Please use this identifier to cite or link to this item: https://zone.biblio.laurentian.ca/handle/10219/3600
Full metadata record
DC FieldValueLanguage
dc.contributor.authorMezouari, Ania-
dc.date.accessioned2020-11-10T15:11:38Z-
dc.date.available2020-11-10T15:11:38Z-
dc.date.issued2020-10-19-
dc.identifier.urihttps://zone.biblio.laurentian.ca/handle/10219/3600-
dc.description.abstractCirculating 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.isoenen_US
dc.subjectPalmitic aciden_US
dc.subjectglycated albuminen_US
dc.subjectGLP-1,en_US
dc.subjecthydrogen sulfideen_US
dc.subjectoxidative stressen_US
dc.titleThe protective role of hydrogen sulfide from obesity-associated metabolic stress in GLP-1 regulationen_US
dc.typeThesisen_US
dc.description.degreeMaster of Science (MSc) in Biologyen_US
dc.publisher.grantorLaurentian University of Sudburyen_US
Appears in Collections:Biology - Master's Theses

Files in This Item:
File Description SizeFormat 
Ania Mezouari MSc Thesis 20_10_2020 Revised.pdf1.49 MBAdobe PDFThumbnail
View/Open


Items in LU|ZONE|UL are protected by copyright, with all rights reserved, unless otherwise indicated.