Why study human disorders at the molecular level?
Simply it is important to understand our disorders and diseases and how to treat them for human health and wellbeing. Our research consider the most interesting species on earth, Homo sapiens. In addition, using of other species in research such as mice and rats is important to understand the mechanisms of incidence of human disorders and the potential strategies for intervention of these disorders.
For example, diabetes mellitus is a common disease and its prevalence is increasing worldwide. Our research showed that induction of diabetes mellitus in rats resulted in changes in glucagon-like peptide -1 receptor (GLP-1R) signaling transduction in the liver. Treatment of these diabetic rats with selenium or exendin-4, GLP-1 analogue, decreased the blood glucose level to near normal values and affected the expression of GLP-1R signal transducers. However, the exact molecular mechanisms for these antidiabetic actions require further detailed investigation.
Our current research program investigates the molecular mechanisms for the antidiabetic effects of selenium and exendin-4 on insulin receptor and GLP-1R signal transduction, glucose transporters and selenoprotein expression in different organs in a model of diabetes in rat.
Research interests extend to studying the association of genetic polymorphism (SNPs) and the human disorders such as on diabetes mellitus. For instance, we investigated the association of transcription factor 7 like 2 (TCF7L2) gene polymorphism with type 2 diabetes in the Lebanese population.
Our research interests also extend to autoimmune diseases, particularly Rheumatoid Arthritis (RA), which is quite common worldwide. We aim to find alternative therapeutic strategies to slow the progression and ease the symptoms of such incurable disease. Current treatments (e.g. Methotrexate) face several obstacles ranging from undesirable side effects to liver toxicity due to long-term usage.
Thus, we focus on testing some promising natural agents and examining their anti-inflammatory, anti-oxidant and hepatoprotective effects against Methotrexate-induced liver injury. We have for this purpose successfully established a well-known experimental RA animal model, which is the Adjuvant Induced-Arthritis (AIA) model. The appearance of arthritis in AIA is demonstrated to quite resemble human RA in terms of clinical, histological and immunological features.
Treatment of arthritic rats with Silibinin, Indole-3-carbinol or Delta-9-Tetrahydrocannabinol showed promising results in diminishing the inflammatory process, modulating the immune response and acting as hepatoprotective agents against Methotrexate-induced liver injury. Future aspects focus on understanding the molecular mechanisms by which these agents exert their protective effects.