Browsing by Author "Adeyemi Fatai Odetayo"

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    Combination Therapy with Vitamin D and Metformin: A Potential Approach to Mitigate Testicular Dysfunction in Type 2 Diabetes Mellitus
    (Reproductive Sciences, 2024-09-25) Adeyemi Fatai Odetayo; Halimat Amin Abdulrahim; Adedotun Muiz Yusuf; Williams Oshetename Aromokhame; Ademola Muritala Olaitan; Mirabel Chisom Ugoji; Moses Agbomhere Hamed; Luqman Aribidesi Olayaki
    Type 2 diabetes mellitus (T2DM) is a multifactorial disease that cannot be linked to a single pathway, causing the observed heterogeneity among T2DM patients. Despite this level of heterogeneity, T2DM is majorly managed by metformin (MET) monotherapy. However, recent fndings have associated long-term metformin intake with progressive oxidative pancreatic β cell damage as the disease progresses. Hence, a signifcant number of patients treated with MET need an alternate therapy. Hence, identifying drug combinations that can efectively alleviate diferent diabetes complications would serve as a more promising therapy that can translate into active use. Hence, this study was designed to explore the possible synergistic efect of vitamin D and metformin on T2DM-induced testicular dysfunction. Thirty healthy male Wistar rats (weight: 120-150 g and age: 10 ± 2 weeks) were randomly divided into control, diabetes untreated (HFD+STZ), diabetes + vitamin D (1000 IU/kg), diabetes + metformin (180 mg/kg), and diabetes + vitamin D + metformin. All treatments lasted for 28 days and animals were sacrifced using IP injection of ketamine and xylaxine (40 and 4 mg/kg respectively). Vitamin D improved the ameliorative efect of metformin on T2DM-induced hyperglycemia and lipid dysmetabolism, accompanied by a signifcant decrease in testicular lactate dehydrogenase and lactate. Also, vitamin D + metformin signifcantly increased serum lutein- izing hormone, follicle-stimulating hormone, testosterone, and testicular 5α reductase activities. Furthermore, vitamin D improved the anti-infammatory and antioxidant efects of metformin by signifcantly decreasing T2DM-induced increase in testicular interleukin 1beta, interleukin 6, TNF-α, nitric oxide, and NF-κB and increasing T2DM-induced decrease in interleukin 10, glutathione, superoxide dismutase, catalase, GPx, and Nrf2. Vitamin D enhanced the ameliorative efect of metformin on T2DM-induced testicular dysfunction.
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    Metformin and vitamin D combination therapy ameliorates type 2 diabetes mellitus‐induced renal injury in male Wistar rats
    (Naunyn-Schmiedeberg's Archives of Pharmacology, 2024-09-30) Halimat Amin Abdulrahim; Emmanuel Aduragbemi Owootori; Adeyemi Fatai Odetayo; Joshua Damrah Bulus; Fatimoh Bolanle Jimoh; Emmanuel Oluwamuyiwa Gabriel; Iyanu Feranmi Odiete; Luqman Aribidesi Olayaki
    Diabetic kidney disease is a major microvascular diabetes mellitus (DM) complication clinically associated with a gradual renal function decline. Although metformin is a common drug for managing DM, however, monotherapy treatment with any antidiabetic drug will necessitate dosage increment since type 2 DM (T2DM) deteriorates over time due to the increasing pancreatic β-cell dysfunction and will eventually require a combination therapy approach with another antidiabetic medica- tion. Vitamin D is a food supplement that has been proven to have antidiabetic and reno-protective activities. Hence, we explore the combination of vitamin D and metformin on T2DM-induced renal dysfunction. Thirty male Wistar rats were randomized into fve (5) groups: control, diabetes untreated, diabetics treated with metformin, vitamin D, and vitamin D+metformin. Vitamin D and metformin signifcantly reversed DM-induced hyperglycemia, electrolyte imbalance, and dyslipidemia. Also, vitamin D and metformin reversed T2DM-induced increase in serum creatinine and urea and renal lactate, LDH, and oxido-infammatory response. These observed alterations were accompanied by an increase in proton pump activities and modulation of Nrf2/Nf-κB and XO/UA signaling. This study revealed that vitamin D and/or metformin ameliorated T2DM-induced renal injury.
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    Synergistic Effects of Vitamin D and Exercise on Diabetes-induced Gonadotoxicity in Male Wistar Rats: Role of Xanthine Oxidase/Uric Acid and Nrf2/NfkB Signaling
    (Cell Biochemistry and Biophysics, 2024-05-13) Adeyemi Fatai Odetayo; Abdulrahim Halimat Amin; Olaoluwa Tolulope Fabiyi; Taiye Abdulmujeeb Adewole; Bright Elijah Ajiboye; Adavize Noah Omeiza; Luqman Aribidesi Olayaki
    Type 2 Diabetes mellitus (T2DM) is one of the oldest known chronic diseases, characterized by elevated fasting blood sugar (FBS). T2DM is a metabolic disorder that can distort the activities of multiple physiological systems, including the reproductive system. Although different drugs have been designed for managing this disorder, these drugs have been reported to have negative side effects. Hence, this study was designed to explore the possible synergistic effect of vitamin D and exercise on T2DM-induced testicular dysfunction. Thirty-six male Wistar rats were randomized into six (6) groups: control, diabetes untreated, diabetes treated with 1000 IU/kg of vitamin D, diabetes treated with 5 min/day of physical exercise, diabetes treated with vitamin D and exercise, diabetes treated with 180 mg/kg of metformin. T2DM induction led to a significant increase in FBS, lactate, and lactate dehydrogenase, and was reversed by vitamin D supplementation and exercise. Also, vitamin D and exercise synergistically blunted T2DM-induced oxido-inflammatory response evidenced by a significant decrease in testicular malondialdehyde, interleukin 1β, interleukin 6, and tumor necrosis factor alpha, and an increase in superoxide dismutase, catalase, glutathione peroxidase, and interleukin 10. These events were associated with a decrease in T2DM-induced increase in XO, UA, and Nf-κb and an increase in T2DM-induced decrease in Nrf2. Also, vitamin D and EX reversed the observed impairment in sperm quality and testicular histology following T2DM-induction. This study revealed the synergistic effect of vitamin D and exercise on T2DM-induced testicular dysfunction.