Prefrontal cortex inflammation and liver pathologies accompany cognitive and motor deficits following Western diet consumption in non-obese female mice

Veniaminova, Ekaterina; Oplatchikova, Margarita; Bettendorff, Lucien; Kotenkova, Elena; Lysko, Alexander; Vasilevskaya, Ekaterina; Kalueff, Allan V.; Fedulova, Liliya; Umriukhin, Aleksei; Lesch, Klaus‐Peter; Anthony, Daniel C.; Strekalova, Tatyana

doi:10.1016/j.lfs.2019.117163

Cited by 37 publications

(34 citation statements)

References 82 publications

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“…These observations will be discussed, in turn, below. The present study on aged mice has, in general, replicated the principal findings reported for young mice fed the WD, such as impaired glucose tolerance, altered expression of Tlr4, Ppargc1a, and Ppargc1b (Strekalova et al, , 2016, and signs of emotional and cognitive abnormalities (Strekalova et al, , 2016Veniaminova et al, 2016Veniaminova et al, , 2017Veniaminova et al, , 2020. In comparison with young mice, aged animals exposed to WD gained weight and exhibited less profound changes in the expression of markers of inflammation and mitochondrial function.…”

Section: Discussionsupporting

confidence: 87%

“…Oral glucose tolerance test (OGTT) was performed as described elsewhere (Veniaminova et al, 2017(Veniaminova et al, , 2020. The test mice were fasted overnight for 18 h, beginning at 1600.…”

Section: Glucose Tolerance Testmentioning

confidence: 99%

“…In the present study, we sought to investigate metabolic, molecular, and behavioral changes induced by the WD in aged mice with complete or partial genetic SERT deficit. We employed a previously validated model that involves feeding mice with the WD for 3 weeks, and we evaluated metabolic and neurobiological hallmarks of the WD-induced syndrome in vitro and ex vivo assays (Strekalova et al, , 2016Veniaminova et al, 2016Veniaminova et al, , 2017Veniaminova et al, , 2020. In this model, impaired glucose tolerance, increases in cholesterol and leptin blood levels, brain and liver overexpression of Toll-like receptor 4 (Tlr4), decreased expression of mitochondrial markers peroxisome proliferatoractivated receptor gamma coactivator 1 (Ppargc1) a and b, and decreased Sert expression in the brain are all features.…”

Section: Introductionmentioning

confidence: 99%

“…In this model, impaired glucose tolerance, increases in cholesterol and leptin blood levels, brain and liver overexpression of Toll-like receptor 4 (Tlr4), decreased expression of mitochondrial markers peroxisome proliferatoractivated receptor gamma coactivator 1 (Ppargc1) a and b, and decreased Sert expression in the brain are all features. These molecular changes are accompanied by depressive-and anxietylike behaviors, signs of impulsivity, lowered sociability, and cognitive deficits (Strekalova et al, , 2016Veniaminova et al, 2016Veniaminova et al, , 2017Veniaminova et al, , 2020. Here, in view of the changes observed in 5-HT receptor densities in aging and in those with SERT deficiency, we also studied gene expression of serotonin receptors Htr1a, Htr1b, and Htr2a in the brain.…”

Section: Introductionmentioning

confidence: 99%

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Metabolic, Molecular, and Behavioral Effects of Western Diet in Serotonin Transporter-Deficient Mice: Rescue by Heterozygosity?

et al. 2020

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Frontiers in Neuroscience | www.frontiersin.org February 2020 | Volume 14 | Article 24 Veniaminova et al.SERT Heterozygosity and Western Diet in glucose tolerance, neuroinflammation, and hippocampus-dependent performance. Thus, complete versus partial Sert inactivation in aged mice results in distinct metabolic, molecular, and behavioral consequences in response to the WD. Our findings show that Sert +/− mice are resilient to certain environmental challenges and support the concept of heterosis as evolutionary adaptive mechanism.

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Section: Discussionsupporting

confidence: 87%

Section: Glucose Tolerance Testmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Metabolic, Molecular, and Behavioral Effects of Western Diet in Serotonin Transporter-Deficient Mice: Rescue by Heterozygosity?

et al. 2020

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“…Mice were allowed to grip a horizontal wire (diameter 0.3 cm, height above the surface 60 cm) for 180s. The latency of falling and the number and percent of mice with falling events (latency < 20s) were recorded as described elsewhere …”

Section: Methodsmentioning

confidence: 99%

Neuro‐Cells therapy improves motor outcomes and suppresses inflammation during experimental syndrome of amyotrophic lateral sclerosis in mice

et al. 2019

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Aims:Mutations in DNA/RNA-binding factor (fused-in-sarcoma) FUS and superoxide dismutase-1 (SOD-1) cause amyotrophic lateral sclerosis (ALS). They were reproduced in SOD-1-G93A (SOD-1) and new FUS[1-359]-transgenic (FUS-tg) mice, where inflammation contributes to disease progression. The effects of standard disease therapy and anti-inflammatory treatments were investigated using these mutants. Methods: FUS-tg mice or controls received either vehicle, or standard ALS treatment riluzole (8 mg/kg/day), or anti-inflammatory drug a selective blocker of cyclooxygenase-2 celecoxib (30 mg/kg/day) for six weeks, or a single intracerebroventricular (i.c.v.) infusion of Neuro-Cells (a preparation of 1.39 × 10 6 mesenchymal and hemopoietic human stem cells, containing 5 × 10 5 of CD34 + cells), which showed antiinflammatory properties. SOD-1 mice received i.c.v.-administration of Neuro-Cells or vehicle.Results: All FUS-tg-treated animals displayed less marked reductions in weight gain, food/water intake, and motor deficits than FUS-tg-vehicle-treated mice. Neuro-Celltreated mutants had reduced muscle atrophy and lumbar motor neuron degeneration.This group but not celecoxib-FUS-tg-treated mice had ameliorated motor performance and lumbar expression of microglial activation marker, ionized calcium-binding adapter molecule-1 (Iba-1), and glycogen-synthase-kinase-3ß (GSK-3ß). The Neuro-Cells-treated-SOD-1 mice showed better motor functions than vehicle-treated-SOD-1 group. Conclusion:The neuropathology in FUS-tg mice is sensitive to standard ALS treatments and Neuro-Cells infusion. The latter improves motor outcomes in two ALS models possibly by suppressing microglial activation. | 505MUNTER ET al.

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A novel fatty acid analogue triggers CD36–GPR120 interaction and exerts anti-inflammatory action in endotoxemia

Boutanquoi,

Khan,

Cabeza

et al. 2024

Cell. Mol. Life Sci.

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Inflammation is a mediator of a number of chronic pathologies. We synthesized the diethyl (9Z,12Z)-octadeca-9,12-dien-1-ylphosphonate, called NKS3, which decreased lipopolysaccharide (LPS)-induced mRNA upregulation of proinflammatory cytokines (IL-1β, IL-6 and TNF-α) not only in primary intraperitoneal and lung alveolar macrophages, but also in freshly isolated mice lung slices. The in-silico studies suggested that NKS3, being CD36 agonist, will bind to GPR120. Co-immunoprecipitation and proximity ligation assays demonstrated that NKS3 induced protein–protein interaction of CD36 with GPR120in RAW 264.7 macrophage cell line. Furthermore, NKS3, via GPR120, decreased LPS-induced activation of TAB1/TAK1/JNK pathway and the LPS-induced mRNA expression of inflammatory markers in RAW 264.7 cells. In the acute lung injury model, NKS3 decreased lung fibrosis and inflammatory cytokines (IL-1β, IL-6 and TNF-α) and nitric oxide (NO) production in broncho-alveolar lavage fluid. NKS3 exerted a protective effect on LPS-induced remodeling of kidney and liver, and reduced circulating IL-1β, IL-6 and TNF-α concentrations. In a septic shock model, NKS3 gavage decreased significantly the LPS-induced mortality in mice. In the last, NKS3 decreased neuroinflammation in diet-induced obese mice. Altogether, these results suggest that NKS3 is a novel anti-inflammatory agent that could be used, in the future, for the treatment of inflammation-associated pathologies.

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Prefrontal cortex inflammation and liver pathologies accompany cognitive and motor deficits following Western diet consumption in non-obese female mice

Cited by 37 publications

References 82 publications

Metabolic, Molecular, and Behavioral Effects of Western Diet in Serotonin Transporter-Deficient Mice: Rescue by Heterozygosity?

Metabolic, Molecular, and Behavioral Effects of Western Diet in Serotonin Transporter-Deficient Mice: Rescue by Heterozygosity?

Neuro‐Cells therapy improves motor outcomes and suppresses inflammation during experimental syndrome of amyotrophic lateral sclerosis in mice

A novel fatty acid analogue triggers CD36–GPR120 interaction and exerts anti-inflammatory action in endotoxemia

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