease Models and Mechanisms (08/14/09)
  • Traveling Fellowship, EMBO (04/12/08)

Boards, Advisory Committees, Professional Organizations

  • Member, American Heart Association (2015 - Present)

Professional Education

  • Bachelor of Science, University of Manchester (2006)
  • Doctor of Philosophy, University of Cambridge (2011)

Stanford Advisors

Research & Scholarship

Current Research and Scholarly Interests

I use optogenetic and chemogenetic techniques to modulate the activity of specific neuronal populations using a candidate-based approach. I couple these manipulations with behavioral and metabolic phenotyping to identify neuronal populations that elicit changes in brown adipose tissue thermogenic activity, basal metabolic rate, lipid and glucose homeostasis and/or arousal state. I then examine circuit connectivity using viral tracing techniques. I am always open to collaborations


All Publications

  • Light and chemical control of neuronal circuits: possible applications in neurotherapy EXPERT REVIEW OF NEUROTHERAPEUTICS Whittle, A. J., Walsh, J., de Lecea, L. 2014; 14 (9): 1007-1017


    Millions of people worldwide suffer from diseases that result from a failure of central pathways to regulate behavioral and physiological processes. Advances in genetics and pharmacology have already allowed us to appreciate that rather than this dysregulation being systemic throughout the brain, it is usually rooted in specific subsets of dysfunctional cells within discrete neurological circuits. This article discusses the advent of opto- and chemogenetic tools and how they are providing the means to dissect these circuits with a degree of temporal and spatial sensitivity not previously possible. We also highlight the potential applications for treating disease and the key developments likely to have the greatest impact over the next 5 years.

    View details for DOI 10.1586/14737175.2014.948850

    View details for Web of Science ID 000341182900004

  • BMP8B Increases Brown Adipose Tissue Thermogenesis through Both Central and Peripheral Actions CELL Whittle, A. J., Carobbio, S., Martins, L., Slawik, M., Hondares, E., Jesus Vazquez, M., Morgan, D., Csikasz, R. I., Gallego, R., Rodriguez-Cuenca, S., Dale, M., Virtue, S., Villarroya, F., Cannon, B., Rahmouni, K., Lopez, M., Vidal-Puig, A. 2012; 149 (4): 871-885


    Thermogenesis in brown adipose tissue (BAT) is fundamental to energy balance and is also relevant for humans. Bone morphogenetic proteins (BMPs) regulate adipogenesis, and, here, we describe a role for BMP8B in the direct regulation of thermogenesis. BMP8B is induced by nutritional and thermogenic factors in mature BAT, increasing the response to noradrenaline through enhanced p38MAPK/CREB signaling and increased lipase activity. Bmp8b(-/-) mice exhibit impaired thermogenesis and reduced metabolic rate, causing weight gain despite hypophagia. BMP8B is also expressed in the hypothalamus, and Bmp8b(-/-) mice display altered neuropeptide levels and reduced phosphorylation of AMP-activated protein kinase (AMPK), indicating an anorexigenic state. Central BMP8B treatment increased sympathetic activation of BAT, dependent on the status of AMPK in key hypothalamic nuclei. Our results indicate that BMP8B is a thermogenic protein that regulates energy balance in partnership with hypothalamic AMPK. BMP8B may offer a mechanism to specifically increase energy dissipation by BAT.

    View details for DOI 10.1016/j.cell.2012.02.066

    View details for Web of Science ID 000303934700019

    View details for PubMedID 22579288