Browsing by Author "Olatunji Lawrence Aderemi"

Now showing 1 - 5 of 5
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    Anti-inflammatory and antithrombotic effects of nicotine exposure in oral contraceptive-induced insulin resistance is glucocorticoid-independent
    (Pharmacological Reports, 2016-12-16) Olatunji Lawrence Aderemi; Michael Olugbenga Samuel; Adeyanju Oluwaseun Aremu; Areola Emmanuel Damilare; Soladoye Ayodele Olufemi
    Background: Reports showed that estrogen-progestin oral contraceptive (COC) or tobacco smoking causes increased risk of cardiovascular diseases (CVD) in premenopausal women. Studies also suggest that nicotine; a major tobacco alkaloid may worsen or improve atherothrombotic CVD. Altered hemorheology, prothrombotic and pro-inflammatory biomarkers, have been implicated in the development of atherothrombotic CVD events. However, the effect of non-smoking nicotine exposure on these biomarkers during COC treatment is not yet established. We therefore sought to determine the effects of nicotine exposure during COC treatment on these biomarkers, and also tested the hypothesis that the nicotine effects would be glucocorticoid-dependent. Methods: Female Sprague-Dawley rats aged 10 weeks were given (po) vehicle, low-dose nicotine (0.1 mg/kg) or high-dose nicotine (1.0 mg/kg) with or without COC steroids (5.0 µg/kg ethinylestradiol and 25.0 µg/kg levonorgestrel) daily for 6 weeks. Results: COC treatment or nicotine exposure led to increased insulin resistance (IR), hemorheological (blood viscosity, hematocrit and plasma viscosity), prothrombotic (plasminogen activator inhibitor-1), pro-inflammatory (uric acid, C-reactive protein, neutrophil/lymphocyte and platelet/lymphocyte ratios) biomarkers and corticosterone. However, these effects except that on corticosterone were abrogated by nicotine exposure during COC treatment. Conclusions: Our study indicates that nicotine- or COC-induced IR may be mediated via inflammatory/thrombotic pathway. The results imply that nicotine exposure could impact negatively on atherothrombotic biomarkers in COC non-users, whereas the impact in COC users could be positive. The results also suggest that the anti-inflammatory, antithrombotic and blood viscosity-lowering effects of nicotine exposure during COC use is circulating glucocorticoid-independent.
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    Dexamethasone Promotes the Risk of Cardiovascular Disease in High Fructose-exposed Wistar Rats
    (2022-10-01) Abdulkareem Adam Olaitan; Abe Emmanuel Olusegun; Olatunji Lawrence Aderemi
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    Inhibition of adenosine deaminase and xanthine oxidase by valproic acid abates hepatic triglyceride accumulation independent of corticosteroids in female rats treated with estrogen-progestin
    (Canadian Journal Publishing, 2018-07-12) Omolekulo Tolulope Eniola; Areola Emmanuel Damilare; Olufunto Olayinka Badmus; Badmus Olayinka Olufunto; Michael Olugbenga Samuel; Kim Inkyeom; Olatunji Lawrence Aderemi
    Elevated circulating uric acid has been postulated to play an important pathophysiological role in estrogen-progestin combined oral contraceptive (COC)-induced hypertension and endothelial dysfunction. We hypothesized that disruption of glucoregulation and liver triglyceride (TG) accumulation induced by COC use would be abated by valproic acid (VPA) treatment through suppression of adenosine deaminase (ADA) and xanthine oxidase (XO) activities. Female Wistar rats aged 9-10 weeks were treated with a combination of estrogen-progestin COC steroids (1.0 μg ethinylestradiol and 5.0 μg levonorgestrel; p.o.) with or without VPA (100.0 mg/kg; p.o.) daily for 6 weeks. The result shows that the disrupted glucoregulation and associated elevated hepatic ADA activity, plasma and hepatic XO activity, uric acid (UA), TG/HDL-cholesterol, total cholesterol, and malondialdehyde induced by COC treatment were attenuated by VPA treatment. However, VPA did not have any effect on plasma aldosterone, corticosterone, ADA, circulating and hepatic free fatty acid. Our results demonstrate that suppression of plasma and hepatic XO activities, along with hepatic ADA activity and UA by VPA treatment, protects against disrupted glucoregulation and increased liver TG by COC independent of elevated corticosteroids. The findings imply that VPA would provide protection against the development of cardiometabolic disorder via inhibition of the ADA/XO/UA-mediated pathway.
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    LETROZOLE ATTENUATES CARDIOMETABOLIC RISK IN PLASMODIUM BERGHEI-INFECTED MICE
    (2023) Abdulkareem Adam Olaitan; Babamale Abdulkareem Olarewaju; Jesutomisin Caleb Omisope; Oluwabunmi Badmos-king A; Ibiwumi Dare B; Olatunji Lawrence Aderemi; Ugbomoiko Uade Samuel
    Malaria is associated with cardiometabolic disorders, promoting the risk of cardiovascular disease (CVD). We recently demonstrated letrozole’s cardioprotective effects in fructose-exposed male rats. Hence, in this study, we investigated the effect of a low-dose letrozole against cardiometabolic risk in Plasmodium berghei-infected female mice. Twenty female mice were randomly grouped into four (n=5/group): uninfected, infected, letrozole (0.24 mg/kg, p.o/day, without infection), and infected + letrozole. Weekly percentage parasitaemia was recorded. At the end of the 21-day exposure, blood and liver were collected and processed for biochemical analyses. P. berghei infection decreased serum estradiol level after 21-day infection and increased serum and liver levels of malondialdehyde, very low-density lipoprotein cholesterol, triglycerides, and triglycerides/high-density lipoprotein cholesterol (TG/HDL-c) index. Similarly, P. berghei elevated serum uric acid and hepatic total cholesterol levels. Meanwhile, the administered dose of letrozole did not significantly affect serum estradiol but lowered lipid peroxidation, attenuated lipid alterations, and reduced serum uric acid level. We reveal that P. berghei-infection lowered serum estradiol and promoted cardiometabolic risk in female mice, while letrozole lowered parasitaemia and mitigated the associated cardiometabolic risk. Thus, this study is suggestive of letrozole’s potential as an adjuvant therapy for improved management of malaria-induced cardiometabolic complications. Further study is recommended to investigate the anti-malaria potency of letrozole, independent of gender.
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    LETROZOLE SUPPRESSES HEPATIC OXIDATIVE STRESS AND AMELIORATES LIPID ACCUMULATION IN FRUCTOSE-EXPOSED WISTER RATS
    (2022-05-08) Abdulkareem Adam Olaitan; Abe Emmanuel Olusegun; Omilana Oluwafemi Ololade; Olatunji Lawrence Aderemi
    An increase in sugar intake, especially fructose or fructose-containing sweeteners, poses a serious public health challenge globally. Unlike glucose, fructose metabolism results in generation of oxidative stress, which promotes hepatic lipid accumulation and consequently increases the risk of non-alcoholic fatty liver disease (NAFLD). Chronic administration of letrozole has been previously reported to decrease lipid peroxidation and increase antioxidants but its effect on fructose-induced lipid accumulation has not been investigated. Thus, the present study sought to investigate the ameliorative effect of letrozole on hepatic oxidative stress and lipid accumulation in high fructose-taking Wister rats. After 3-week of exposure, our results reveal that fructose intake increased hepatic total cholesterol (p< 0.01), triglycerides (p< 0.001) and free fatty acid (p< 0.001). Similarly, fructose increased hepatic malondialdehyde (MDA) (p< 0.001 vs. control) and decreased catalase and superoxide dismutase activities (p< 0.001 and p < 0.05 vs. control, respectively). Furthermore, our data show that high fructose intake elevated levels of uric acid and xanthine oxidase activity in the liver (p< 0.001 vs. control). However, letrozole treatment attenuated the hepatic lipid accumulation, reduced MDA level, and suppressed uric acid biosynthesis in high fructose-taking rats. Conclusively, this study has demonstrated that high fructose intake induces hepatic uric acid synthesis, generating oxidative stress and promoting hepatic lipid accumulation in male Wister rats, while administration of letrozole attenuates the fructose effects. Our findings, therefore, suggest the efficacy of letrozole in attenuating hepatic lipid accumulation, hence, lowering the risk of NAFLD associated with excessive fructose intake.