Understanding the molecular basis for the development of type-2 diabetes
Type-2 diabetes (T2D) is a highly prevalent disease whose incidence is increasing at an alarming rate due to the obesity epidemic. This is because obesity results in the development of insulin resistance. Although the majority of obese people develop insulin resistance, they do not develop diabetes due to a compensatory increase in insulin secretion from the pancreatic beta-cells. This is enabled by an increase in both pancreatic beta-cell function and mass. Critically, it is the failure of the beta-cells to compensate and/or maintain a compensatory phenotype that ultimately leads to the development of T2DM. This is characterised by the development of beta-cell dysfunction and ultimately beta-cell death. My laboratory is focused on understanding the molecular basis for beta-cell compensation and the development of beta-cell dysfunction. This work is important not only in the development of a fundamental understanding of beta-cell physiology but also in understanding the pathophysiology of type-2 diabetes, which in turn may lead to the identification of new rational strategies for the treatment and possible prevention of this disease.
Current areas of active research
- The role of mTOR in beta-cell compensation and dysfunction.
- ER stress and the unfolded protein response (UPR) in health and disease (principally in relation to type-2 diabetes).
- The role of amino acid transporters in beta-cell function and type-2 diabetes.
PhD opportunities are currently available in Dr Herbert's laboratory. If you are interested in applying for PhD position in his laboratory (self-funded or through a Scholarship Scheme) please contact him by e-mail.
- Associate Professor of Pharmacology
- Principal Investigator of the Islet Molecular and Cellular Biology Group
- BSc (Hons), University of Newcastle (UK)
- PhD, University of Cambridge (UK)
- 1995–1997 Juvenile Diabetes Research Foundation (JDRF) Research Fellow, Joslin Diabetes Center (Harvard Affiliate), Boston, MA, U.S.A. Supervisor: Professor Christopher Rhodes
- 1997–1998 Postdoctoral Research Fellow, Department of Biology, Tufts University, MA 02155, USA. Supervisor: Professor Norman Hecht
- 1998–2001 Postdoctoral Research Fellow, Department of Anatomy and Physiology, University of Dundee, Dundee, Scotland, UK. Supervisor: Professor Christopher Proud
- 2001-2003 University Lecturer, Department of Biochemistry, University of Leicester, England, UK
- 2003-2007 University Lecturer, Department of Cell Physiology and Pharmacology, University of Leicester, England, UK
- 2007-2014 Senior Lecturer, Department of Cell Physiology and Pharmacology, University of Leicester, England, UK
- Editorial advisor for the Biochemical Journal
- Biochemical Journal
- Journal of Endocrinology
- Journal of Cell Biology
- PLoS one
- Nutrition Research Reviews
- Clinical Science
- Journal Biochimica et Biophysica Acta
- ….and many more.
- Australian Research Council
- Wellcome Trust
- Diabetes UK
- Leverhulme Trust
- "InBev-Baillet Latour Grant for Medical Research" Belgium
Membership of Learned societies
- Member of the Biochemical Society
- Member of the European Association for the Study of Diabetes
- Member of the Islet Study Group
- Cheung, J.,Li, S.,Zhang, X.,Wang, H.,Herbert, T.,Jenkins, T.,Xu, A.,Ye, J. (2017). Chronic activation of PPAR alpha with fenofibrate reduces autophagic proteins in the liver of mice independent of FGF21 In: PLoS ONE, 12, 1 - 10
- Cheng, Q.,Diez Beltran, V.,Chan, S.,Brown, J.,Bevington, A.,Herbert, T. (2016). System-L amino acid transporters play a key role in pancreatic beta-cell signalling and function In: Journal of Molecular Endocrinology, 56, 175 - 187
- Herbert, T.,Laybutt, R. (2016). A reevaluation of the role of the unfolded protein response in islet dysfunction: Maladaptation or a failure to adapt? In: Diabetes, 65, 1472 - 1480
- Wang, H.,Sun, R.,Camera, D.,Zeng, X.,Jo, E.,Chan, S.,Herbert, T.,Molero - Navajas, J.,Ye, J. (2016). Endoplasmic reticulum stress up-regulates Nedd4-2 to induce autophagy In: The FASEB Journal, 30, 2549 - 2556
- Johnson, C.,Hunt, D.,Wiltshire, M.,Herbert, T.,Sampson, J.,Errington, R.,Davies, D.,Tee, A. (2015). Endoplasmic reticulum stress and cell death in mTORC1-overactive cells is induced by nelfinavir and enhanced by chloroquine In: Molecular Oncology, 9, 675 - 688
- Xie, J.,El Sayed, N.,Qi, C.,Zhao, X.,Moore, C.,Herbert, T. (2014). Exendin-4 stimulates islet cell replication via the IGF1 receptor activation of mTORC1/S6K1 In: Journal of Molecular Endocrinology, 53, 105 - 115
- Chen, C.,Cano, M.,Wang, J.,Li, J.,Huang, C.,Yu, Q.,Herbert, T.,Handa, J.,Zhang, S. (2014). Role of unfolded protein response dysregulation in oxidative injury of retinal pigment epithelial cells In: Antioxidants & Redox Signaling, 20, 2091 - 2106
- Omikorede, O.,Qi, C.,Gorman, T.,Chapman, P.,Yu, A.,Smith, D.,Herbert, T. (2013). ER stress in rodent islets of langerhans is concomitant with obesity and beta-cell compensation but not with beta-cell dysfunction and diabetes In: Nutrition and Diabetes, 3, 1 - 9
- Barlow, A.,Nicholson, M.,Herbert, T. (2013). Evidence for rapamycin toxicity in pancreatic beta-cells and a review of the underlying molecular mechanisms In: Diabetes, 62, 2674 - 2682
- Selway, J.,Rigatti, R.,Storey, N.,Lu, J.,Willars, G.,Herbert, T. (2012). Evidence that Ca2+ within the microdomain of the l-type voltage gated Ca2+ channel activates ERK in MIN6 cells in response to glucagon-like peptide-1 In: PLoS One, 7, 1 - 10
1 PhD Current Supervisions