Long term effects of high fat diet given early in life in prenatally stressed rats: role of the inflammatory response

2019 ◽  
Vol 29 ◽  
pp. S225-S226
Author(s):  
M. Mazzelli ◽  
N. Cattane ◽  
C. Mora ◽  
V. Begni ◽  
A. Berry ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
High Fat Diet ◽  
Long Term Effects ◽  
High Fat ◽  
Prenatally Stressed

scholarly journals Maternal Exposure to High-Fat Diet Induces Long-Term Derepressive Chromatin Marks in the Heart

Nutrients ◽  
2020 ◽  
Vol 12 (1) ◽  
pp. 181 ◽  
Author(s):  
Guillaume Blin ◽  
Marjorie Liand ◽  
Claire Mauduit ◽  
Hassib Chehade ◽  
Mohamed Benahmed ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Heart Development ◽  
High Fat Diet ◽  
Target Genes ◽  
Critical Role ◽  
Maternal Exposure ◽  
High Fat ◽  
Cardiac Alterations

Heart diseases are a leading cause of death. While the link between early exposure to nutritional excess and heart disease risk is clear, the molecular mechanisms involved are poorly understood. In the developmental programming field, increasing evidence is pointing out the critical role of epigenetic mechanisms. Among them, polycomb repressive complex 2 (PRC2) and DNA methylation play a critical role in heart development and pathogenesis. In this context, we aimed at evaluating the role of these epigenetic marks in the long-term cardiac alterations induced by early dietary challenge. Using a model of rats exposed to maternal high-fat diet during gestation and lactation, we evaluated cardiac alterations at adulthood. Expression levels of PRC2 components, its histone marks di- and trimethylated histone H3 (H3K27me2/3), associated histone mark (ubiquitinated histone H2A, H2AK119ub1) and target genes were measured by Western blot. Global DNA methylation level and DNA methyl transferase 3B (DNMT3B) protein levels were measured. Maternal high-fat diet decreased H3K27me3, H2Ak119ub1 and DNA methylation levels, down-regulated the enhancer of zeste homolog 2 (EZH2), and DNMT3B expression. The levels of the target genes, isl lim homeobox 1 (Isl1), six homeobox 1 (Six1) and mads box transcription enhancer factor 2, polypeptide C (Mef2c), involved in cardiac pathogenesis were up regulated. Overall, our data suggest that the programming of cardiac alterations by maternal exposure to high-fat diet involves the derepression of pro-fibrotic and pro-hypertrophic genes through the induction of EZH2 and DNMT3B deficiency.

Stress Aggravates High-Fat-Diet-Induced Insulin Resistance via a Mechanism That Involves the Amygdala and Is Associated with Changes in Neuroplasticity

2018 ◽  
Vol 107 (2) ◽  
pp. 147-157 ◽  
Author(s):  
Sheng-Feng Tsai ◽  
Hung-Tsung Wu ◽  
Pei-Chun Chen ◽  
Yun-Wen Chen ◽  
Megan Yu ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
High Fat Diet ◽  
Tissue Expansion ◽  
Plasma Corticosterone ◽  
High Fat ◽  
Obesity In Mice ◽  
Bilateral Lesions

Background: The notion that exposure to chronic stress predisposes individuals to developing type 2 diabetes (T2D) has gained much attention in recent decades. Long-term stress induces neuroadaptation in the amygdala and increases corticosterone levels. Corticosterone, the major stress hormone in rodents, induces insulin resistance and obesity in mice. However, little is known about whether the stress-induced amygdalar neuroadaptation could promote the risk of T2D. Methods: We used an 11-week high-fat diet (HFD) feeding paradigm to induce insulin dysfunction in mice, followed by implementation of a 10-day social defeat (SD) stress protocol. Results: Mice receiving SD at the beginning of the HFD feeding aggravated HFD-induced insulin resistance and white adipose tissue expansion. HFD mice had higher levels of plasma corticosterone, which was not affected by the SD. The SD stress upregulated the expression of TrkB and synaptotagmin-4 in the amygdala of HFD mice. Bilateral lesions of the central amygdalae before SD stress inhibited the stress-induced aggravating effect without affecting the HFD-induced elevation of plasma corticosterone. Conclusions: Stress aggravates HFD-induced insulin resistance and neuroadaptation in the amygdala. The HFD-induced insulin resistance is amygdala-dependent. Understanding the role of stress-induced amygdalar adaptation in the development of T2D could inform therapies aimed at reducing chronic stressors to decrease the risk for T2D.

scholarly journals Long-term impact of maternal high-fat diet on offspring cardiac health: role of micro-RNA biogenesis

2019 ◽  
Vol 5 (1) ◽  
Author(s):  
Benazir Siddeek ◽  
Claire Mauduit ◽  
Hassib Chehade ◽  
Guillaume Blin ◽  
Marjorie Liand ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Micro Rna ◽  
High Fat ◽  
Cardiac Health ◽  
Rna Biogenesis ◽  
Long Term Impact

Short- and long-term effects of high-fat diet feeding and voluntary exercise on hepatic lipid metabolism in mice

2018 ◽  
Vol 507 (1-4) ◽  
pp. 291-296 ◽  
Author(s):  
Saki Yoshimura ◽  
Shihoko Nakashima ◽  
Yuki Tomiga ◽  
Shotaro Kawakami ◽  
Yoshinari Uehara ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
High Fat Diet ◽  
Voluntary Exercise ◽  
Long Term Effects ◽  
High Fat ◽  
Hepatic Lipid Metabolism ◽  
Hepatic Lipid ◽  
Short And Long Term

scholarly journals La capacidad de inhibición de respuesta y la memoria a corto plazo son robustos a los efectos de la dieta alta en grasa (HFD) durante la pre y periadolescencia

2014 ◽  
Vol 13 (3) ◽  
Author(s):  
Elizabeth Watterson ◽  
Arturo R Zavala ◽  
Gregory J Privitera ◽  
Federico Sanabria
Keyword(s):  
Response Inhibition ◽  
High Fat Diet ◽  
Short Term Memory ◽  
Rule Learning ◽  
Long Term Effects ◽  
High Fat ◽  
Reinforcer Efficacy ◽  
Low Fat Diet ◽  
Diet Exposure

Several lines of evidence demonstrate that high fat diet exposure can be detrimental to cognition across the lifespan. We have previously shown that context-stimulus learning is sensitive to high fat diet effects during adolescence but not adulthood. In the present study we determined if pre and periadolescent high fat diet exposure interferes with response-inhibition capacity, rule- learning, and memory during adulthood. Rats were fed a high fat or low fat diet during pre and periadolescence and completed behavioral testing as adults to assess response-inhibition capacity and reinforcer efficacy rule-learning and short-term memory. Results indicate pre and periadolescent high fat diet may have long-term effects on reinforcer efficacy and sustained attention. However, results indicate that either the pre and periadolescence period is too short for a high fat diet to induce long-term deficits in response-inhibition, rule-learning, or memory, or that maturation in the absence of a high fat diet rescued these deficits.

The role of oxidative stress and inflammatory response in high-fat diet induced peripheral neuropathy

2014 ◽  
Vol 55 ◽  
pp. 51-57 ◽  
Author(s):  
Rafet Ozay ◽  
Ertugrul Uzar ◽  
Abit Aktas ◽  
Mehtap Erkmen Uyar ◽  
Bora Gürer ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Peripheral Neuropathy ◽  
Inflammatory Response ◽  
High Fat Diet ◽  
High Fat

scholarly journals Impact of high-fat diet on lifespan, metabolism, fecundity and behavioral senescence in Drosophila

2020 ◽  
Author(s):  
Sifang Liao ◽  
Mirjam Amcoff ◽  
Dick R. Nässel
Keyword(s):  
Body Mass ◽  
High Fat Diet ◽  
Normal Diet ◽  
Long Term Effects ◽  
High Fat ◽  
Adipokinetic Hormone ◽  
Age Related ◽  
Lipid Stores ◽  
And Behavior

AbstractExcess consumption of high-fat diet (HFD) is likely to result in obesity and increases the predisposition to associated health disorders. Drosophila melanogaster has emerged as an important model to study the effects of HFD on metabolism, gut function, behavior, and ageing. In this study, we investigated the effects of HFD on physiology and behavior of female flies at different time-points over several weeks. We found that HFD decreases lifespan, and also with age leads to accelerated decline of climbing ability in both virgins and mated flies. In virgins HFD also increased sleep fragmentation with age. Furthermore, long-term exposure to HFD results in elevated adipokinetic hormone (AKH) transcript levels and an enlarged crop with increased lipid stores. We detected no long-term effects of HFD on body mass, or levels of triacylglycerides (TAG), glycogen or glucose, although fecundity was diminished. However, one week of HFD resulted in decreased body mass and elevated TAG levels in mated flies. Finally, we investigated the role of AKH in regulating effects of HFD during aging. Both with normal diet (ND) and HFD, Akh mutant flies displayed increased longevity compared to control flies. However, both mutants and controls showed shortened lifespan on HFD compared to ND. In flies exposed to ND, fecundity is decreased in Akh mutants compared to controls after one week, but increased after three weeks. However, HFD leads to a similar decrease in fecundity in both genotypes after both exposure times. Thus, long-term exposure to HFD increases AKH signaling, impairs lifespan and fecundity and augments age-related behavioral senescence.

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