Dr. Mohammed Dehbi
Principal Investigator (QBRI)
Assistant Professor (HBKU)
Tel: + 974 4454 6339
Dr. Dehbi obtained his M.Sc. degree in molecular and cellular biology from Université Louis Pasteur, France in 1988. In 1995, he obtained his Ph.D. in biochemistry from l’Université de Montreal, Canada. His Ph.D thesis was on understanding the mechanisms of cell transformation by oncogenic retroviruses. He then pursued his postdoctoral training on kidney cancer at McGill University, Canada.
In 1997, he joined Targanta Therapeutics Inc; (now The Medicine Company) as a Senior Scientist and was later promoted to Research Fellow. His work focused on developing new classes of antibiotics based on phage genomics.
In 2005, Dr. Dehbi moved to the King Faisal Specialist Hospital in Saudi Arabia to setup and head the Cell Injury & Inflammation Research Unit. His research interest was to understand the mechanisms of heat injury “heatstroke” using animal models.
In 2009, he joined the Dasman Diabetes Institute in Kuwait as a Senior Scientist and Head of the Biochemistry & Molecular Biology Unit, where he played an instrumental role in establishing the unit and developing research programs on obesity and diabetes. In 2013, he moved to Qatar and joined QBRI as a Principal Investigator and he is still pursuing his research on metabolic diseases.
In 2015, he received a joint appointment with Hamad Bin Khalifa University as Assistant Professor. Dr Dehbi has 35 peer-reviewed publications in major journals, such as Nature Biotechnology, EMBO. J. He has received several awards and fellowships, including the two highly prestigious fellowships from the National Cancer Institute of Canada and the Natural Sciences & Engineering Research Council of Canada.
Defects in the heat shock response system have been observed in obese and diabetic patients in a manner that correlates with the degree of insulin resistance. Consistent with these clinical observations, interventions that restored the heat shock response such heat therapy, electrical stimulation, physical exercise and pharmacological modulators improved the clinical outcomes both in human and experimental animal models. In mice models of diet or obesity-induced insulin resistance and diabetes, overexpression of HSP-72; a key component of the heat shock response protected animals from developing insulin resistance and improved significantly their glyceamic control and thus supporting the direct cause-relationship between the heat shock response, insulin resistance and diabetes. Data from our group and others are in support of proposing the metabolic vicious cycle paradigm leading to type 2 diabetes. Over the last 6 years, our efforts have been devoted to understanding the role and mechanisms by which physical exercise modulates the inflammatory and metabolic stresses in obese/diabetic subjects. Accordingly, we identified two protein candidates namely DNAJB3; a member of the heat shock protein-40 (HSP-40) and the histone deacetylase-4 (HDAC4) that were significantly downregulated in obese/diabetic patients and up-regulated by physical exercise with concomitant improvement of the outcomes. Dr. Dehbi is still pursuing vigorously his research activities on the role and mechanisms of DNAJB3 and HDAC-4 on insulin resistance and diabetes in vitro and in vivo using animal models. He is using state of the art technology used for target identification, validation and characterization including mass spectrometry, Biacore, FRET and multiplexing technologies. The ultimate objective is to translate the knowledge gained from the various approaches into clinical outcomes such as development of small molecules that promote the heat shock response with therapeutic feature or preventative strategies to control and manage obesity and its related disorders.
Our current research efforts focus on elucidating the in vivo and in vitro role of DNAJB3 in the pathophysiology of insulin resistance and diabetes. We recently demonstrated that DNAJB3 stimulates glucose uptake in vitro, but the molecular mechanisms remain to be elucidated. As there is strong evidence suggesting that epigenetic regulation could impact the heat shock response, we have also an interest to dissect the relationship between DNAJB3 and HDAC-4 at the molecular level and evaluating the relevance of such relationship to obesity, insulin resistance and diabetes. More specifically, our research questions are as follow:
- Role and mechanisms by which DNAJB3 regulate glucose homeostasis?
- Role of DNAJB3 in modulating metabolic stress?
- Effect of DNAJB3 on Beta cell integrity and function?
List of Publications on Pubmed
||Cell biology, glucose and lipid metabolisms, insulin secretion and action.
|Dr. M. Chikri
||Gene expression profiling, pathways analysis
Role of circulating microRNA in insulin resistance, Role of TMEM-143 in diabetes.
||Gene silencing via siRNA, CRISPR, characterization of the interacting partners.
||Structure-function analysis of the chaperone network.
|The iTRI, HMC
||Mass spectrometry analysis, epigenetic modifications.
|The iTRI, HMC
||Flow cytometry analysis, immune modulation.
|Dr. M. Prentki
||Montreal Diabetes Center, University of Montreal, Canada
||Development of animal models of diet-induced obesity and diabetes, monitoring β-Cell integrity and function (in vivo & ex-vivo studies).
|Drs. J. Abubaker,
A. Tiss &
|Dasman Diabetes Institute, Kuwait
||Physiology of physical exercise.
|Hamad Bin Khalifa
|Advanced Cell Biology
|Qatar University (2014-2015)
||Biomedical Sciences Program for Master Students
||Coordinator of QBRI/Qatar University Courses
|Qatar University (2014)
||The Endocrine Disorders and Function (BIOM-660)
||Lecturer (2 hours)
|Techniques in Biochemistry (BCM 6100)
(2 consecutive weeks/year)
||Carnegie Melon University, Qatar
||Carnegie Melon University, Qatar
|Nora Al Khaddari
||Dasman Diabetes Institute, Kuwait
|King Faisal Specialist Hospital,
Riyadh, Saudi Arabia
- Member of QBRI Recruitment Committee.
- Regular reviewer of QNRF-NPRP grants and King Abdulaziz City of Sciences & Technology (KACST) grants.
- Referee for various peer reviewed scientific journals.