Please use this identifier to cite or link to this item: https://scholarhub.balamand.edu.lb/handle/uob/7523
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dc.contributor.advisorEchtay, Karimen_US
dc.contributor.authorHakam, Hanin-Khaulaen_US
dc.date.accessioned2024-09-23T10:18:11Z-
dc.date.available2024-09-23T10:18:11Z-
dc.date.issued2024-
dc.identifier.urihttps://scholarhub.balamand.edu.lb/handle/uob/7523-
dc.descriptionIncludes bibliographical references (p. 65-84)en_US
dc.description.abstractIn the past few years, there has been a heightened interest in exploiting the immunomodulatory properties of mycobacteria to manage diabetes. In this context, Bacillus Calmette-Guerin (BCG), the live attenuated strain of Mycobacterium bovis, has been reported to optimize glycemic control in patients with type 1 diabetes and to reduce hyperglycemia in several experimental animal models of diabetes. Lately, heat-killed (HK) Mycobacterium aurum (M. aurum) was developed as a natural supplement with a capacity to reduce or prevent stress-induced inflammation; however, its bioactive properties are yet to be revealed. Therefore, our current study aimed to evaluate the therapeutic anti-diabetic potential of HK M. aurum in streptozotocin (STZ)-induced diabetic mice. Male BALB/c mice were divided into 3 groups: the vehicle group (CB + BBS) received one dose (intraperitoneal administration) of citrate buffer (CB) followed by 6 doses (intradermal administration) of borate buffer saline (BBS) , the untreated diabetic group (STZ + BBS) was injected with a single high dose (150 mg/Kg) (intraperitoneal administration) of STZ followed by 6 doses of BBS, and the treated diabetic group (STZ + HK M. aurum) received a single high dose (150 mg/Kg) (intraperitoneal administration) of STZ followed by 6 doses of HK M. aurum. Body weight, glycemia, and urine glucose were measured on a weekly basis. At week 6, all mouse groups were evaluated for their serum insulin levels using ELISA as well as for their liver catalase (CAT), lactate dehydrogenase (LDH), uncoupling protein 2 (UCP2) and skeletal muscle LDH, UCP3 and GLUT4 protein expression levels by western blot. Administration of HK M. aurum to normal non-diabetic mice did not result in significant alterations in their blood glucose levels. We also found that HK M. aurum-treated diabetic mice exhibited lower blood glucose levels and higher serum insulin levels as compared to untreated diabetic mice. Treatment of diabetic mice with 6 doses of HK M. aurum restored the altered protein expression levels of their liver UCP2 and LDH as well as of their skeletal muscle UCP3 and LDH. Our findings demonstrate a novel ability for HK M. aurum to lower hyperglycemia and to ameliorate dysregulated expression of metabolism-related proteins in STZ-induced diabetic mice. In conclusion, these results suggest that HK M. aurum can be used as a potential therapeutic agent for the management of diabetes.en_US
dc.description.statementofresponsibilityby Hanin-Khaula Hakamen_US
dc.format.extent1 online resource (ix, 84 pages) : ill., tablesen_US
dc.language.isoengen_US
dc.publisher[Kalhat, Lebanon] : [University of Balamand], 2024en_US
dc.rightsThis object is protected by copyright, and is made available here for research and educational purposes. Permission to reuse, publish, or reproduce the object beyond the personal and educational use exceptions must be obtained from the copyright holderen_US
dc.subject.lcshUniversity of Balamand--Dissertationsen_US
dc.subject.lcshDissertations, Academicen_US
dc.titleExploring the potential therapeutic effect of heat-killed mycobacterium aurum on glycemic management and glucose metabolism in streptozotocin-induced diabetic BALB/c miceen_US
dc.typeThesisen_US
dc.contributor.corporateUniversity of Balamanden_US
dc.contributor.departmentDepartment of Biologyen_US
dc.contributor.facultyFaculty of Arts and Sciencesen_US
dc.contributor.institutionUniversity of Balamanden_US
dc.date.catalogued2024-09-23-
dc.description.degreeMSc in Biologyen_US
dc.description.statusUnpublisheden_US
dc.relation.ispartofbookseriesUniversity of Balamand. Thesis. Bioen_US
dc.rights.accessrightsThis item is under embargo until end of year 2026en_US
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