Mohammed Dehbi

ORCID: 0000-0002-1808-2564
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About
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Research Areas
  • Thermoregulation and physiological responses
  • Adipose Tissue and Metabolism
  • Heat shock proteins research
  • Endoplasmic Reticulum Stress and Disease
  • Climate Change and Health Impacts
  • Bacteriophages and microbial interactions
  • Adipokines, Inflammation, and Metabolic Diseases
  • Thermal Regulation in Medicine
  • Renal and related cancers
  • Exercise and Physiological Responses
  • RNA Research and Splicing
  • Bacterial Genetics and Biotechnology
  • Pancreatic function and diabetes
  • GDF15 and Related Biomarkers
  • RNA and protein synthesis mechanisms
  • Protein Tyrosine Phosphatases
  • Histone Deacetylase Inhibitors Research
  • Mitochondrial Function and Pathology
  • Genetics, Aging, and Longevity in Model Organisms
  • Virus-based gene therapy research
  • Diabetes Management and Research
  • Hyperglycemia and glycemic control in critically ill and hospitalized patients
  • RNA Interference and Gene Delivery
  • Biochemical Acid Research Studies
  • Diabetes and associated disorders

Hamad bin Khalifa University
2016-2023

Qatar Foundation
2014-2023

Biomedical Research Institute
2016

Qatar Airways (Qatar)
2015

Dasman Diabetes Institute
2010-2014

King Faisal Specialist Hospital & Research Centre
2006-2012

Université Paris-Sud
2008

Inserm
2008

Alfaisal University
2007

McGill University
1995-1998

Sedentary lifestyle and excessive energy intake are prominent contributors to obesity; a major risk factors for the development of insulin resistance, type 2 diabetes cardiovascular diseases. Elucidating molecular mechanisms underlying these chronic conditions is relevant importance as it might lead identification novel anti-obesity targets. The purpose current study investigate differentially expressed proteins between lean obese subjects through shot-gun quantitative proteomics approach...

10.1371/journal.pone.0075342 article EN cc-by PLoS ONE 2013-09-24

Recent studies have demonstrated a protective role for IL-33 against obesity-associated inflammation, atherosclerosis and metabolic abnormalities. promotes the production of T helper type 2 (Th2) cytokines, polarizes macrophages towards alternatively activated phenotype, reduces lipid storage decreases expression genes associated with metabolism adipogenesis. Our objective was to determine level serum in non-diabetic diabetic subjects, correlate these levels clinical (BMI body weight) (serum...

10.1186/1471-2172-15-19 article EN cc-by BMC Immunology 2014-05-10

Obesity is a major risk factor for myriad of disorders such as insulin resistance and diabetes. The mechanisms underlying these chronic conditions are complex but low grade inflammation alteration the endogenous stress defense system well established. Previous studies indicated that impairment HSP-25 HSP-72 was linked to obesity, diabetes in humans animals while their induction associated with improved clinical outcomes. In an attempt identify additional components heat shock response may be...

10.1371/journal.pone.0069217 article EN cc-by PLoS ONE 2013-07-24

Chronic low-grade inflammation and dysregulation of the stress defense system are cardinal features obesity, a major risk factor for development insulin resistance diabetes. Dual-specificity protein phosphatase 1 (DUSP1), known also as MAP kinase (MKP1), is implicated in metabolism energy expenditure. Mice lacking DUSP1 resistant to high-fat diet-induced obesity. However, expression has not been investigated human In current study, we compared pattern between lean obese nondiabetic subjects...

10.1152/ajpendo.00577.2013 article EN AJP Endocrinology and Metabolism 2014-11-05

Objective: Excessive activation of coagulation, which can culminate in overt disseminated intravascular is a prominent feature heat stroke. However, neither the mechanism that initiates coagulation nor its pathogenic role known. We examined whether tissue factor/factor VIIa complex stroke and, if so, upstream inhibition through neutralization may minimize cellular injury and organ dysfunction. also influences stroke-induced fibrinolytic inflammatory responses. Design: Randomized controlled...

10.1097/ccm.0b013e3182387bef article EN Critical Care Medicine 2011-11-11

Obesity is characterized by a chronic low-grade inflammation and altered stress responses in key metabolic tissues. Impairment of heat shock response (HSR) has been already linked to diabetes insulin resistance as reflected decrease proteins (HSPs) expression. However, the status HSR non-diabetic human obese not yet elucidated. The aim current study was investigate whether obesity triggers change pattern impact physical exercise on this at protein mRNA levels. Two groups adult subjects...

10.1186/1476-511x-13-106 article EN cc-by Lipids in Health and Disease 2014-07-01

RANTES and its CCR5 receptor trigger inflammation progression to insulin resistance in obese. In the present study, we investigated for first time effect of physical exercise on expression obese humans. Fifty-seven adult nondiabetic subjects (17 lean 40 obese) were enrolled a 3-month supervised exercise. expressions measured PBMCs subcutaneous adipose tissue before after Circulating plasma levels also investigated. There was significant increase compared lean. PBMCs, however, while mRNA...

10.1155/2014/627150 article EN cc-by Mediators of Inflammation 2014-01-01

Streptococcus pneumoniae causes several diseases, including pneumonia, septicemia, and meningitis. Phage Dp-1 is one of the very few isolated virulent S. bacteriophages, but only a partial characterization currently available. Here, we confirmed that belongs to family Siphoviridae. Then, determined its complete genomic sequence 56,506 bp. It encodes 72 open reading frames, which 44 have been assigned function. We identified putative promoters, Rho-independent terminators, clusters. provide...

10.1128/jb.01117-10 article EN Journal of Bacteriology 2010-11-20

Objectives— We tested the hypothesis that antithrombotic and cytoprotective effects of recombinant human activated protein C (rhAPC) protect baboons against lethal heatstroke. Methods Results— Fourteen anesthetized assigned randomly to rhAPC (n=7) or control group were heat-stressed in a prewarmed incubator at 44 47°C until systolic blood pressure fell below 90 mm Hg, which signaled severe was administered intravenously (24 μg/kg/h) for 12 hours onset Heat stress induced coagulation...

10.1161/atvbaha.107.161737 article EN Arteriosclerosis Thrombosis and Vascular Biology 2008-05-04

The molecular mechanisms that initiate the inflammatory response in heatstroke and their relation with tissue injury lethality are not fully elucidated. We examined whether endogenous ligands released by damaged/stressed cells such as high-mobility group box 1 (HMGB1) signaling through Toll-like receptor 4 (TLR4) may play a pathogenic role heatstroke. Mutant TLR4-defective (C3H/HeJ) wild type (C3H/HeOuJ) mice were subjected to heat stress an environmental chamber pre-warmed at 43.5 °C until...

10.1371/journal.pone.0044100 article EN cc-by PLoS ONE 2012-09-04

Heat shock protein 60 (HSP60) is a key in the crosstalk between cellular stress and inflammation. However, status of HSP60 diabetes obesity unclear. In present study, we investigated adipose tissue obese adults with without changes its expression response to supervised 3-month physical exercise program. Subcutaneous (SAT) blood samples were collected from (n=138 n=92, respectively, at baseline; n=43 for both groups after 3 months exercise). Conventional RT-PCR, immunohistochemistry,...

10.3389/fendo.2018.00016 article EN cc-by Frontiers in Endocrinology 2018-02-05

Abstract Heat shock response (HSR) is an essential host-defense mechanism that dysregulated in obesity-induced insulin resistance and type 2 diabetes (T2D). Our recent data demonstrated DNAJB3 was downregulated obese human subjects showed negative correlation with inflammatory markers. Nevertheless, expression pattern diabetic its mode of action are not yet known. In this study, we reduction transcript protein levels PBMC subcutaneous adipose tissue T2D compared to non-diabetic subjects....

10.1038/srep14448 article EN cc-by Scientific Reports 2015-09-24

Abstract Persistent ER stress, mitochondrial dysfunction and failure of the heat shock response (HSR) are fundamental hallmarks insulin resistance (IR); one early core metabolic aberrations that leads to type 2 diabetes (T2D). The antioxidant α-lipoic acid (ALA) has been shown attenuate stress improve sensitivity in part through activation (HSR). However, these studies have focused on a subset proteins (HSPs). In current investigation, we assessed whether ALA an effect modulating expression...

10.1038/s41598-020-77621-x article EN cc-by Scientific Reports 2020-11-24
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