DPP-4 Inhibitor and PPARγ Agonist Restore the Loss of CA1 Dendritic Spines in Obese Insulin-resistant Rats

Sripetchwandee, Jirapas; Pipatpiboon, Noppamas; Pratchayasakul, Wasana; Chattipakorn, Nipon; Chattipakorn, Siriporn C.

doi:10.1016/j.arcmed.2014.09.002

Cited by 31 publications

(15 citation statements)

References 53 publications

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“…As previously demonstrated, long-term HFD consumption could lead to the induction of cognitive impairment in association with a reduction in dendritic spine density10. Consistent with a previous study, HFD consumption in the present study also caused memory impairment indicated by the increased time to reach the platform (Fig.…”

Section: Resultssupporting

confidence: 93%

“…To examine dendritic spine density, Golgi staining was performed following Sripetchwandee et al 10. Briefly, the brain was transferred to Golgi staining solution according to FD Rapid Golgistain™ Kits (FD Neuro Technologies, Baltimore, MD, USA) and cut at 60 μm of thickness using Cyostat (Leica CM1950, Leica Biosystem Nussloch GmbH, Nussloch, Germany).…”

Section: Methodsmentioning

confidence: 99%

“…It has been shown that insulin resistance is associated with learning impairment and memory decline56. Previous studies from our group and others have demonstrated that obese rats, induced by high-fat diet (HFD) consumption, not only caused peripheral insulin resistance, but also brain insulin resistance, increased pro-inflammatory cytokines, increased brain oxidative stress, brain mitochondrial dysfunction, hippocampal synaptic dysfunction, decreased dendritic spine density, and instigated cognitive decline267891011.…”

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confidence: 99%

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Vagus Nerve Stimulation Exerts the Neuroprotective Effects in Obese-Insulin Resistant Rats, Leading to the Improvement of Cognitive Function

Chunchai

Samniang

Sripetchwandee

et al. 2016

Sci Rep

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Vagus nerve stimulation (VNS) therapy was shown to improve peripheral insulin sensitivity. However, the effects of chronic VNS therapy on brain insulin sensitivity, dendritic spine density, brain mitochondrial function, apoptosis and cognition in obese-insulin resistant subjects have never been investigated. Male Wistar rats (n = 24) were fed with either a normal diet (n = 8) or a HFD (n = 16) for 12 weeks. At week 13, HFD-fed rats were divided into 2 groups (n = 8/group). Each group was received either sham therapy or VNS therapy for an additional 12 weeks. At the end of treatment, cognitive function, metabolic parameters, brain insulin sensitivity, brain mitochondrial function, brain apoptosis, and dendritic spines were determined in each rat. The HFD-fed with Sham therapy developed brain insulin resistance, brain oxidative stress, brain inflammation, and brain apoptosis, resulting in the cognitive decline. The VNS group showed an improvement in peripheral and brain insulin sensitivity. VNS treatment attenuated brain mitochondrial dysfunction and cell apoptosis. In addition, VNS therapy increased dendritic spine density and improved cognitive function. These findings suggest that VNS attenuates cognitive decline in obese-insulin resistant rats by attenuating brain mitochondrial dysfunction, improving brain insulin sensitivity, decreasing cell apoptosis, and increasing dendritic spine density.

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Section: Resultssupporting

confidence: 93%

Section: Methodsmentioning

confidence: 99%

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confidence: 99%

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Vagus Nerve Stimulation Exerts the Neuroprotective Effects in Obese-Insulin Resistant Rats, Leading to the Improvement of Cognitive Function

Chunchai

Samniang

Sripetchwandee

et al. 2016

Sci Rep

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“…In addition, another DPP-IV inhibitor, vildagliptin, effectively restored neuronal IR function, increased GLP-1 levels, and prevented brain mitochondrial dysfunction, thus attenuating the impaired cognitive function caused by HFD Pipatpiboon et al, 2013). Vildagliptin also restored the loss of hippocampus CA1 dendritic spines, which was associated with cognitive decline caused by HFD (Sripetchwandee et al, 2014). Furthermore, vildagliptin ameliorated cognitive deficits and pathology observed in the STZ-induced AD animal model (Kosaraju et al, 2013b).…”

Section: Effects Of Dpp-iv Inhibitors On Neurodegenerative Diseasesmentioning

confidence: 74%

Incretin-based therapy for type 2 diabetes mellitus is promising for treating neurodegenerative diseases

Hölscher

2016

Reviews in the Neurosciences

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AbstractIncretin hormones include glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). Due to their promising action on insulinotropic secretion and improving insulin resistance (IR), incretin-based therapies have become a new class of antidiabetic agents for the treatment of type 2 diabetes mellitus (T2DM). Recently, the links between neurodegenerative diseases and T2DM have been identified in a number of studies, which suggested that shared mechanisms, such as insulin dysregulation or IR, may underlie these conditions. Therefore, the effects of incretins in neurodegenerative diseases have been extensively investigated. Protease-resistant long-lasting GLP-1 mimetics such as lixisenatide, liraglutide, and exenatide not only have demonstrated promising effects for treating neurodegenerative diseases in preclinical studies but also have shown first positive results in Alzheimer’s disease (AD) and Parkinson’s disease (PD) patients in clinical trials. Furthermore, the effects of other related incretin-based therapies such as GIP agonists, dipeptidyl peptidase-IV (DPP-IV) inhibitors, oxyntomodulin (OXM), dual GLP-1/GIP, and triple GLP-1/GIP/glucagon receptor agonists on neurodegenerative diseases have been tested in preclinical studies. Incretin-based therapies are a promising approach for treating neurodegenerative diseases.

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“…After decapitation, brains were removed and rinsed with double distilled water, and they were then processed for Golgi staining using a commercially available kit (FD Neurotechnologies kit, PK 401, Ellicott City, USA). The details of dendritic spine density analysis were previously described (Sripetchwandee et al, 2014). Briefly, two segments from a pyramidal cell in the CA1 area of the hippocampus were randomly measured.…”

Section: Golgi Impregnation and Analysismentioning

confidence: 99%

Obesity accelerates cognitive decline by aggravating mitochondrial dysfunction, insulin resistance and synaptic dysfunction under estrogen-deprived conditions

Pratchayasakul

Sa‐nguanmoo

Sivasinprasasn

et al. 2015

Hormones and Behavior

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DPP-4 Inhibitor and PPARγ Agonist Restore the Loss of CA1 Dendritic Spines in Obese Insulin-resistant Rats

Cited by 31 publications

References 53 publications

Vagus Nerve Stimulation Exerts the Neuroprotective Effects in Obese-Insulin Resistant Rats, Leading to the Improvement of Cognitive Function

Vagus Nerve Stimulation Exerts the Neuroprotective Effects in Obese-Insulin Resistant Rats, Leading to the Improvement of Cognitive Function

Incretin-based therapy for type 2 diabetes mellitus is promising for treating neurodegenerative diseases

Obesity accelerates cognitive decline by aggravating mitochondrial dysfunction, insulin resistance and synaptic dysfunction under estrogen-deprived conditions

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