Transcriptomic Analysis of High Fat Diet Fed Mouse Brain Cortex

Yoon, Gil-Sang; Cho, Kyung A; Song, Jeong Sup; Kim, Young‐Kook

doi:10.3389/fgene.2019.00083

Cited by 32 publications

(35 citation statements)

References 104 publications

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“…Another interesting variance in the results regards the effects of the HFD manipulation, where the present study found that the HFD impairs apoE3 mice, rendering them similar to apoE4 mice in various parameters; Zhao et al [48] observed no effect on apoE3 mice following the HFD. In this context, it is interesting to note that many studies have shown that HFD-induced insulin resistance impairs control wildtype (WT) mice [91,94,95], meaning that the results revealed in the present study may be compatible with effects of this pattern. Although some specifics of the Zhao et al study [48] and the current one differ, the general concept that CNS insulin signaling is affected by apoE4 while peripheral parameters are not seems to be consistent between the two.…”

Section: Discussionsupporting

confidence: 72%

Central and Peripheral Mechanisms in ApoE4-Driven Diabetic Pathology

Koren-Iton

Salomon-Zimri

Smolar

et al. 2020

IJMS

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Apolipoprotein E (APOE) ε4 gene allele and type 2 diabetes mellitus (T2DM) are prime risk factors for Alzheimer’s disease (AD). Despite evidence linking T2DM and apoE4, the mechanism underlying their interaction is yet to be determined. In the present study, we employed a model of APOE-targeted replacement mice and high-fat diet (HFD)-induced insulin resistance to investigate diabetic mechanisms associated with apoE4 pathology and the extent to which they are driven by peripheral and central processes. Results obtained revealed an intriguing pattern, in which under basal conditions, apoE4 mice display impaired glucose and insulin tolerance and decreased insulin secretion, as well as cognitive and sensorimotor characteristics relative to apoE3 mice, while the HFD impairs apoE3 mice without significantly affecting apoE4 mice. Measurements of weight and fasting blood glucose levels increased in a time-dependent manner following the HFD, though no effect of genotype was observed. Interestingly, sciatic electrophysiological and skin intra-epidermal nerve fiber density (IENFD) peripheral measurements were not affected by the APOE genotype or HFD, suggesting that the observed sensorimotor and cognitive phenotypes are related to central nervous system processes. Indeed, measurements of hippocampal insulin receptor and glycogen synthase kinase-3β (GSK-3β) activation revealed a pattern similar to that obtained in the behavioral measurements while Akt activation presented a dominant effect of diet. HFD manipulation induced genotype-independent hyperlipidation of apoE, and reduced levels of brain apoE in apoE3 mice, rendering them similar to apoE4 mice, whose brain apoE levels were not affected by the diet. No such effect was observed in the peripheral plasma levels of apoE, suggesting that the pathological effects of apoE4 under the control diet and apoE3 under HFD conditions are related to the decreased levels of brain apoE. Taken together, our data suggests that diabetic mechanisms play an important role in mediating the pathological effects of apoE4 and that consequently, diabetic-related therapy may be useful in treating apoE4 pathology in AD.

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Section: Discussionsupporting

confidence: 72%

Central and Peripheral Mechanisms in ApoE4-Driven Diabetic Pathology

Koren-Iton

Salomon-Zimri

Smolar

et al. 2020

IJMS

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“…In a recent study, using RNA sequencing of coding and noncoding RNAs, it was demonstrated that the expression levels of mRNAs related to neurogenesis, synaptic plasticity and calcium signalling were decreased after HFD. Interesting, several ncRNAs were also differentially expressed in HFD mice compared to control [ 73 ], suggesting a crucial role played by ncRNAs in linking nutritional influence, metabolic disease and neuronal plasticity.…”

Section: Overnutrition and Synaptic Plasticitymentioning

confidence: 99%

Interplay between Peripheral and Central Inflammation in Obesity-Promoted Disorders: The Impact on Synaptic Mitochondrial Functions

Crispino

Trinchese

Penna

et al. 2020

IJMS

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The metabolic dysfunctions induced by high fat diet (HFD) consumption are not limited to organs involved in energy metabolism but cause also a chronic low-grade systemic inflammation that affects the whole body including the central nervous system. The brain has been considered for a long time to be protected from systemic inflammation by the blood–brain barrier, but more recent data indicated an association between obesity and neurodegeneration. Moreover, obesity-related consequences, such as insulin and leptin resistance, mitochondrial dysfunction and reactive oxygen species (ROS) production, may anticipate and accelerate the physiological aging processes characterized by systemic inflammation and higher susceptibility to neurological disorders. Here, we discussed the link between obesity-related metabolic dysfunctions and neuroinflammation, with particular attention to molecules regulating the interplay between energetic impairment and altered synaptic plasticity, for instance AMP-activated protein kinase (AMPK) and Brain-derived neurotrophic factor (BDNF). The effects of HFD-induced neuroinflammation on neuronal plasticity may be mediated by altered brain mitochondrial functions. Since mitochondria play a key role in synaptic areas, providing energy to support synaptic plasticity and controlling ROS production, the negative effects of HFD may be more pronounced in synapses. In conclusion, it will be emphasized how HFD-induced metabolic alterations, systemic inflammation, oxidative stress, neuroinflammation and impaired brain plasticity are tightly interconnected processes, implicated in the pathogenesis of neurological diseases.

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“…The sequencing reads with low quality were trimmed using the Trimmomatic (Bolger et al, 2014). To quantify the expression levels of mRNAs and lncRNAs, we used two independent analysis pipelines and intersected the results as shown in our previous article (Yoon et al, 2019). In the first approach, the trimmed sequences were aligned into the mouse genome (mm10) using the STAR aligner (Dobin et al, 2013), while the Cuffnorm was used to calculate normalized values of fragments per kilobase of transcript per million mapped reads (FPKM) based on GENCODE annotation (Release M17, GRCm38.p6; Harrow et al, 2006;Trapnell et al, 2012).…”

Section: Analysis Of Rna Sequencing Datamentioning

confidence: 99%

“…In our previous study, we combined the results from two different pipelines for RNA sequencing analysis to increase the reliability of the expression measurement ( Figure 1A; see the ''Materials and Methods'' section; Yoon et al, 2019). In the first pipeline, the sequences from each sample were aligned to the mouse genome by STAR, while the expression level of each gene was measured by Cuffnorm (Trapnell et al, 2012;Dobin et al, 2013).…”

Section: Transcriptome Analysis Of Pineal Gland From Mouse Ad Modelmentioning

confidence: 99%

“…Moreover, one to six exons were combined to compose circRNAs with three exons as the highest frequency ( Figure 4C). In our previous analysis of the circRNAs in the brain cortex, the combination of three exons was also the most frequent choice for the production of circRNA (Yoon et al, 2019). Therefore, there may be a similar principle to produce circRNA by combining exons between the brain cortex and the pineal gland.…”

Section: Analysis Of Circrnas Change In the Mouse Pineal Gland With Admentioning

confidence: 99%

See 1 more Smart Citation

Transcriptome Analysis of Pineal Glands in the Mouse Model of Alzheimer’s Disease

Nam

Yoon

Kim

et al. 2020

Front. Mol. Neurosci.

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The pineal gland maintains the circadian rhythm in the body by secreting the hormone melatonin. Alzheimer's disease (AD) is the most common neurodegenerative disease. Pineal gland impairment in AD is widely observed, but no study to date has analyzed the transcriptome in the pineal glands of AD. To establish resources for the study on pineal gland dysfunction in AD, we performed a transcriptome analysis of the pineal glands of AD model mice and compared them to those of wild type mice. We identified the global change of diverse protein-coding RNAs, which are implicated in the alteration in cellular transport, protein transport, protein folding, collagen expression, histone dosage, and the electron transfer system. We also discovered various dysregulated long noncoding RNAs and circular RNAs in the pineal glands of mice with AD. This study showed that the expression of diverse RNAs with important functional implications in AD was changed in the pineal gland of the AD mouse model. The analyzed data reported in this study will be an important resource for future studies to elucidate the altered physiology of the pineal gland in AD.

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Transcriptomic Analysis of High Fat Diet Fed Mouse Brain Cortex

Cited by 32 publications

References 104 publications

Central and Peripheral Mechanisms in ApoE4-Driven Diabetic Pathology

Central and Peripheral Mechanisms in ApoE4-Driven Diabetic Pathology

Interplay between Peripheral and Central Inflammation in Obesity-Promoted Disorders: The Impact on Synaptic Mitochondrial Functions

Transcriptome Analysis of Pineal Glands in the Mouse Model of Alzheimer’s Disease

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