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However, these cocktails have been independently associated with the aetiopathogenesis of metabolic syndrome. This study investigated whether or not the co-administration of antikoch and anti-retroviral, as seen in tuberculosis\/Human Immunodeficiency Virus co-infection, will produce a similar effect. Also, it evaluated the role of glutathione and adenine deaminase\/xanthine oxidase\/uric acid signaling in antikoch\/anti-retroviral-induced cardiometabolic dysfunction.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Methods<\/jats:title>\n                <jats:p>Male rats of Wistar strain were randomized into four groups: the control, which had 0.5 mL of distilled water as a vehicle, anti-Koch-treated rats that were administered a cocktail of anti-Koch, HAART-treated rats that had a combination of anti-retroviral drugs, and anti-Koch\u2009+\u2009HAART-treated rats that had treatments as anti-Koch-treated and HAART-treated rats. The treatment was once daily and lasted for eight weeks. One way-analysis of variance followed by Tukey\u2019s posthoc test was used to test for significance and pairwise comparisons respectively.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Results<\/jats:title>\n                <jats:p>Although no changes in body weight gain and cardiac weight were noted, it was found that antikoch and\/or HAART caused insulin resistance and elevated blood glucose level. In addition, antikoch and\/or HAART led to dyslipidaemia, increased atherogenic indices, and elevated cardiac injury markers. These were accompanied by increased plasma and cardiac concentrations of malondialdehyde and nitric oxide, C-reactive protein, and myeloperoxidase activity, as well as suppressed activities of glutathione peroxidase and glutathione-S-transferase, and a fall in reduced glutathione level. The observed alterations were more pronounced in animals that received a combination of antikoch and HAART.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Conclusions<\/jats:title>\n                <jats:p>This study provides the first evidence that antikoch and\/or HAART induce cardiometabolic dysfunction via glutathione suppression and up-regulation of adenine deaminase\/xanthine oxidase\/uric acid-dependent oxidative stress and inflammatory response. These events were associated with dyslipidaemia and increased atherogenic indices. This infers that regular monitoring of glucose level, insulin sensitivity, lipid profile, and oxido-inflammatory markers is important in patients on antikoch and\/or HAART for prompt diagnosis and management of cardiometabolic disorder if it ensues.<\/jats:p>\n              <\/jats:sec>","DOI":"10.1186\/s12944-021-01493-x","type":"journal-article","created":{"date-parts":[[2021,7,5]],"date-time":"2021-07-05T12:03:44Z","timestamp":1625486624000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":21,"title":["Co-administration of HAART and antikoch triggers cardiometabolic dysfunction through an oxidative stress-mediated pathway"],"prefix":"10.1186","volume":"20","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3874-5927","authenticated-orcid":false,"given":"RE","family":"Akhigbe","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3378-6794","authenticated-orcid":false,"given":"MA","family":"Hamed","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2021,7,5]]},"reference":[{"key":"1493_CR1","unstructured":"World Health Organization. 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