Browsing by Author "Bensmail, Halima"
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Item Harnessing Qatar Biobank to understand type 2 diabetes and obesity in adult Qataris from the First Qatar Biobank Project(2018) Ullah, Ehsan; Mall, Raghvendra; Rawi, Reda; Moustaid, Naima M. (TTU); Butt, Adeel A.; Bensmail, HalimaBackground: Human tissues are invaluable resources for researchers worldwide. Biobanks are repositories of such human tissues and can have a strategic importance for genetic research, clinical care, and future discoveries and treatments. One of the aims of Qatar Biobank is to improve the understanding and treatment of common diseases afflicting Qatari population such as obesity and diabetes. Methods: In this study we apply a panorama of state-of-the-art statistical methods and machine learning algorithms to investigate associations and risk factors for diabetes and obesity on a sample of 1000 Qatari population. Results: Regarding diabetes, we identified pronounced associations and risk factors in Qatari population including magnesium, chloride, c-peptide of insulin, insulin, and uric acid. Similarly, for obesity, significant associations and risk factors include insulin, c-peptide of insulin, albumin, and uric acid. Moreover, our study has revealed interactions of hypomagnesemia with HDL-C, triglycerides, and free thyroxine. Conclusions: Our study strongly confirms known associations and risk factors associated with diabetes and obesity in Qatari population as previously found in other population studies in different parts of the world. Moreover, interactions of hypomagnesemia with other associations and risk factors merit further investigations.Item Role of microRNA 690 in Mediating Angiotensin II Effects on Inflammation and Endoplasmic Reticulum Stress(2020) Menikdiwela, Kalhara R. (TTU); Ramalingam, Latha (TTU); Abbas, Mostafa M.; Bensmail, Halima; Scoggin, Shane (TTU); Kalupahana, Nishan S. (TTU); Palat, Asha; Gunaratne, Preethi; Moustaid-Moussa, Naima (TTU)Overactivation of the renin-angiotensin system (RAS) during obesity disrupts adipocyte metabolic homeostasis and induces endoplasmic reticulum (ER) stress and inflammation; however, underlying mechanisms are not well known. We propose that overexpression of angiotensinogen (Agt), the precursor protein of RAS in adipose tissue or treatment of adipocytes with Angiotensin II (Ang II), RAS bioactive hormone, alters specific microRNAs (miRNA), that target ER stress and inflammation leading to adipocyte dysfunction. Epididymal white adipose tissue (WAT) from B6 wild type (Wt) and transgenic male mice overexpressing Agt (Agt-Tg) in adipose tissue and adipocytes treated with Ang II were used. Small RNA sequencing and microarray in WAT identified differentially expressed miRNAs and genes, out of which miR-690 and mitogen-activated protein kinase kinase 3 (MAP2K3) were validated as significantly up- and down-regulated, respectively, in Agt-Tg, and in Ang II-treated adipocytes compared to respective controls. Additionally, the direct regulatory role of miR-690 on MAP2K3 was confirmed using mimic, inhibitors and dual-luciferase reporter assay. Downstream protein targets of MAP2K3 which include p38, NF-κB, IL-6 and CHOP were all reduced. These results indicate a critical post-transcriptional role for miR-690 in inflammation and ER stress. In conclusion, miR-690 plays a protective function and could be a useful target to reduce obesity.Item Sex Differences in Fish Oil and Olanzapine Effects on Gut Microbiota in Diet-Induced Obese Mice(2022) Abbas, Mostafa M.; Soto, Paul (TTU); Ramalingam, Latha (TTU); El-Manzalawy, Yasser; Bensmail, Halima; Moustaid-Moussa, Naima (TTU)Children are prescribed second-generation antipsychotic (SGA) medications, such as olanzapine (OLZ) for FDA-approved and “off-label” indications. The long-term impact of early-life SGA medication exposure is unclear. Olanzapine and other SGA medications are known to cause excessive weight gain in young and adult patients, suggesting the possibility of long-term complications associated with the use of these drugs, such as obesity, diabetes, and heart disease. Further, the weight gain effects of OLZ have previously been shown to depend on the presence of gut bacteria and treatment with OLZ, which shifts gut bacteria toward an “obesogenic” profile. The purpose of the current study was to evaluate changes in gut bacteria in adult mice following early life treatment with OLZ and being fed either a high-fat diet or a high-fat diet supplemented with fish oil, which has previously been shown to counteract gut dysbiosis, weight gain, and inflammation produced by a high-fat diet. Female and male C57Bl/6J mice were fed a high fat diet without (HF) or with the supplementation of fish oil (HF-FO) and treated with OLZ from postnatal day (PND) 37–65 resulting in four groups of mice: mice fed a HF diet and treated with OLZ (HF-OLZ), mice fed a HF diet and treated with vehicle (HF), mice fed a HF-FO diet and treated with OLZ (HF-FO-OLZ), and mice fed a HF-FO diet and treated with vehicle (HF-FO). Following euthanasia at approximately 164 days of age, we determined changes in gut bacteria populations and serum LPS binding protein, an established marker of gut inflammation and dysbiosis. Our results showed that male HF-FO and HF-FO-OLZ mice had lower body weights, at sacrifice, compared to the HF group, with a comparable body weight across groups in female mice. HF-FO and HF-FO-OLZ male groups also exhibited lower serum LPS binding protein levels compared to the HF group, with no differences across groups in female mice. Gut microbiota profiles were also different among the four groups; the Bacteroidetes-to-Firmicutes (B/F) ratio had the lowest value of 0.51 in the HF group compared to 0.6 in HF-OLZ, 0.9 in HF-FO, and 1.1 in HF-FO-OLZ, with no differences in female mice. In conclusion, FO reduced dietary obesity and its associated inflammation and increased the B/F ratio in male mice but did not benefit the female mice. Although the weight lowering effects of OLZ were unexpected, FO effects persisted in the presence of olanzapine, demonstrating its potential protective effects in male subjects using antipsychotic drugs.