Investigation of brain-derived neurotrophic factor (BDNF) gene expression in hypothalamus of obese rats: Modulation by omega-3 fatty acids

Abdel-Maksoud, Sahar M.; Hassanein, Sally I.; Gohar, Neveen A; Attia, Saad M M; Gad, Mohamed Z.

doi:10.1080/1028415x.2016.1180859

Cited by 25 publications

(7 citation statements)

References 27 publications

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“…Exenatide treatment positively affects BDNF signaling in 3xTg-AD CD mice and prevents the development of neurotrophic signaling impairment in 3xTg-AD HFD animals HFD administration impairs BDNF neurotrophic signaling along with the downstream activation of the cAMP response element-binding (CREB) protein, a transcription factor essential for synaptic plasticity and learning and memory processes 35,36 . Compared to 3xTg-AD CD animals, WB analysis performed on hippocampal, cortical, and cerebellar homogenates obtained from the study animals showed decreased BDNF levels in 3xTg-AD HFD mice (Fig.…”

Section: Aβ-and Tau-pathology In 3xtg-ad CD and 3xtg-ad Hfd Micementioning

confidence: 99%

Exenatide Reverts the High-Fat-Diet-Induced Impairment of BDNF Signaling and Inflammatory Response in an Animal Model of Alzheimer’s Disease

Bomba

Granzotto

Castelli

et al. 2019

JAD

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Background: preclinical, clinical, and epidemiological evidence support the notion that Alzheimer's disease (AD) is a multifactorial condition in which, along with β-amyloid (Aβ) and tau-related pathology, the synergistic activity of genetic, environmental, vascular, metabolic, and inflammatory factors promote the onset and progression of the disease. Epidemiological evidence indicate that glucose intolerance, deficits in insulin secretion or type 2 diabetes mellitus (T2DM) participate in increasing the risk of developing cognitive impairment or dementia. A pivotal role in the process is played by insulin as the hormone critically regulates brain functioning. GLP-1, the glucagon-like peptide 1, facilitates insulin signaling, regulates glucose homeostasis, and modulates synaptic plasticity. Exenatide is a GLP-1R agonist, characterized by an extended half-life, employed in T2DM. However, exenatide has also been shown to affect the signaling of the brain-derived neurotrophic factor (BDNF), synaptic plasticity, and cognitive performances in animal models of brain aging and neurodegeneration.Methods: in this study, we tested whether exenatide exerts neuroprotection in a preclinical AD model set to mimic the clinical complexity of the human disease. To that aim, we investigated the effects of 3-month exenatide treatment in 3xTg-AD mice challenged for six months with a high-fat diet (HFD). Endpoints of the study were variations in systemic metabolism, insulin and neurotrophic signaling, neuroinflammation, levels of Aβ and tau pathology as well as changes in cognitive performances.Findings and interpretation: results of the study indicate that exenatide reverts the adverse changes of BDNF signaling and the neuroinflammation status of 3xTg-AD mice undergoing HFD.

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Section: Aβ-and Tau-pathology In 3xtg-ad CD and 3xtg-ad Hfd Micementioning

confidence: 99%

Exenatide Reverts the High-Fat-Diet-Induced Impairment of BDNF Signaling and Inflammatory Response in an Animal Model of Alzheimer’s Disease

Bomba

Granzotto

Castelli

et al. 2019

JAD

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“…The effect of n -3 PUFA in the brain alterations related to obesity was less studied, with hypothalamus being the major focus of the investigation. n -3 PUFA showed beneficial effects on modulating inflammation and hypothalamic function in rodents ( 23 , 26 , 33 ) and was able to reverse the negative effect on the brain-derived neurotrophic factor (BDNF) gene expression caused by obesity in the hypothalamus of rats ( 31 ) . A review of animal studies on n -3 PUFA for obesity (and related alterations) is summarised in Table 1.…”

Section: N-3 Pufa and Obesitymentioning

confidence: 99%

n-3 PUFA and obesity: from peripheral tissues to the central nervous system

et al. 2018

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The current paradigms of prevention and treatment are unable to curb obesity rates, which indicates the need to explore alternative therapeutic approaches. Obesity leads to several damages to the body and is an important risk factor for a number of other chronic diseases. Furthermore, despite the first alterations in obesity being observed and reported in peripheral tissues, studies indicate that obesity can also cause brain damage. Obesity leads to a chronic low-grade inflammatory state, and the therapeutic manipulation of inflammation can be explored. In this context, the use of n-3 PUFA (especially in the form of fish oil, rich in EPA and DHA) may be an interesting strategy, as this substance is known by its anti-inflammatory effect and numerous benefits to the body, such as reduction of TAG, cardiac arrhythmias, blood pressure and platelet aggregation, and has shown potential to help treat obesity. Thereby, the aim of this narrative review was to summarise the literature related to n-3 PUFA use in obesity treatment. First, the review provides a brief description of the obesity pathophysiology, including alterations that occur in peripheral tissues and at the central nervous system. In the sequence, we describe what are n-3 PUFA, their sources and their general effects. Finally, we explore the main topic linking obesity and n-3 PUFA. Animal and human studies were included and alterations on the whole organism were described (peripheral tissues and brain).

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“…Essential fatty acids ω-3 can contribute to an increase in the proliferation and differentiation of hippocampal cells [52,53,55] which can reverse the decline of substances affecting neurogenesis process caused by aging [56]. DHA has a positive effect on the viability of neurons by inducing the formation of the neurotrophic factor BDNF [57] and own metabolic changes, in which it is metabolized to derivatives having neuroprotective activity -N-docosahexaenoylethanolamid (DEA) [58] and neuroprotectin D1 (NPD1) [59,60] .…”

Section: The Role Of Efas In the Functioning Of Cnsmentioning

confidence: 99%

“…NNKT ω-3 mogą wpływać na wzrost proliferacji i różnicowania komórek hipokampa [52,53,55] oraz odwracać spowodowany wiekiem spadek substancji oddziałujących na proces neurogenezy [56]. DHA wywiera korzystny efekt na żywotność neuronów poprzez indukcję powstawania czynnika neurotroficznego BDNF [57] oraz przemiany własne, w których metabolizowany jest do pochodnych o neuroprotekcyjnym działaniu -N-docosahexaenoylethanolamid (DEA) [58] oraz neuroprotektyny 1 (NPD1) [59,60].…”

Section: Rola Nnkt W Funkcjonowaniu Oununclassified

Omega – 3 fatty acids in schizophrenia – part I: importance in the pathophysiology of schizophrenia

Róg

Karakuła-Juchnowicz

2016

Current Problems of Psychiatry

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Despite the increasing offer of antipsychotic drugs, the effectiveness of pharmacotherapy in schizophrenia is still unsatisfactory. Drug resistance, lack of complete remission and the increasing risk of metabolic complications are the reasons why the new forms of therapy in schizophrenia among which unsaturated essential fatty acids omega 3 (EFAs ω-3) affecting the proper functioning of nervous system, are mentioned, are being looked for.Fatty acids represent 50-60% of the dry weight of the brain and diet is one of the factors that influence the value of each of the fat fractions in the neuron membranes. Patients with schizophrenia tend to have irregular nutritional status concerning essential fatty acids ω-3, which might result from metabolic disorders or irregular consumption of fatty acids.Apart from being a review of the literature on this subject, this very paper characterizes essential fatty acids ω-3, their metabolism, the most important sources in the diet and the opinions of experts in the field about the recommended intake. It pays attention to the role of essential fatty acids in both the structure and functioning of the central nervous system is, as well as their role in the pathophysiology of schizophrenia, with particular emphasis on the membrane concept by David Horrobin. The assessment of the errors in consumption and metabolism of essential fatty acids are described as well.The evidence was found both in epidemiological and modeling studies. It supports the participation of EFAs in etiopathogenesis and pathophysiology of schizophrenia. Further research is needed, both observational and interventional, as to the role of essential fatty acids ω-3 in the functioning of the CNS as well as the development and course of schizophrenia.

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Investigation of brain-derived neurotrophic factor (BDNF) gene expression in hypothalamus of obese rats: Modulation by omega-3 fatty acids

Abstract: Obesity causes down-regulation of BDNF gene expression that can be reversed by ω-3 FAs treatment, making them an interesting treatment approach for obesity and metabolic disease.

Cited by 25 publications

References 27 publications

Exenatide Reverts the High-Fat-Diet-Induced Impairment of BDNF Signaling and Inflammatory Response in an Animal Model of Alzheimer’s Disease

Exenatide Reverts the High-Fat-Diet-Induced Impairment of BDNF Signaling and Inflammatory Response in an Animal Model of Alzheimer’s Disease

n-3 PUFA and obesity: from peripheral tissues to the central nervous system

Omega – 3 fatty acids in schizophrenia – part I: importance in the pathophysiology of schizophrenia

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