Browsing by Author "Olaniyi, Kehinde"

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    Estrogen-progestin oral contraceptive and nicotine exposure synergistically confers cardio-renoprotection in female Wistar rats
    (Elsevier, 2020-06-07) Michael, Olugbenga Samuel; Dibia, Chinaza; Adeyanju, Oluwaseun; Olaniyi, Kehinde; Areola, Emmanuel; Olatunji, Lawrence Aderemi
    Approximately fifty percent of premenopausal women who smoke cigarettes or on nicotine replacement therapy are also on hormonal contraceptives, especially oral estrogen-progestin. Oral estrogen-progestin therapy has been reported to promote insulin resistance (IR) which causes lipid influx into non-adipose tissue and impairs Na+/K+ -ATPase activity, especially in the heart and kidney. However, the effects of nicotine on excess lipid and altered Na+/K+ -ATPase activity associated with the use of estrogen-progestin therapy have not been fully elucidated. This study therefore aimed at investigating the effect of nicotine on cardiac and renal lipid influx and Na+/K+ -ATPase activity during estrogen-progestin therapy. Twenty-four female Wistar rats grouped into 4 (n = 6/group) received (p.o.) vehicle, nicotine (1.0 mg/kg) with or without estrogen-progestin steroids (1.0 μg ethinyl estradiol and 5.0 μg levonorgestrel) and estrogen-progestin only daily for 6 weeks. Data showed that estrogen-progestin treatment or nicotine exposure caused IR, hyperinsulinemia, increased cardiac and renal uric acid, malondialdehyde, triglyceride, glycogen synthase kinase-3, plasminogen activator inhibitor-1, reduced bilirubin and circulating estradiol. Estrogen-progestin treatment led to decreased cardiac Na+/K+-ATPase ac tivity while nicotine did not alter Na+/K+-ATPase activity but increased plasma and tissue cotinine. Renal Na+/K+-ATPase activity was not altered by the treatments. However, all these alterations were reversed following combined administration of oral estrogen-progestin therapy and nicotine. The present study therefore demon strates that oral estrogen-progestin therapy and nicotine exposure synergistically prevents IR-linked cardio-renotoxicity with corresponding improvement in cardiac and renal lipid accumulation, oxidative stress, in- flammation and Na+/K+-ATPase activity
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    Low-dose spironolactone combats dyslipidemia and hepatic inflammation by modulating PCSK9 in rat model of polycystic ovarian syndrome
    (Elsevier, 2023-06-13) Olaniyi, Kehinde; Areloegbe, Stephanie; Areola, Emmanuel; Sabinari, Isaiah; Fafure, Adedamola; Agbana, Richard; Atuma, Chukwubueze; ul haq Shah, Mohd Zahoor; Ajadi, Isaac; Olatunji, Lawrence
    Polycystic ovarian syndrome (PCOS) is the most common endocrine disorder among women and it is associated with overt metabolic derangement. Circulating lipids are regulated by proprotein convertase subtilisin/kexin type 9 (PCSK9) which blocks low density lipoprotein (LDL) receptors especially in the liver. The liver is highly vulnerable in dyslipidemia as lipid accumulation leads to progression of non-alcoholic fatty liver disease (NAFLD). An array of scientific endeavours hold that low-dose spironolactone (LDS) is beneficial as intervention for PCOS traits, but this claim is yet to be fully elucidated. The aim of this study was to investigate the effect of LDS on dyslipidemia and hepatic inflammation in rats with letrozole (LET)-induced PCOS and to assess the possible involvement of PCSK9 in these effects. Eighteen female Wistar rats were randomly assigned into 3 groups. The control group received vehicle (distilled water; p.o.), LET-treated group received letrozole (1 mg/kg; p.o.), LET+LDS-treated group received LET plus LDS (0.25 mg/kg, p.o.) for 21 days. Exposure to LET increased body and hepatic weights, plasma and hepatic total cholesterol (TC), TC/HDL, LDL, interleukin-6, MDA, PCSK9, ovarian degenerated follicles and hepatic NLRP3 intensity, reduced GSH and normal ovarian follicles. Interest ingly, LDS averted dyslipidemia, NLRP3-dependent hepatic inflammation and ovarian PCOS traits. It is evident herein that LDS ameliorates PCOS traits and combats dyslipidemia and hepatic inflammation in PCOS by a PCSK9-dependent mechanism.
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    Regulatory effects of quercetin on testicular histopathology induced by cyanide in Wistar rats
    (Elsevier, 2021-07-24) Oyewopo, Adeoye; Adeleke, Opeyemi; Johnson, Olawumi; Akingbade, Adebanji; Olaniyi, Kehinde; Areola, Emmanuel; Tokunbo, Olorunfemi
    Several causes of infertility have been identified, and several papers have documented some compounds that cause infertility. One of the compounds reported to be toxic to the reproductive system is cyanide. In the management of infertility, various mechanisms ranging from synthetic drugs, natural products and supplements have been employed. Quercetin is an antioxidant supplement that has been used in the treatment of a variety of ailments. This work is aimed at investigating the role of quercetin in attenuating spermato-toxicity and testicular-histopathology induced by cyanide. Seventy-two (72) male wistar rat (weight 190 g ± 10 g) were divided into nine groups (n = 8) except for groups 4 and 5 with (n = 16). Group 1 (control) received physiological saline while Groups 2 and 3 received 0.5 and 1 mg/kg body weight (bwt) cyanide respectively for 56 days, groups 4 and 5 received 0.5 and 1 mg/kg bwt cyanide respectively for 30 days. At day 30, eight animals were sacrificed from Groups 4 and 5 and the remaining eight (8) rats were subdivided into groups (6 and 7) and were given 20 and 40 mg/kg bwt of quercetin respectively for twenty-six days. Co-administration of cyanide and quercetin at a dose of 0.5 mg/kg cyanide +20 mg/kg quercetin and 1 mg/kg cyanide +40 mg/kg quercetin were given to group 8 and 9 respectively for 56 days. Significant decreases in sperm parameters (count, motile and normal sperm) and increases in malondiadehyde concentration were observed in the cyanide treated groups. Testicular histoarchitecture showed few to no spermatozoa in the lumen of rats treated with cyanide. All these effects were attenuated by quercetin. In conclusion, quercetin regulates testicular histopathology induced by cyanide in Wistar rats. Data from this work suggests potential preventive or therapeutic applications of quercetin for individuals subjected to cyanide environmental pollution.
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    Sodium acetate protects against nicotine-induced excess hepatic lipid in male rats by suppressing xanthine oxidase activity
    (Elsevier, 2019-12-15) Dangana, Elizabeth; Omolekulo, Tolulope; Areola, Emmanuel; Olaniyi, Kehinde; Soladoye, Ayodele; Olatunji, Lawrence Aderemi
    Fatty liver is the hepatic consequence of chronic insulin resistance (IR) and related syndromes. It is mostly accompanied by inflammatory and oxidative molecules. Increased activity of xanthine oxidase (XO) exerts both inflammatory and oxidative effects and has been implicated in metabolic derangements including non-alcoholic fatty liver disease. Short chain fatty acids (SCFAs) elicit beneficial metabolic alterations in IR and related syn dromes. In the present study, we evaluated the preventive effects of a SCFA, acetate, on nicotine-induced dys metabolism and fatty liver. Twenty-four male Wistar rats (n = 6/group): vehicle-treatment (p.o.), nicotine treated (1.0 mg/kg; p.o.), sodium acetate-treated (200 mg/kg; p.o.) and nicotine + sodium acetate-treated groups. The treatments lasted for 8 weeks. IR was estimated by oral glucose tolerance test and homeostatic model assessment of IR. Plasma and hepatic free fatty acid, triglyceride (TG), glutathione peroxidase, adenosine deaminase (ADA), XO and uric acid (UA) were measured. Nicotine exposure resulted in reduced body weight, liver weight, visceral adiposity, glycogen content and glycogen synthase activity. Conversely, exposure to ni cotine increased fasting plasma glucose, lactate, IR, plasma and hepatic TG, free fatty acid, TG/HDL-cholesterol ratio, lipid peroxidation, liver function enzymes, plasma and hepatic UA, XO and ADA activities. However, plasma and hepatic glucose-6-phosphate dehydrogenase-dependent antioxidant defense was not affected by nicotine. Concomitant treatment with acetate ameliorated nicotine-induced effects. Taken together, these results indicate that nicotine exposure leads to excess deposition of lipid in the liver by enhancing XO activity. The results also imply that acetate confers hepatoprotection and is accompanied by decreased XO activity.
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    Sodium butyrate recovers high-fat diet-fed female Wistar rats from glucose dysmetabolism and uric acid-associated cardiac tissue damage
    (Springer, 2019-06-29) Badejogbin, Caroline; Areola, Damilare; Olaniyi, Kehinde; Adeyanju, Oluwaseun; Adeosun, Isaac
    Increased global consumption of high-fat/high-calorie diet has led to higher incidence of the multifactorial cardiometabolic syndrome especially among women. The links between glucose deregulation and eventual mortal cardiac diseases are still being investigated. However, several reports have implicated elevated uric acid (UA) in the progression of metabolic disorders especially during high-fructose diet. Also, butyrate (BUT) a short-chain fatty acid is being identified with intriguing therapeutic potentials in metabolic disorders. We therefore hypothesized that high-fat diet-induced glucose deregulation and cardiac tissue damage are associated with elevated UA and attenuated by BUT in female rats. Twenty-four 10-week-old female Wistar rats with weights ranging from 135 to 150 g were treated with normal rat chow and distilled water (po) or sodium butyrate (200 mg/kg; po) or high-fat diet and distilled water (po) or high-fat diet and sodium butyrate. Treatments lasted for 6 weeks. Results showed that high-fat diet caused glucose dysmetabolism, elevated plasma triglyceride (TG), total cholesterol (TC), corticosterone, malondialdehyde (MDA), plasma and cardiac UA, and lactate dehydrogenase (LDH). High-fat diet also led to depressed reduced glutathione (GSH). Histological analysis of cardiac tissue showed cellular infarction, infiltration, and fibrosis in high-fat diet-fed rats. However, all these effects were ameliorated by BUT treatment. The findings here showed that high-fat diet resulted in glucose dysmetabolism and cardiac tissue damage through a UA-dependent mechanism and that BUT can protect against high-fat diet-induced cardiometabolic disorders through UA suppression and augmentation of glutathione antioxidant defenses.
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    Suppression of HDAC by sodium acetate rectifies cardiac metabolic disturbance in streptozotocin-nicotinamide-induced diabetic rats
    (Society for Experimental Biology and Medicine, 2020-03-17) Olaniyi, Kehinde; Amusa, Oluwatobi; Areola, Emmanuel; Olatunji, Lawrence
    Diabetes mellitus, particularly type 2 occurs at global epidemic proportions and leads to cardiovascular diseases. Molecular studies suggest the involvement of epigenetic altera tions such as histone code modification in the progression of cardiometabolic disorders. However, short chain fatty acids (SCFAs) are recognized as epigenetic modulators by their histone deacetylase inhibitory property. It is therefore hypothesized that cardiac histone deacetylase activity increases in type II diabetes and SCFA, acetate, would inhibit histone deacetylase with accompanying restoration of glucose dysregulation, cardiac lipid deposi tion, and tissue damage in male Wistar rats. Twenty-four male rats (240–270 g) were allotted into four groups (n ¼ 6 per group) namely: vehicle-treated (p.o.), sodium acetate-treated (200 mg/kg), diabetic, and diabeticþ sodium acetate-treated groups. Diabetes was induced by intraperitoneal injection of streptozotocin 65 mg/kg after a dose of nicotinamide 110 mg/kg. The results showed that diabetic rats had, glucose dysregulation, elevated serum and cardiac triglyc eride, malondialdehyde, alanine aminotransferase, histone deacetylase, serum aspartate transaminase, cardiac low density lipoprotein cholesterol (LDLc), glutathione/glutathione disulphide ratio (GSH/GSSG), reduced serum and cardiac high density lipoprotein cholesterol (HDLc), and serum GSH/GSSG. Histological analysis revealed disrupted cardiac fiber in diabetic rats. However, sodium acetate attenuated glucose dysregulation and improved serum and cardiac GSH/GSSG. Sodium acetate normalized cardiac triglyceride accumulation, malondialdehyde, serum aspartate transaminase levels and prevented cardiac tissue damage in diabetic rats. These effects were associated with suppressed histone deacetylase activity. Therefore, sodium acetate attenuated but failed to normalize glucoregulation. Nevertheless, it ameliorated oxidative stress- and lipid dysmetabolism-driven cardiovascular complications in diabetic rats by the suppression of histone deacetylase activity.