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182 results on '"Kochumon, Shihab"'

2. Unraveling Verapamil's Multidimensional Role in Diabetes Therapy: From β-Cell Regeneration to Cholecystokinin Induction

Author

Arefanian, Hossein, primary, Al Madhoun, Ashraf, additional, Al-Rashed, Fatema, additional, Alzaid, Fawaz, additional, Bahman, Fatemah, additional, Nizam, Rasheeba, additional, Alhusayan, Mohammed, additional, John, Sumi Elsa, additional, Jacob, Sindhu, additional, Williams, Michayla R, additional, Abu Khalaf, Nermeen, additional, Shenouda, Steve, additional, Joseph, Shibu, additional, AlSaeed, Halemah, additional, Kochumon, Shihab, additional, Mohammad, Anwar, additional, Koti, Lubaina, additional, Sindhu, Sardar, additional, Abu-Farha, Mohamed, additional, Abubaker, Jehad, additional, Thanaraj, Thangavel Alphonse, additional, Ahmad, Rasheed, additional, and Al-Mulla, Fahd, additional

Published
2024
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3. Differential effects of fish-oil and cocoa-butter based high-fat/high-sucrose diets on endocrine pancreas morphology and function in mice

Author

Albeloushi, Shaima, primary, Hasan, Amal, additional, Arefanian, Hossein, additional, Sindhu, Sardar, additional, Al-Rashed, Fatema, additional, Kochumon, Shihab, additional, Abukhalaf, Nermeen, additional, Jacob, Texy, additional, Shenouda, Steve, additional, Al Madhoun, Ashraf, additional, Al-Mulla, Fahd, additional, and Ahmad, Rasheed, additional

Published
2024
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4. Gut Dysbiosis Shaped by Cocoa Butter-Based Sucrose-Free HFD Leads to Steatohepatitis, and Insulin Resistance in Mice.

Author

Kochumon, Shihab, Malik, Md. Zubbair, Sindhu, Sardar, Arefanian, Hossein, Jacob, Texy, Bahman, Fatemah, Nizam, Rasheeba, Hasan, Amal, Thomas, Reeby, Al-Rashed, Fatema, Shenouda, Steve, Wilson, Ajit, Albeloushi, Shaima, Almansour, Nourah, Alhamar, Ghadeer, Al Madhoun, Ashraf, Alzaid, Fawaz, Thanaraj, Thangavel Alphonse, Koistinen, Heikki A., and Tuomilehto, Jaakko

Abstract

Background: High-fat diets cause gut dysbiosis and promote triglyceride accumulation, obesity, gut permeability changes, inflammation, and insulin resistance. Both cocoa butter and fish oil are considered to be a part of healthy diets. However, their differential effects on gut microbiome perturbations in mice fed high concentrations of these fats, in the absence of sucrose, remains to be elucidated. The aim of the study was to test whether the sucrose-free cocoa butter-based high-fat diet (C-HFD) feeding in mice leads to gut dysbiosis that associates with a pathologic phenotype marked by hepatic steatosis, low-grade inflammation, perturbed glucose homeostasis, and insulin resistance, compared with control mice fed the fish oil based high-fat diet (F-HFD). Results: C57BL/6 mice (5–6 mice/group) were fed two types of high fat diets (C-HFD and F-HFD) for 24 weeks. No significant difference was found in the liver weight or total body weight between the two groups. The 16S rRNA sequencing of gut bacterial samples displayed gut dysbiosis in C-HFD group, with differentially-altered microbial diversity or relative abundances. Bacteroidetes, Firmicutes, and Proteobacteria were highly abundant in C-HFD group, while the Verrucomicrobia, Saccharibacteria (TM7), Actinobacteria, and Tenericutes were more abundant in F-HFD group. Other taxa in C-HFD group included the Bacteroides, Odoribacter, Sutterella, Firmicutes bacterium (AF12), Anaeroplasma, Roseburia, and Parabacteroides distasonis. An increased Firmicutes/Bacteroidetes (F/B) ratio in C-HFD group, compared with F-HFD group, indicated the gut dysbiosis. These gut bacterial changes in C-HFD group had predicted associations with fatty liver disease and with lipogenic, inflammatory, glucose metabolic, and insulin signaling pathways. Consistent with its microbiome shift, the C-HFD group showed hepatic inflammation and steatosis, high fasting blood glucose, insulin resistance, increased hepatic de novo lipogenesis (Acetyl CoA carboxylases 1 (Acaca), Fatty acid synthase (Fasn), Stearoyl-CoA desaturase-1 (Scd1), Elongation of long-chain fatty acids family member 6 (Elovl6), Peroxisome proliferator-activated receptor-gamma (Pparg) and cholesterol synthesis (β-(hydroxy β-methylglutaryl-CoA reductase (Hmgcr). Non-significant differences were observed regarding fatty acid uptake (Cluster of differentiation 36 (CD36), Fatty acid binding protein-1 (Fabp1) and efflux (ATP-binding cassette G1 (Abcg1), Microsomal TG transfer protein (Mttp) in C-HFD group, compared with F-HFD group. The C-HFD group also displayed increased gene expression of inflammatory markers including Tumor necrosis factor alpha (Tnfa), C-C motif chemokine ligand 2 (Ccl2), and Interleukin-12 (Il12), as well as a tendency for liver fibrosis. Conclusion: These findings suggest that the sucrose-free C-HFD feeding in mice induces gut dysbiosis which associates with liver inflammation, steatosis, glucose intolerance and insulin resistance. [ABSTRACT FROM AUTHOR]

Published
2024
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5. Unraveling Verapamil's Multidimensional Role in Diabetes Therapy: From β-Cell Regeneration to Cholecystokinin Induction in Zebrafish and MIN6 Cell-Line Models.

Author

Arefanian, Hossein, Al Madhoun, Ashraf, Al-Rashed, Fatema, Alzaid, Fawaz, Bahman, Fatemah, Nizam, Rasheeba, Alhusayan, Mohammed, John, Sumi, Jacob, Sindhu, Williams, Michayla R., Abukhalaf, Nermeen, Shenouda, Steve, Joseph, Shibu, AlSaeed, Halemah, Kochumon, Shihab, Mohammad, Anwar, Koti, Lubaina, Sindhu, Sardar, Abu-Farha, Mohamed, and Abubaker, Jehad

Subjects
VERAPAMIL, BRACHYDANIO, PEPTIDE hormones, CHOLECYSTOKININ, CARDIAC regeneration, DIABETES
Abstract

This study unveils verapamil's compelling cytoprotective and proliferative effects on pancreatic β-cells amidst diabetic stressors, spotlighting its unforeseen role in augmenting cholecystokinin (CCK) expression. Through rigorous investigations employing MIN6 β-cells and zebrafish models under type 1 and type 2 diabetic conditions, we demonstrate verapamil's capacity to significantly boost β-cell proliferation, enhance glucose-stimulated insulin secretion, and fortify cellular resilience. A pivotal revelation of our research is verapamil's induction of CCK, a peptide hormone known for its role in nutrient digestion and insulin secretion, which signifies a novel pathway through which verapamil exerts its therapeutic effects. Furthermore, our mechanistic insights reveal that verapamil orchestrates a broad spectrum of gene and protein expressions pivotal for β-cell survival and adaptation to immune-metabolic challenges. In vivo validation in a zebrafish larvae model confirms verapamil's efficacy in fostering β-cell recovery post-metronidazole infliction. Collectively, our findings advocate for verapamil's reevaluation as a multifaceted agent in diabetes therapy, highlighting its novel function in CCK upregulation alongside enhancing β-cell proliferation, glucose sensing, and oxidative respiration. This research enriches the therapeutic landscape, proposing verapamil not only as a cytoprotector but also as a promoter of β-cell regeneration, thereby offering fresh avenues for diabetes management strategies aimed at preserving and augmenting β-cell functionality. [ABSTRACT FROM AUTHOR]

Published
2024
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7. Endoplasmic Reticulum Stress Promotes the Expression of TNF-α in THP-1 Cells by Mechanisms Involving ROS/CHOP/HIF-1α and MAPK/NF-κB Pathways

Author

Akhter, Nadeem, primary, Wilson, Ajit, additional, Arefanian, Hossein, additional, Thomas, Reeby, additional, Kochumon, Shihab, additional, Al-Rashed, Fatema, additional, Abu-Farha, Mohamed, additional, Al-Madhoun, Ashraf, additional, Al-Mulla, Fahd, additional, Ahmad, Rasheed, additional, and Sindhu, Sardar, additional

Published
2023
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11. IRF3 reduces adipose thermogenesis via ISG15-mediated reprogramming of glycolysis

Author

Yan, Shuai, Kumari, Manju, Xiao, Haopeng, Jacobs, Christopher, Kochumon, Shihab, Jedrychowski, Mark, Chouchani, Edward, Ahmad, Rasheed, and Rosen, Evan D.

Subjects
Obesity -- Development and progression, Adipose tissues -- Health aspects, Thermogenesis -- Genetic aspects -- Health aspects, Glycolysis -- Genetic aspects -- Health aspects, Transcription factors -- Health aspects, Health care industry
Abstract

Adipose thermogenesis is repressed in obesity, reducing the homeostatic capacity to compensate for chronic overnutrition. Inflammation inhibits adipose thermogenesis, but little is known about how this occurs. Here we showed that the innate immune transcription factor IRF3 is a strong repressor of thermogenic gene expression and oxygen consumption in adipocytes. IRF3 achieved this by driving expression of the ubiquitin-like modifier ISG15, which became covalently attached to glycolytic enzymes, thus reducing their function and decreasing lactate production. Lactate repletion was able to restore thermogenic gene expression, even when the IRF3/ISG15 axis was activated. Mice lacking ISG15 phenocopied mice lacking IRF3 in adipocytes, as both had elevated energy expenditure and were resistant to diet-induced obesity. These studies provide a deep mechanistic understanding of how the chronic inflammatory milieu of adipose tissue in obesity prevents thermogenic compensation for overnutrition., Introduction Body weight is under homeostatic control, in that both gain and loss of body weight initiate physiological events that tend to restore energy balance to normal (1). Thus, short-term [...]

Published
2021
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13. Expression of Steroid Receptor RNA Activator 1 (SRA1) in the Adipose Tissue Is Associated with TLRs and IRFs in Diabesity

Author

Kochumon, Shihab, primary, Arefanian, Hossein, additional, Sindhu, Sardar, additional, Thomas, Reeby, additional, Jacob, Texy, additional, Al-Sayyar, Amnah, additional, Shenouda, Steve, additional, Al-Rashed, Fatema, additional, Koistinen, Heikki A., additional, Al-Mulla, Fahd, additional, Tuomilehto, Jaakko, additional, and Ahmad, Rasheed, additional

Published
2022
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14. Caveolin-1 rs1997623 Single Nucleotide Polymorphism Creates a New Binding Site for the Early B-Cell Factor 1 That Instigates Adipose Tissue CAV1 Protein Overexpression

Author

Al Madhoun, Ashraf, primary, Haddad, Dania, additional, Nizam, Rasheeba, additional, Miranda, Lavina, additional, Kochumon, Shihab, additional, Thomas, Reeby, additional, Thanaraj, Thangavel Alphonse, additional, Ahmad, Rasheed, additional, Bitar, Milad S., additional, and Al-Mulla, Fahd, additional

Published
2022
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15. Increased Adipose Tissue Expression of IL-23 Associates with Inflammatory Markers in People with High LDL Cholesterol

Author

Kochumon, Shihab, primary, Hasan, Amal, additional, Al-Rashed, Fatema, additional, Sindhu, Sardar, additional, Thomas, Reeby, additional, Jacob, Texy, additional, Al-Sayyar, Amnah, additional, Arefanian, Hossein, additional, Al Madhoun, Ashraf, additional, Al-Ozairi, Ebaa, additional, Alzaid, Fawaz, additional, Koistinen, Heikki A., additional, Al-Mulla, Fahd, additional, Tuomilehto, Jaakko, additional, and Ahmad, Rasheed, additional

Published
2022
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20. FSL-1 Induces MMP-9 Production through TLR-2 and NF-κB /AP-1 Signaling Pathways in Monocytic THP-1 Cells

Author

Rasheed Ahmad, Puthiyaveetil Kochumon Shihab, Sara Jasem, and Kazem Behbehani

Subjects
p38, ERK, MyD88, MMP-9, TLR-2, Physiology, QP1-981, Biochemistry, QD415-436
Abstract

Background: Matrix metalloproteinase-9 (MMP-9) is known to be implicated in the pathogenesis of many inflammatory disorders. FSL-1 (fibroblast-stimulating lipopeptide-1) induces cytokine production by monocytes/macrophages. However, it is unclear whether FSL-1 is also able to induce MMP-9 production. Herein, we determined whether FSL-1 could induce MMP-9 production, and if so, which signal transduction pathway(s) were involved. Methods: MMP-9 expression was assessed with real-time qPCR and ELISA. Signaling pathways were studied by using THP1-XBlue™ cells, THP1-XBlue™-defMyD cells, anti-TLR2 mAb and pharmacological inhibitors. Phospho and total proteins were determined by Western blotting. Results: FSL-1 induces MMP-9 expression (PP-/- THP-1 cells did not express MMP-9 in response to FSL-1 treatment. By small interfering RNA-mediated knockdown, we also show that FSL-1-induced up-regulation of MMP-9 requires MyD88. Pre-treatment of THP-1 cells with inhibitors of JNK (SP600125), MEK/ERK (U0126; PD98056; XMD 8-92), p38 MAPK (SB203580) and NF-κB (BAY11-7085, Triptolide, Resveratrol) significantly suppressed (PConclusion: These findings provide the first evidence that FSL-1 induces TLR-2-dependent MMP-9 gene expression which requires the recruitment of MyD88 and leads to activation of MEK1/2 /ERK 1/2, MEK5/ERK5, JNK, p38 MAPK and NF-κB/AP-1.

Published
2014
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21. Urocortin Neuropeptide Levels Are Impaired in the PBMCs of Overweight Children

Author

Kavalakatt, Sina, primary, Khadir, Abdelkrim, additional, Kochumon, Shihab, additional, Madhu, Dhanya, additional, Devarajan, Sriraman, additional, Hammad, Maha, additional, Alam-Eldin, Nada, additional, Warsame, Samia, additional, Al-Kandari, Hessa, additional, AlMahdi, Maria, additional, Ahmad, Rasheed, additional, Koistinen, Heikki A., additional, Tuomilehto, Jaakko, additional, Al-Mulla, Fahd, additional, Abubaker, Jehad, additional, and Tiss, Ali, additional

Published
2022
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22. Short-Term Palmitate Exposure or Acute High Fat Feeding Promotes a Foamy and Inflammatory Macrophage Phenotype Which Involves ACSL1-Associated Signaling via the CD36/FABP4/P38/PPARδ Axis

Author

Al-Rashed, Fatema, primary, Haddad, Dania, additional, Al Madhoun, Ashraf, additional, Sindhu, Sardar, additional, Jacob, Texy, additional, Kochumon, Shihab, additional, Obeid, Lina M., additional, Al-Mulla, Fahd, additional, Hannun, Yusuf A., additional, and Ahmad, Rasheed, additional

Published
2022
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25. ROS/TNF-α Crosstalk Triggers the Expression of IL-8 and MCP-1 in Human Monocytic THP-1 Cells via the NF-κB and ERK1/2 Mediated Signaling

Author

Akhter, Nadeem, primary, Wilson, Ajit, additional, Thomas, Reeby, additional, Al-Rashed, Fatema, additional, Kochumon, Shihab, additional, Al-Roub, Areej, additional, Arefanian, Hossein, additional, Al-Madhoun, Ashraf, additional, Al-Mulla, Fahd, additional, Ahmad, Rasheed, additional, and Sindhu, Sardar, additional

Published
2021
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30. sj-pdf-1-tae-10.1177_2042018820930902 – Supplemental material for Adipose tissue gene expression of CXCL10 and CXCL11 modulates inflammatory markers in obesity: implications for metabolic inflammation and insulin resistance

Author

Kochumon, Shihab, Madhoun, Ashraf Al, Al-Rashed, Fatema, Azim, Rafaat, Ebaa Al-Ozairi, Al-Mulla, Fahd, and Ahmad, Rasheed

Subjects
FOS: Clinical medicine, 111403 Paediatrics, 110306 Endocrinology, 111599 Pharmacology and Pharmaceutical Sciences not elsewhere classified
Abstract

Supplemental material, sj-pdf-1-tae-10.1177_2042018820930902 for Adipose tissue gene expression of CXCL10 and CXCL11 modulates inflammatory markers in obesity: implications for metabolic inflammation and insulin resistance by Shihab Kochumon, Ashraf Al Madhoun, Fatema Al-Rashed, Rafaat Azim, Ebaa Al-Ozairi, Fahd Al-Mulla and Rasheed Ahmad in Therapeutic Advances in Endocrinology and Metabolism

Published
2020
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31. Stearic Acid and TNF-α Co-Operatively Potentiate MIP-1α Production in Monocytic Cells via MyD88 Independent TLR4/TBK/IRF3 Signaling Pathway

Author

Kochumon, Shihab, primary, Arefanian, Hossein, additional, Azim, Rafaat, additional, Shenouda, Steve, additional, Jacob, Texy, additional, Abu Khalaf, Nermeen, additional, Al-Rashed, Fatema, additional, Hasan, Amal, additional, Sindhu, Sardar, additional, Al-Mulla, Fahd, additional, and Ahmad, Rasheed, additional

Published
2020
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33. Repetitive Intermittent Hyperglycemia Drives the M1 Polarization and Inflammatory Responses in THP-1 Macrophages Through the Mechanism Involving the TLR4-IRF5 Pathway

Author

Al-Rashed, Fatema, primary, Sindhu, Sardar, additional, Arefanian, Hossein, additional, Al Madhoun, Ashraf, additional, Kochumon, Shihab, additional, Thomas, Reeby, additional, Al-Kandari, Sarah, additional, Alghaith, Abdulwahab, additional, Jacob, Texy, additional, Al-Mulla, Fahd, additional, and Ahmad, Rasheed, additional

Published
2020
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43. FSL-1 Induces MMP-9 Production through TLR-2 and NF-κB /AP-1 Signaling Pathways in Monocytic THP-1 Cells

Author

Kazem Behbehani, Puthiyaveetil Kochumon Shihab, Sara Jasem, and Rasheed Ahmad

Subjects
MAPK/ERK pathway, Gene knockdown, lcsh:QP1-981, Physiology, medicine.medical_treatment, p38 mitogen-activated protein kinases, TLR-2, NF-κB, p38, Triptolide, MyD88, lcsh:Physiology, Cell biology, lcsh:Biochemistry, chemistry.chemical_compound, ERK, Cytokine, chemistry, medicine, THP1 cell line, lcsh:QD415-436, Signal transduction, MMP-9
Abstract

Background: Matrix metalloproteinase-9 (MMP-9) is known to be implicated in the pathogenesis of many inflammatory disorders. FSL-1 (fibroblast-stimulating lipopeptide-1) induces cytokine production by monocytes/macrophages. However, it is unclear whether FSL-1 is also able to induce MMP-9 production. Herein, we determined whether FSL-1 could induce MMP-9 production, and if so, which signal transduction pathway(s) were involved. Methods: MMP-9 expression was assessed with real-time qPCR and ELISA. Signaling pathways were studied by using THP1-XBlue™ cells, THP1-XBlue™-defMyD cells, anti-TLR2 mAb and pharmacological inhibitors. Phospho and total proteins were determined by Western blotting. Results: FSL-1 induces MMP-9 expression (PP-/- THP-1 cells did not express MMP-9 in response to FSL-1 treatment. By small interfering RNA-mediated knockdown, we also show that FSL-1-induced up-regulation of MMP-9 requires MyD88. Pre-treatment of THP-1 cells with inhibitors of JNK (SP600125), MEK/ERK (U0126; PD98056; XMD 8-92), p38 MAPK (SB203580) and NF-κB (BAY11-7085, Triptolide, Resveratrol) significantly suppressed (PConclusion: These findings provide the first evidence that FSL-1 induces TLR-2-dependent MMP-9 gene expression which requires the recruitment of MyD88 and leads to activation of MEK1/2 /ERK 1/2, MEK5/ERK5, JNK, p38 MAPK and NF-κB/AP-1.

Published
2014

45. The Synergy between Palmitate and TNF-α for CCL2 Production Is Dependent on the TRIF/IRF3 Pathway: Implications for Metabolic Inflammation

Author

Ahmad, Rasheed, primary, Al-Roub, Areej, additional, Kochumon, Shihab, additional, Akther, Nadeem, additional, Thomas, Reeby, additional, Kumari, Manju, additional, Koshy, Merin S., additional, Tiss, Ali, additional, Hannun, Yusuf A., additional, Tuomilehto, Jaakko, additional, Sindhu, Sardar, additional, and Rosen, Evan D., additional

Published
2018
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50. Additional file 3: of Increased adipose tissue expression of TLR8 in obese individuals with or without type-2 diabetes: significance in metabolic inflammation

Author

Ahmad, Rasheed, Kochumon, Shihab, Reeby Thomas, Atizado, Valerie, and Sindhu, Sardar

Abstract

Correlation between macrophage markers expression in the adipose tissue and body mass index. The adipose tissue gene expression of various monocyte/macrophage markers including CD68, CD86, and CD163 in 94 individuals (49 non-diabetic and 45 type-2 diabetic) was determined by using quantitative real-time RT-PCR as described in Methods. The data show significant positive associations between body mass index (BMI) and adipose tissue gene expression of (A) CD68 (r = 0.26, P = 0.007), (B) CD86 (r = 0.20, P = 0.04), and (C) CD163 (r = 0.27, P = 0.005) macrophage markers. (PDF 115 kb)

Published
2016
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