Oluwole Akinola
@unilorin.edu.ng
Professor, Faculty of Basic Medical Sciences
Dean, Faculty of Basic Medical Sciences
University of Ilorin, Nigeria
Oluwole B. Akinola is a Professor of Anatomy and the Dean of Basic Medical Sciences. He was the Head of Anatomy and presently PI of the Laboratory of Neuro-endocrinology. Akinola’s Laboratory seeks to understand the link between androgen deprivation, insulin resistance and synaptic plasticity; including understanding how impaired insulin receptor signalling contributes to the pathogenesis and progression of neurodegenerative diseases. His lab also studies the association between heavy metals, obesogenic diets and corticogenesis. Specifically, he studies how gestational co-exposure to these environmental factors impact the migration of GABAergic and glutamatergic neurons during corticogenesis in rodent models, in a bid to understand the developmental mechanisms of certain neurological conditions such as autism spectrum disorders, epilepsy and schizophrenia. Prof. Akinola is the recipient of the IBRO Research Fellowship, UniLecce Pre-doctoral Fellowship and IBRO Return Home Fellowship.
EDUCATION
Postdoctoral Research Fellowship, 2012-2013; Uniformed Services University of the Health Sciences, Bethesda, USA.
Doctor of Philosophy (PhD Anatomy), 2007-2011; University of Ilorin, Nigeria.
Pre-doctoral Research Fellowship, 2007-2008; University of Lecce, Italy.
Master of Science (MSc Anatomy), 1999-2001; University of Lagos, Nigeria.
Bachelor of Science (BSc Anatomy), 1992-1997; University of Ilorin, Nigeria.
RESEARCH, TEACHING, or OTHER INTERESTS
Anatomy, Endocrinology, Structural Biology, Developmental Neuroscience
Scopus Publications
Scholar Citations
Scholar h-index
Scholar i10-index
Scopus Publications
S. Olorunnado and O. Akinola
African Journals Online (AJOL)
INTRODUCTION: The incidence of insulin resistance is on the increase globally. Earlier reports linked impaired insulin signaling and glucose intolerance to cognitive decline, suggesting that improving insulin signaling could enhance neuronal survival. Trans-cinnamaldehyde (TCA) is an active component of cinnamon and has many pharmacological importance. However, the effects of TCA on insulin resistance-induced neurodegenerative changes are unclear. This study, therefore, aimed at evaluating the effects of trans-cinnamaldehyde on hippocampal histoarchitecture in insulin-resistant rats. METHODS: Twenty adult Wistar rats were fed with a high-fat diet for 8 weeks and then injected with a low dose of STZ (30 mg/kg body weight intraperitoneally). 60mg/kg of TCA was orally administered once daily for 4 weeks. Histological and immunohistochemical techniques were used to investigate the ameliorative potentials of TCA on the hippocampus of Wistar Rats. RESULTS: TCA administration to insulin-resistant rats histologically and immunohistochemically reduced pyknosis, astrogliosis, and neurodegenerative changes in the hippocampus when compared with untreated insulin-resistant rats. CONCLUSION: TCA prospect as a novel therapy in insulin-resistant subjects with neurogenerative diseases could be further explored.
A. A. Mohammed and O. B. Akinola
African Journals Online (AJOL)
INTRODUCTION: The primary mechanism connecting Type 2 diabetes mellitus (T2DM) to the neurodegenerative deficits in brain regions such as the hippocampus is insulin resistance. Neurodegenerative deficits in the form of amyloid aggregation and Tau hyperphosphorylation, which are hallmarks of Alzheimer's disease, are documented for both conditions in scientific literature. A mouse model of insulin resistance was used to study this relationship, and curcumin, a flavonoid contained in the spice turmeric, was evaluated as a potential treatment because of its reported benefits in lowering hyperglycemia and hyperlipidemia in diabetes mellitus. Curcumin is a prime contender against these pervasive diseases due to its efficacy, accessibility, affordability, and safety. METHODS: The study methodology included measuring fasting blood glucose levels, staining hippocampal sections for histomorphological examination, and ELISA to quantify hippocampal PI3K expression, AKT expression, and GSK3-β. Data were processed using one-way ANOVA and Turkey's post hoc test. RESULTS: The findings demonstrated that oral curcumin effectively corrected hyperglycemia and reduced insulin resistance. The study further revealed that insulin resistance was related to hippocampal atrophy and related deficits in the assessed rat model. Curcumin ameliorated these changes, reduced the aggregation of Aβ in the hippocampus, and reversed impaired signaling of proteins PI3K, AKT, and GSK-3β. CONCLUSION: The study's findings imply that oral curcumin has potential therapeutic advantages against prevalent neuronal death linked to abnormalities mimicking Alzheimer's disease and insulin resistance. Hence, curcumin may benefit dementia patients who also have insulin resistance.
Olumayowa K. Idowu, Olushola O. Oluyomi, Oluwatomisin O. Faniyan, Olufunke O. Dosumu, and Oluwole B. Akinola
Wiley
AbstractInsulin resistance (IR) is a risk factor for metabolic disorders and neurodegeneration. Peroxisome proliferator‐activated receptor (PPAR) agonists have been proven to mitigate the neuronal pathology associated with IR. However, the synergetic efficacy of these agonists is yet to be fully described. Hence, we aimed to investigate the efficacy of PPARα/γ agonists (fenofibrate and pioglitazone) on a high‐fat diet (HFD) and streptozotocin (STZ)‐induced hippocampal neurodegeneration. Male Wistar rats (200 ± 25 mg/body weight [BW]) were divided into five groups. The experimental groups were fed on an HFD for 12 weeks coupled with 5 days of an STZ injection (30 mg/kg/BW, i.p) to induce IR. Fenofibrate (FEN; 100 mg/kg/BW, orally), pioglitazone (PIO; 20 mg/kg/BW, orally), and their combination were administered for 2 weeks postinduction. Behavioral tests were conducted, and blood was collected to determine insulin sensitivity after treatment. Animals were killed for assessment of oxidative stress, cellular morphology characterization, and astrocytic evaluation. HFD/STZ‐induced IR increased malondialdehyde (MDA) levels and decreased glutathione (GSH) levels. Evidence of cellular alterations and overexpression of astrocytic protein was observed in the hippocampus. By contrast, monotherapy of FEN and PIO increased the GSH level (p < 0.05), decreased the MDA level (p < 0.05), and improved cellular morphology and astrocytic expression. Furthermore, the combined treatment led to improved therapeutic activities compared to monotherapies. In conclusion, FEN and PIO exerted a therapeutic synergistic effect on HFD/STZ‐induced IR in the hippocampus.
Enya Joseph Igbo and
Negah Scientific Publisher
Introduction: Polycystic ovary syndrome (PCOS) is a complex endocrine disorder in women that is associated with an increased risk of infertility. This study aims to evaluate the neurobehavioral and neurochemical changes along with the associated changes in the medial prefrontal cortex (mPFC) and anterior cingulate cortex (ACC) of the dehydroepiandrosterone (DHEA)-induced PCOS model rats. Methods: A total of 12 female juvenile Wistar rats (30 to 50 g) about 22 to 44 days old were divided into 2 groups. The control group received sesame oil while the PCOS group received sesame oil plus DHEA. All treatment was done via daily subcutaneous injection for 21 days. Results: Subcutaneous DHEA-induced PCOS significantly depleted the line crossing and rearing frequency in the open field, along with the percentage of the time in the white box, line crossing, rearing, and peeping frequency in the black and white box, and the percentage of alternation in the Y-maze. PCOS significantly increased the immobility time, freezing period, and the percentage of time in the dark area in the forced swim test, open field test, and black and white box, respectively. The level of luteinizing hormone, follicle-stimulating hormone, malondialdehyde (MDA), reactive oxygen species (ROS), and interleukin-6 (IL-6) increased significantly, while norepinephrine depleted significantly with an obvious decrease in the brain-derived neurotrophic factor level in the PCOS model rats. PCOS rats exhibited cystic follicles in the ovaries and necrotic or degenerative like features in the hippocampal pyramidal cells. Conclusion: DHEA-induced PCOS results in anxiety and depressive behavior with structural alteration in rats, possibly through the elevation of MDA, ROS, and IL-6 levels, which also attributes to impaired emotional and executive functions in the mPFC and ACC.
Oluwatomilayo Patience Ojo, Paula Andrea Perez-Corredor, Johanna Andrea Gutierrez-Vargas, Oluwole Busayo Akinola, and Gloria Patricia Cardona-Gómez
Informa UK Limited
ABSTRACT Introduction: Obesity is a public health problem that is associated with cerebrovascular diseases, such as ischemic stroke. The coexistence of obesity with cerebral ischemia has been suggested to be considerably detrimental to the neurological system. Objective: Hence, in this study, we evaluated the long-term effects of a 20% high fructose diet (HFD) and global cerebral ischemia on neurological, cognitive and emotional performance in three-month-old male Wistar rats. Results: Our results demonstrated that fructose intake led to increases in body weight and blood glucose, as well as reduced insulin sensitivity. The co-morbidity of fructose intake and cerebral ischemia resulted to hyperlipidemia, as well as increases in liver and adipocyte damage, which worsened neurological performance and resulted in alterations in learning and emotional skills at two weeks post-ischemia. No significant biochemical changes in autophagy and plasticity markers at the late stage of ischemia were observed. Conclusion: These results suggested that obesity causes a lasting effect on metabolic disorders that can contribute to increased neurological impairment after cerebral ischemia.
Emmanuel O. Yawson and Oluwole B. Akinola
Springer Science and Business Media LLC
Leke Jacob Medubi, Oluwole Busayo Akinola, and Adeoye Oyetunji Oyewopo
Hindawi Limited
Psychological stress is a known aetiology of infertility. However, the mechanisms translating it to reproductive dysfunction are not fully elucidated. Three experiments were performed on Wistar rats were designed to evaluate Sertoli cell function under stress. In Experiment I, rats were randomised into three groups: saline baseline group given saline, ASEMA baseline group given aqueous extract of Massularia acuminata, zinc baseline group administered zinc orally. In Experiment II, exposure to psychological stress (for 1 hour per day) was layered on Experiment I while Experiment III substituted stress with administration of dexamethasone (DX). Six rats were sacrificed per group per experiment on days 7 and 14 and the right testis was excised and processed for PAS‐haematoxylin staining and the left used for Zn determination. Results show significantly lower testicular Zn level as well more intensely immunoexpression of p53 in saline stress and saline DX groups compared with other groups. Also seen are the presence of residual bodies in the seminiferous tubular lumen of saline groups in Experiments II and III suggesting failure of residual bodies to be transported back towards the basement membrane. This study demonstrates that psychological stress impairs the ability of Sertoli cells to recycle residual bodies.
Aboyeji L. Oyewole, Oluwole Akinola, and Bamidele V. Owoyele
AOSIS
Various types of pain were reported by people with Plasmodium falciparum and were mostly attributed to a symptom of malarial infection. Neural processes of pain sensation during malarial infection and their contributions to malaria-related death are poorly understood. Thus, these form the focus of this study. Swiss mice used for this study were randomly divided into two groups. Animals in the first group (Pb-infected group) were inoculated with Plasmodium berghei to induce malaria whilst the other group (intact group) was not infected. Formalin test was used to assess pain sensitivity in both groups and using various antagonists, the possible mechanism for deviation in pain sensitivity was probed. Also, plasma and brain samples collected from animals in both groups were subjected to biochemical and/or histological studies. The results showed that Pb-infected mice exhibited diminished pain-related behaviours to noxious chemical. The observed parasite-induced analgesia appeared to be synergistically mediated via µ-opioid, α2 and 5HT2A receptors. When varied drugs capable of decreasing pain threshold (pro-nociceptive drugs) were used, the survival rate was not significantly different in the Pb-infected mice. This showed little or no contribution of the pain processing system to malaria-related death. Also, using an anti-CD68 antibody, there was no immunopositive cell in the brain to attribute the observed effects to cerebral malaria. Although in the haematoxylin and eosin-stained tissues, there were mild morphological changes in the motor and anterior cingulate cortices. In conclusion, the pain symptom was remarkably decreased in the animal model for malaria, and thus, the model may not be appropriate for investigating malaria-linked pain as reported in humans. This is the first report showing that at a critical point, the malaria parasite caused pain-relieving effects in Swiss mice.
Michael O. Gabriel, Maria Nikou, Oluwole B. Akinola, Daniela D. Pollak, and Spyridon Sideromenos
Elsevier BV
G.O. Omotoso, O.J. Olajide, I.T. Gbadamosi, J.O. Adebayo, B.U. Enaibe, O.B. Akinola, and B.V. Owoyele
Elsevier BV
O. B. Akinola and M. O. Gabriel
Springer Science and Business Media LLC
Francis T. Djankpa, Oluwole B. Akinola, and Sharon L. Juliano
S. Karger AG
KCC2 (a brain-specific potassium-chloride cotransporter) affects development of the cerebral cortex, including aspects of neuronal migration and cellular maturation and differentiation. KCC2 also modulates chloride homeostasis by influencing the switch of GABA from depolarizing in young neurons to hyperpolarizing in mature neurons. We describe the expression pattern, regional distribution, and cellular colocalization of KCC2 in the ferret cortex in normal kits and those treated with methylazoxymethanol acetate (MAM). We earlier developed a model of impaired cortical development by injecting MAM during mid-cortical gestation, which briefly interferes with neuronal production and additionally results in increased levels of KCC2 at P0. Using immunohistochemistry, we show a shift in KCC2 expression during development, being high in the subplate at P0, repositioning into a subtle laminar pattern in the neocortex at P7-P14, and becoming homogeneous at P35. KCC2 colocalizes with neuronal markers in the developing and mature cerebral cortex of normal ferrets and those treated with MAM, but shows a differential pattern of expression at different ages and locates in distinct cellular compartments during development. Subcellular localization shows that KCC2 predominantly situates in the membrane fraction of neocortical samples. These findings reveal that KCC2 colocalizes differentially with neurons and its expression pattern alters during development.
O. B. Akinola
Springer Science and Business Media LLC
O. B. Akinola, S. A. Biliaminu, O. G. Adedeji, B. S. Oluwaseun, O. M. Olawoyin, and T. A. Adelabu
Hindawi Limited
Exposure to either environmental toxicants or chronic hyperglycaemia could impair male reproductive function. However, the extent to which exposure to such toxicants, in the presence of pre‐existing metabolic dysfunction, could affect male reproduction is unclear. Streptozotocin‐induced diabetic Wistar rats (12 weeks old) were exposed to oral aluminium chloride at 250 ppm for 30 days; followed by evaluation of caudal epididymal sperm count and motility, assay for serum follicle stimulating hormone (FSH), testosterone (T) and oestradiol; and assessment of testicular histology. Moreover, blood glucose was evaluated by the glucose oxidase method. In rats treated with streptozotocin (STZ) or aluminium (Al) alone, erosion of testicular parenchyma and stroma was observed. This effect was most severe in diabetic rats simultaneously exposed to Al; coupled with reduced caudal epididymal sperm count that was least in this (STZ+Al) group (18.75 × 106 ml−1) compared with controls (61.25 × 106 ml−1; P < 0.05), STZ group or Al group. Moreover, these reproductive perturbations (in the STZ+Al group) were associated with reduced sperm motility and significantly reduced serum FSH (P < 0.05); but elevated serum T and oestradiol (P < 0.05), compared with control. These suggest that diabetes‐induced testicular lesion is exacerbated by simultaneous oral Al toxicity in Wistar rats.
Adejoke J. Adekanmbi, Adefisayo A. Adekanmbi, and Oluwole B. Akinola
Hindawi Limited
This paper reports a study of cone photoreceptors present in the retina ofManis tricuspis. Specifically, the LWS (L-) opsin expressed in longwave-sensitive cones and SWS1 (S-) opsin shortwave-sensitive cones were targeted. Vertical sections revealed reactivity to a cone marker, peanut agglutinin (PNA), and to an LWS antibody, but not to an SWS1 antibody. This suggests that theManis tricuspisvisual system is not able to discriminate shorter wavelengths from longer wavelengths because the short wavelength cones are not expressed in their retina.
Oluwole B. Akinola, Sikiru A. Biliaminu, Rianat A. Adediran, Kehinde A. Adeniye, and Fatimah C. Abdulquadir
Springer Science and Business Media LLC
O.B. Akinola, O.O. Dosumu, S.A. Sanusi, T.F. Ajayi, and T.H. Olajide
Springer Science and Business Media LLC