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DC Field | Value | Language |
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dc.contributor.author | Mezouari, Ania | - |
dc.date.accessioned | 2020-11-10T15:11:38Z | - |
dc.date.available | 2020-11-10T15:11:38Z | - |
dc.date.issued | 2020-10-19 | - |
dc.identifier.uri | https://zone.biblio.laurentian.ca/handle/10219/3600 | - |
dc.description.abstract | Circulating palmitic acid (PA) and glycated albumin (GA) are increased in obesity and cause metabolic stress leading to diabetes. This includes the impairment of the glucoregulatory hormone glucagon-like peptide-1 (GLP-1) secreted from intestinal L-cells. Recently, the gasotransmitter hydrogen sulfide (H2S) has been implicated in the enhancement of GLP-1 secretion. We hypothesized that H2S can reduce the oxidative stress caused by PA and GA, and play a protective role in L-cell function. In mouse and human L-cell models, PA and GA caused an increase in reactive oxygen species (ROS). The H2S donor GYY4137 partially blocked PA- ROS induction. In mice, PA-enriched Western diet (WD) elevated body weight in both sexes and elevated fasting blood glucose and lipid peroxidation in males. A single GYY4137 injection improved oral glucose tolerance in WD-fed male mice and also enhanced glucose-stimulated GLP-1 release. To conclude, H2S reduces oxidative stress in GLP-1 cells and can improve glucose clearance in mice. | en_US |
dc.language.iso | en | en_US |
dc.subject | Palmitic acid | en_US |
dc.subject | glycated albumin | en_US |
dc.subject | GLP-1, | en_US |
dc.subject | hydrogen sulfide | en_US |
dc.subject | oxidative stress | en_US |
dc.title | The protective role of hydrogen sulfide from obesity-associated metabolic stress in GLP-1 regulation | en_US |
dc.type | Thesis | en_US |
dc.description.degree | Master of Science (MSc) in Biology | en_US |
dc.publisher.grantor | Laurentian University of Sudbury | en_US |
Appears in Collections: | Biology - Master's Theses Master's Theses |
Files in This Item:
File | Description | Size | Format | |
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Ania Mezouari MSc Thesis 20_10_2020 Revised.pdf | 1.49 MB | Adobe PDF | View/Open |
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