Abstract:
:The aim of the present work was to investigate the role of ondansetron on the high fat diet (HFD) induced obese mice for behavioral and biochemical alterations using chronic unpredictable mild stress (CUMS) model of depression. Animals were fed with high fat diet for 14 weeks and subjected to different stress procedures for 4 weeks. Treatment with ondansetron was started on day 15. After day 28 behavioral assays and biochemical estimations were performed. Behavioral paradigms viz. sucrose preference test, locomotor score, forced swim test (FST) and elevated plus maze (EPM), whereas biochemical parameters like plasma glucose, total cholesterol, triglycerides and total proteins were estimated. Results examines that in behavioral assays, ondansetron significantly (P < 0.05) increased sucrose consumption, reduced immobility time in FST, increased the percent entries and time in open arm in EPM. In biochemical assessments elevated plasma glucose, total cholesterol, triglycerides and total proteins were significantly (P < 0.05) reversed by ondansetron treatment in HFD obese animals subjected to CUMS. The study indicates that the obese mice subjected to CUMS exhibited severe depressive-like symptoms and ondansetron significantly reversed the behavioral and biochemical alterations. In the present study the plasma glucose level indicates that, it could be "altered glucose level" playing an important role in depression co-morbid with obesity. Ondansetron through allosteric modulation of serotonergic system elevates the serotonin level and thereby regulates the insulin secretion and hence, reversing the "altered glucose level", could be the possible antidepressive-like mechanism against depression co-morbid with obesity.
journal_name
Metab Brain Disjournal_title
Metabolic brain diseaseauthors
Kurhe Y,Radhakrishnan M,Gupta Ddoi
10.1007/s11011-014-9574-8subject
Has Abstractpub_date
2014-09-01 00:00:00pages
701-10issue
3eissn
0885-7490issn
1573-7365journal_volume
29pub_type
杂志文章abstract::Hypoxic-ischemia (HI) is a widely used animal model to mimic the preterm or perinatal sublethal hypoxia, including hypoxic-ischemic encephalopathy. It causes diffuse neurodegeneration in the brain and results in mental retardation, hyperactivity, cerebral palsy, epilepsy and neuroendocrine disturbances. Herein, we exa...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-016-9816-z
更新日期:2016-08-01 00:00:00
abstract::Effects of sertraline, haloperidol or olanzapine administration on ketamine-induced behaviours in mice were examined. The aim was to ascertain the degree of reversal of such behaviours by sertraline, and compare its effectiveness to haloperidol and olanzapine. Ten-week old mice (N = 120) were equally divided into main...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-017-0031-3
更新日期:2017-10-01 00:00:00
abstract::The effects of chronic and repeated radiofrequency electromagnetic radiation (RFEMR) exposure on spatial cognition and hippocampal architecture were investigated in prepubescent rats. Four weeks old male Wistar rats were exposed to RF-EMR (900 MHz; SAR-1.15 W/kg with peak power density of 146.60 μW/cm(2)) for 1 h/day,...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-015-9689-6
更新日期:2015-10-01 00:00:00
abstract::First-episode psychosis (FEP) patients are more sensitive to neuroleptic side-effects such as hyperprolactinemia. We examined the prolactin levels of previously minimally treated patients with first episode schizophrenia over their first year of treatment with flupenthixol decanoate and the relationship between prolac...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-019-00474-5
更新日期:2019-12-01 00:00:00
abstract::Brain glucose uptake is usually reduced in type 2 diabetes owing to downregulation of brain glucose transporters. The ability of Vernonia amygdalina to stimulate glucose uptake as well as ameliorate glucose-induced oxidative stress and proinflammation were investigated in rat brain. Hot infusion of V. amygdalina leave...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-018-0363-7
更新日期:2019-06-01 00:00:00
abstract::Cyclic AMP is part of an endogenous mechanism that downregulates inflammatory response, and its intracellular concentration is regulated chiefly by cyclic nucleotide phosphodiesterases type 4. The goal of the present study was to determine whether phosphodiesterases 4 are involved in the inflammatory response of astro...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-009-9150-9
更新日期:2009-09-01 00:00:00
abstract::A rat model of glucose-precipitated Wernicke's encephalopathy (WE) has been developed in which glucose loading (10 g/kg, i.p.) of ataxic thiamin-deficient (TD) rats induced episodes of gross neurological dysfunction and sometimes death. The acute effects of a glucose load on the neurological state of thiamin-replete c...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1023/a:1020653312697
更新日期:1999-03-01 00:00:00
abstract::We aimed to evaluate the effect of in vitro galactosaemia on acetylcholinesterase (AChE) activity in different suckling rat brain regions. Various concentrations of galactose (Gal), galactose-1-phosphate (Gal-1-P) and/or galactitol (Galtol) were preincubated for 1 h with homogenates from frontal cortex, hippocampus an...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-005-7210-3
更新日期:2005-09-01 00:00:00
abstract::As studies of brain metabolism grow in complexity, investigators turn increasingly to nuclear magnetic resonance spectroscopy combined with 13C isotopic labeling. The unique ability to detect labeling non-destructively in specific carbon positions of individual compounds has opened the way to investigate brain metabol...
journal_title:Metabolic brain disease
pub_type: 杂志文章,评审
doi:10.1007/BF02029492
更新日期:1996-12-01 00:00:00
abstract::Acute and chronic administration of Al-gluconate (12.7% Al) at the concentration of 1 mg/kg produces edema in the rat brain, as reflected by the increase in water and Na+ content. The permeability for Evans blue is also increased, which indicates the opening of the blood-brain barrier. Higher concentrations of the Al-...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/BF00996974
更新日期:1990-03-01 00:00:00
abstract::The cholesterol-raising properties of the apolipoprotein E (APOE) epsilon-4 (ε-4) allele has been validated in the South African population. Mounting evidence supports the added value of APOE genotyping for the evaluation of cardiovascular risk in dyslipidemic patients beyond its established role in the diagnosis of l...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-015-9737-2
更新日期:2016-02-01 00:00:00
abstract::Hereditary tyrosinemia type I (HT1) is caused by mutations in the fumarylacetoacetate hydrolase (FAH) gene, the template for the final enzyme in the tyrosine catabolism pathway. If left untreated this deficiency of functional FAH leads to a buildup of toxic metabolites that can cause liver disease, kidney dysfunction ...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-017-0071-8
更新日期:2017-12-01 00:00:00
abstract::Chronic liver disease (CLD) leads to a spectrum of neuropsychiatric disorders named hepatic encephalopathy (HE). Even though brain energy metabolism is believed to be altered in chronic HE, few studies have explored energy metabolism in CLD-induced HE, and their findings were inconsistent. The aim of this study was to...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-015-9715-8
更新日期:2016-12-01 00:00:00
abstract::The availability of an animal model is crucial in studying the pathophysiological mechanisms of disease and to test possible therapies. Now, there are several models for the study of liver diseases, but there still remains a lack of a satisfactory animal model of chronic liver disease with hepatic encephalopathy (HE) ...
journal_title:Metabolic brain disease
pub_type: 杂志文章,评审
doi:10.1007/s11011-005-7925-1
更新日期:2005-12-01 00:00:00
abstract::Mutations in NADH dehydrogenase (ND) subunits of complex I lead to mitochondrial encephalomyopathies associated with various phenotypes. This report aims to present the patient's clinical symptomatology in the context of a very rare 13042G>A de novo mutation and with an emphasis on changing phenotypic expression and p...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-014-9645-x
更新日期:2015-08-01 00:00:00
abstract::Adult-onset type II citrullinemia (CTLN2), characterized by a liver-specific deficiency of urea cycle enzyme, argininosuccinate synthetase, is caused by mutations in SLC25A13 that encodes a calcium binding mitochondrial solute carrier protein, citrin. Citrin deficiency causes not only CTLN2 but also neonatal intrahepa...
journal_title:Metabolic brain disease
pub_type: 杂志文章,评审
doi:10.1023/a:1021961919148
更新日期:2002-12-01 00:00:00
abstract::It has been suggested that alterations of GABAergic neurotransmission are implicated in the pathophysiology of hepatic encephalopathy (HE). Increased concentrations of endogenous benzodiazepines with positive allosteric modulatory properties at the GABA-A receptor complex were proposed as a pathophysiological mechanis...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1023/b:mebr.0000043974.89820.22
更新日期:2004-12-01 00:00:00
abstract::In Alzheimer's disease (AD) basal forebrain cholinergic neurons appear to be targeted primarily in early stages of the disease. Scopolamine (muscarinic receptor antagonist) has been used for decades to induce working and reference memory impairment in rodents. In this study, we evaluated the protective effect of kolav...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-016-9902-2
更新日期:2017-02-01 00:00:00
abstract::In this work, we evaluated the effects of Psidium cattleianum (Red Type) (PcRT) fruit extract on metabolic, behavioral, and neurochemical parameters in rats fed with a highly palatable diet (HPD) consisted of sucrose (65% carbohydrates being 34% from condensed milk, 8% from sucrose and 23% from starch, 25% protein and...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-018-0262-y
更新日期:2018-10-01 00:00:00
abstract::The sprouting of new blood vessels from pre-existing vasculature (angiogenesis) is essential for tumour survival, influenced by tumour cell-endothelial cell interactions and is tightly regulated by biochemical cues including the kallikrein-kinin system (KKS). We examined the structural interaction between neuroblastom...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-006-9008-3
更新日期:2006-09-01 00:00:00
abstract::Parkinson's disease is a neurodegenerative disease whose hallmark pathological features include a selective loss of dopaminergic neurons in the midbrain. Ciclooxygenase-2 activity induction and oxidative stress have been implicated in the aetiology of Parkinson's disease and in the 1-methyl-4-phenyl-1,2,3,6-tetrahydro...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-013-9416-0
更新日期:2013-12-01 00:00:00
abstract::There is abundant evidence showing that repeated use of MDMA (3, 4-Methylenedioxymethamphetamine, ecstasy) has been associated with depression, anxiety and deficits in learning and memory, suggesting detrimental effects on hippocampus. Adenosine is an endogenous purine nucleoside that has a neuromodulatory role in the...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-012-9334-6
更新日期:2012-12-01 00:00:00
abstract::Mitochondrial glutathione (mGSH) is a critical factor in the cell defense against oxidative and nitrosative stress (ONS), and ONS is a key pathogenic event in hepatic encephalopathy (HE). Acute HE in the thioacetamide (TAA) model caused a 54 % decrease of mGSH content in the rat prefrontal cortex (pfc), but not in the...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-012-9342-6
更新日期:2013-03-01 00:00:00
abstract::To characterize an Egyptian patient with glutaric acidemia type I (GA I) and to identify the causative mutation(s) that may be responsible for the disease phenotype. MRI was performed on the patient using the 1.5 T magnet, biochemical analysis was carried out using gas chromatography/mass spectrometry on the patient's...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-016-9879-x
更新日期:2017-02-01 00:00:00
abstract::The developing facial neurons of a series of hamsters ranging in age from the 14-day fetus to the 9 day postnatal were axotomized. Postoperative times were graded for each age so that the retrograde response could be observed before any significant amount of cell degeneration or death occurred. The incorporation of tr...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/BF00996894
更新日期:1993-06-01 00:00:00
abstract::Amyloid-beta (Aβ) interacts with the serine/threonine protein kinase AKT (also known as protein kinase B)/glycogen synthase kinase 3β (GSK3β) pathway and deactivates GSK3β signaling, which result in microtubule protein tau phosphorylation. Atorvastatin, a HMG-CoA reductase inhibitor, has been proven to improve learnin...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-016-9803-4
更新日期:2016-06-01 00:00:00
abstract::Sepsis is a major clinical challenge that is associated with encephalopathy and multi-organ dysfunction. Current therapeutic interventions are relatively ineffective and the development of novel treatments is hampered by the lack of a well-characterised animal model. Therefore, the behavioural, metabolic, physiologica...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-007-9058-1
更新日期:2007-12-01 00:00:00
abstract::We report reversible abnormalities in magnetic resonance spectra acquired from a patient with AIDS undergoing antibiotic and corticosteroid therapy for disseminated nocardiosis, a rare opportunistic infection of immunosuppressed patients which can cause cerebral abscess formation. There was no clinical, CT or MRI evid...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1023/a:1020733024934
更新日期:1999-12-01 00:00:00
abstract::Hyperammonemia is necessary for development of the cerebral complications to liver disease including hepatic encephalopathy and cerebral edema but the mechanisms are unclear. Ammonia is taken up by the brain in proportion to its arterial concentration. The flux into the brain is most likely by both diffusion of NH3 an...
journal_title:Metabolic brain disease
pub_type: 杂志文章,评审
doi:10.1007/s11011-014-9494-7
更新日期:2014-12-01 00:00:00
abstract::The present experiments were conducted to investigate the direct effects of ethanol on the energy metabolism of astrocytes and C6-glioma cells. Primary astrocytes were prepared from cerebral cortices of neonatal rats, and C6-glioma cells were purchased from American Type Culture Collection (ATCC). These cells were exp...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1023/a:1020606607729
更新日期:1999-09-01 00:00:00