Professor Hari Hundal FHEA FRSB
The research programme in the Hundal lab is aimed at defining the intracellular signalling processes that regulate uptake, storage and metabolism of nutrients (e.g. glucose, fatty acids and amino acids) with particular focus on how cells sense nutrient availability and how nutrient over-load can induce metabolic disorders such as insulin resistance and diabetes. More recently, the Hundal lab has also opened up a new and exciting area of study that principally aims to develop our understanding of the action of a class of compounds, termed cannabinoids, in peripheral tissues such as skeletal muscle. Cannabinoids are present in cannabis, but our bodies naturally create cannabinoid-like chemicals, known as endocannabinoids that lock-on to protein molecules found on the surface of cells called cannabinoid receptors (i.e. CB1 and CB2). Pathological over-activation of the endocannabinoid system (ECS) is a feature of obesity and diabetes and one that we have recently discovered to be upregulated during aging and to influence insulin signalling and energy metabolism in skeletal muscle. For more detail and information of our research in the above areas please visit the research page on the Hundal Lab website.
I am involved in the delivery and management of taught modules to undergraduate students at Level 3 and Level 4 taking degrees within our Biomedicial Sciences teaching programme.
BS31013 - Biomembranes
BS31019 - Regulatory Physiology and Pharmacology
BS42014 – Diabetes, Obesity and Metabolic Dysfunction
Lipina, C. and Hundal, H.S. (2017) The endocannabinoid system: no longer anonymous in the control of nitrergic signalling? Journal of molecular cell biologyd.o.i 10.1093/jmcb/mjx008
Lipina, C. and Hundal, H. S. (2016) Lipid modulation of skeletal muscle mass and function. Journal of cachexia, sarcopenia and muscled.o.i 10.1002/jcsm.12144
Lipina, C. and Hundal, H.S. (2016) Is REDD1 a Metabolic Eminence Grise? Trends in endocrinology and metabolism: TEM. 27, 868-880
Watson, A., Lipina, C., McArdle, H. J., Taylor, P. M. and Hundal, H. S. (2016) Iron depletion suppresses mTORC1-directed signalling in intestinal Caco-2 cells via induction of REDD1. Cellular signalling. 28, 412-424
Lipina, C. and Hundal, H. S. (2016) Modulation of cellular redox homeostasis by the endocannabinoid system. Open biology. 6, 150276
Lipina, C., Vaanholt, L. M., Davidova, A., Mitchell, S. E., Storey-Gordon, E., Hambly, C., Irving, A. J., Speakman, J. R. and Hundal, H. S. (2016) CB1 receptor blockade counters age-induced insulin resistance and metabolic dysfunction. Aging cell. 15, 325-335
Nardi, F., Hoffmann, T. M., Stretton, C., Cwiklinski, E., Taylor, P. M. and Hundal, H. S. (2015) Proteasomal modulation of cellular SNAT2 (SLC38A2) abundance and function by unsaturated fatty acid availability. The Journal of biological chemistry. 290, 8173-8184
Stretton, C., Hoffmann, T. M., Munson, M. J., Prescott, A., Taylor, P. M., Ganley, I. G. and Hundal, H. S. (2015) GSK3-mediated raptor phosphorylation supports amino-acid-dependent mTORC1-directed signalling. The Biochemical journal. 470, 207-221
Lipina, C., Macrae, K., Suhm, T., Weigert, C., Blachnio-Zabielska, A., Baranowski, M., Gorski, J., Burgess, K. and Hundal, H. S. (2013) Mitochondrial substrate availability and its role in lipid-induced insulin resistance and proinflammatory signaling in skeletal muscle. Diabetes. 62, 3426-3436
Macrae, K., Stretton, C., Lipina, C., Blachnio-Zabielska, A., Baranowski, M., Gorski, J., Marley, A. and Hundal, H. S. (2013) Defining the role of DAG, mitochondrial function, and lipid deposition in palmitate-induced proinflammatory signaling and its counter-modulation by palmitoleate. Journal of lipid research. 54, 2366-2378