Department of Pharmacy

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Author: search.filters.author.Taliyan, RajeevSubject: search.filters.subject.High Fat Diet (HFD)

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    [P2–130]: AR-A014418, A GSK-3β INHIBITOR, ATTENUATES ALZHEIMER'S- LIKE PATHOLOGY IN HIGH FAT DIET-INDUCED COGNITIVE DEFICIT IN MICE
    (Wiley, 2017-07) Taliyan, Rajeev
    Alzheimer's disease (AD) is characterized by the progressive deposition of fibrillar amyloid-β (Aβ) in the form of extracellular plaques and hyperphosphorylated tau as intraneuronal neuro fibrillary tangles (NFTs). Studies have reported that increased Glycogen synthase kinase-3β (GSK-3β) activity has been associated with hyper phosphorylation of tau. However, the molecular mechanisms of association still remain elusive. Thus, the present study was designed to explore the potential of GSK-3β inhibitor, AR-A014418 in high fat diet (HFD) induced cognitive impairment and AD like pathology.
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    Epigenetic Regulation of Mammalian Target of Rapamycin Debilitates Insulin Resistance Associated Alzheimer Disease Condition in Rats
    (Research Square, 2021) Taliyan, Rajeev
    Insulin resistance (IR) and accumulation of amyloid beta (Aβ) oligomers are potential causative factor for Alzheimer Disease (AD). Simultaneously, enhanced clearance level of these oligomers through autophagy activation bring novel insights into their therapeutic paradigm. Autophagy activation is negatively correlated with mammalian target of rapamycin (mTOR) and dysregulated mTOR level due to epigenetic alterations can further culminate towards AD pathogenesis. Therefore, in the current study we explored the neuroprotective efficacy of rapamycin and vorinostat in-vitro and in-vivo. Aβ1−42 treated SH-SY5Y cells were exposed to rapamycin (20µM) and vorinostat (4µM) to analyse mRNA expression of amyloid precursor protein (APP), brain derived neurotrophic factor (BDNF), glial cell derived neurotrophic factor (GDNF), neuronal growth factor (NGF), beclin-1, microtubule-associated protein 1A/1B-light chain 3-phosphatidylethanolamine conjugate, lysosome-associated membrane protein 2 and microtubule associated protein 2. In order to develop IR condition, rats were fed a high fat diet (HFD) for 8weeks and then subjected to intracerebroventricular Aβ1−42 administration. Subsequently, their treatment was initiated with rapa (1mg/kg, i.p.) and vori (50mg/kg, i.p.) once daily for 28days. Morris water maze was performed to govern cognitive impairment followed by sacrification for subsequent biochemical and histological estimations. For all the measured parameters, a significant improvement was observed amongst the combination treatment group in contrast to that of the HFD + Aβ1−42 group and that of the groups treated with the drugs alone. Outcomes of the present study thus suggest that combination therapy with rapa and vori provide a prospective therapeutic approach to ameliorate AD symptoms exacerbated by IR.
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    High fat diet feeding induced insulin resistance exacerbates 6-OHDA mediated neurotoxicity and behavioral abnormalities in rats
    (Elsevier, 2018-10) Taliyan, Rajeev
    Some of the clinical reports suggest that insulin resistance could be a risk factor for Parkinson’s disease (PD) development, however experimental data is scarce. Our previous work has suggested that insulin resistance could be an important factor that leads to diabetes associated neurodegeneration. In the present study, we evaluated whether insulin resistance is linked to PD pathology or not. For this purpose, we first standardized an animal model which could mimic the co-morbid insulin resistance and PD condition. For development of insulin resistance, we fed the male Wistar rats with high fat diet (HFD) for eight weeks, followed by 6-hydroxydopamine (6-OHDA) administration, a toxin widely used for PD induction, in medial forebrain bundle (MFB) of rats. The 6-OHDA treatment resulted in neuronal damage and loss of striatal dopamine level. This dopamine loss was correlated with impaired performance in behavioral tasks such as rotarod, narrow beam walk test and locomotor activity. Interestingly, we found that exposure to HFD exacerbated the effects of 6-OHDA on striatal dopamine loss and behavioral parameters in rats, indicating that HFD-induced insulin resistance is associated with a diminished capacity of dopaminergic neurons to cope with 6-OHDA mediated neurotoxicity. Based upon these findings, it can be suggested that HFD feeding induced insulin resistance exacerbates the PD pathology.