Early adaptive response of the retina to a pro-diabetogenic diet: Impairment of cone response and gene expression changes in high-fructose fed rats

2015 ◽  
Vol 135 ◽  
pp. 37-46 ◽  
Author(s):  
Magalie Thierry ◽  
Bruno Pasquis ◽  
Bénédicte Buteau ◽  
Cynthia Fourgeux ◽  
Doulaye Dembele ◽  
...  
Keyword(s):  
Gene Expression ◽  
Adaptive Response ◽  
High Fructose ◽  
Cone Response

scholarly journals Effects of Exercise Training on Molecular Markers of Lipogenesis and Lipid Partitioning in Fructose-Induced Liver Fat Accumulation

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Siham Yasari ◽  
Denis Prud'homme ◽  
Frédérique Tesson ◽  
Marek Jankowski ◽  
Jolanta Gutkowska ◽  
...  
Keyword(s):  
Gene Expression ◽  
Exercise Training ◽  
Unsaturated Fatty Acids ◽  
Regulatory Element ◽  
Female Rats ◽  
Liver Fat ◽  
Standard Diet ◽  
Fat Accumulation ◽  
High Fructose ◽  
The Impact

The present study was designed to investigate the impact of exercise training on lipogenic gene expression in liver and lipid partitioning following the ingestion of a high fructose load. Female rats were exercise-trained for 8 wk or kept sedentary before being submitted to a fasting/refeeding protocol. Rats were further subdivided as follow: rats were fasted for 24 h, refed a standard diet for 24 h, starved for another 24 h, and refed with a standard or a high-fructose diet 24 h before sacrifice. Fructose refeeding was associated with an increase in hepatic lipid content, endocannabinoid receptor 1, sterol regulatory element-binding protein1c, and stearoyl-CoA desaturase1 gene expression in both Sed and TR rats. However, desaturation indexes measured in liver (C16 : 1/C16 : 0 and C18 : 1/C18 : 0) and plasma (C18 : 1/C18 : 0) were higher (P<0.01) in TR than in Sed rats following fructose refeeding. It is concluded that exercise training does not significantly affect fat accumulation and the molecular expression of genes involved in lipogenesis after fasting and fructose refeeding but does modify the partitioning of lipids so as to provide more unsaturated fatty acids in liver without affecting liver fat content.

scholarly journals A ‘phenotypic hangover’ – the predictive adaptive response and multigenerational effects of altered nutrition on the transcriptome of Drosophila melanogaster

2017 ◽  
Author(s):  
Amy J. Osborne ◽  
Peter K. Dearden
Keyword(s):  
Gene Expression ◽  
Drosophila Melanogaster ◽  
Adaptive Response ◽  
Communicable Disease ◽  
Later Life ◽  
Standard Diet ◽  
Expression Of Genes ◽  
Postnatal Environment ◽  
Predictive Adaptive Response ◽  
Epigenetic Processes

AbstractThe Developmental Origins of Health and Disease (DOHaD) hypothesis predicts that early-life environmental exposures can be detrimental to later-life health, and that mismatch between the pre- and postnatal environment may contribute to the growing non-communicable disease (NCD) epidemic. Within this is an increasingly recognised role for epigenetic mechanisms; epigenetic modifications can be influenced by, e.g., nutrition, and can alter gene expression in mothers and offspring. Currently, there are no whole-genome transcriptional studies of response to nutritional alteration. Thus, we sought to explore how nutrition affects the expression of genes involved in epigenetic processes in Drosophila melanogaster. We manipulated Drosophila food macronutrient composition at the F0 generation, mismatched F1 offspring back to a standard diet, and analysed the transcriptome of the F0 – F3 generations by RNA-sequencing. At F0, the altered (high protein, low carbohydrate, HPLC) diet increased expression of genes involved in epigenetic processes, with coordinated downregulation of genes involved in immunity, neurotransmission and neurodevelopment, oxidative stress and metabolism. Upon reversion to standard nutrition, mismatched F1 and F2 generations displayed multigenerational inheritance of altered gene expression. By the F3 generation, gene expression had reverted to F0 (matched) levels. These nutritionally-induced gene expression changes demonstrate that dietary alteration can upregulate epigenetic genes, which may influence the expression of genes with broad biological functions. Further, the multigenerational inheritance of the gene expression changes in F1 and F2 mismatched generations suggests a predictive adaptive response (PAR) to maternal nutrition. Our findings may help to understand the interaction between maternal diet and future offspring health, and have direct implications for the current NCD epidemic.

scholarly journals Mechanisms of short-term and long-term adaptation

2020 ◽  
pp. 77-86
Author(s):  
Н.Б. Панкова
Keyword(s):  
Gene Expression ◽  
Epigenetic Regulation ◽  
Adaptive Response ◽  
Educational Environment ◽  
Stress Factors ◽  
Short Term ◽  
Functional Reserve ◽  
Short Term Adaptation ◽  
Expression Program

В лекции рассмотрены общие представления об адаптации, основанные на классических работах Г. Селье, Ф.З. Меерсона, Н.А. Агаджаняна, а также особенности адаптивного ответа развивающегося организма. Рассмотрены механизмы срочной адаптации как мобилизации функциональных резервов организма. В качестве одного из механизмов долговременной адаптации представлена эпигенетическая регуляция, которая позволяет выбрать и реализовать программу экспрессии генов - в соответствии с этапом онтогенетического развития, или средовым окружением. В качестве ещё одного механизма долговременной адаптации рассмотрено воздействие на генетический материал. Приведены примеры формирования адаптивного ответа организма на физико-химические и климатогеографические стрессорные факторы. Отдельно проанализированы механизмы адаптивного ответа организма детей на факторы образовательной среды. The lecture addresses general ideas about adaptation based on classic studies by H. Selye, F.Z. Meerson, and N.A. Agadzhanyan and features of the adaptive response in a developing body. Mobilization of the functional reserve is considered as a mechanism of short-term adaptation. Epigenetic regulation is presented as one of mechanisms for long-term adaptation, which allows selecting and implementing a gene expression program consistent with the stage of ontogenetic development or the environment. Another mechanism of long-term adaptation is influence on the genome. The lecture provides examples of adaptation to physicochemical and climatic geographical stress factors. Mechanisms of the adaptive response to factors of the educational environment in children are analyzed separately.

Curcumin ameliorates protein expression changes involved in mitochondrial fatty acids metabolism in heart of mice fed a high-fructose diet

2020 ◽  
Author(s):  
Cecilia Gabriela Meléndez-Salcido ◽  
Katya Vargas-Ortiz ◽  
Oscar Gerardo Silva-Gaona ◽  
María Cristina León-García ◽  
Luz Arcelia Ortega-Hernández ◽  
...  
Keyword(s):  
Gene Expression ◽  
Fatty Acids ◽  
Beneficial Effect ◽  
Therapeutic Potential ◽  
Cardiometabolic Disease ◽  
Control Group ◽  
Standard Diet ◽  
High Fructose Diet ◽  
High Fructose ◽  
Fatty Acids Metabolism

Abstract Background: It has been proposed that curcumin modulates the gene expression of different signaling pathways, improve the fatty acids metabolism and exerts a potential beneficial effect on cardiometabolic disease, but this has not been thoroughly demonstrated. In the present study, we evaluated the effect of curcumin upon the expression of PPARα, CPT1, MCAD, VLCAD and ACAA2 in heart of mice fed a high-fructose diet (HFD). Methods: Twenty-four mice C57BL/6 were divided into four groups (n=6) and treated for 15 weeks. Control group (C) received standard diet (SD), Curcumin group (C+Cur), Fructose group (F) and Fructose with Curcumin group (F+Cur). The groups were treated with 0.75% w/w curcumin mixed in the SD and 30% w/v fructose in water, respectively. Heart proteins expression were analyzed by Western Blot. Results: Curcumin supplementation increased PPARα and ACAA2 expression and decreased CPT1 and MCAD expression in heart of mice fed a HFD. However, it did not modify the VLCAD expression. Conclusions: Curcumin regulated PPARα, CPT1 and MCAD expression and increased ACAA2 expression; suggesting a therapeutic potential in the prevention of alterations in mitochondrial fatty acids metabolism in heart of mice fed a HFD.

Dietary carbohydrates as a means to prevent obesity and adipose tissue inflammation

2020 ◽  
Vol 79 (OCE2) ◽  
Author(s):  
Ellen Vercalsteren ◽  
Christine Vranckx ◽  
Liesbeth Frederix ◽  
Max Gooijen ◽  
Ilse Scroyen
Keyword(s):  
Gene Expression ◽  
Body Weight ◽  
Adipose Tissue ◽  
Plasma Cholesterol ◽  
Inflammatory Cells ◽  
Mannose Receptor ◽  
Foxp3 Expression ◽  
Blood Stream ◽  
Dietary Carbohydrates ◽  
High Fructose

AbstractWhen obesity arises, adipose tissue (AT) expands and shifts to an influx of pro-inflammatory cells, leading to a state of chronic AT-inflammation.Furthermore, a western diet (WD) modulates the gut microbiome, increasing intestinal permeability. This facilitates the translocation of endotoxins and even entire bacteria into the blood stream, further contributing to the pro-inflammatory state. Even though it is evident a WD, high in fat and carbohydrates (CHO), can cause AT-inflammation, it is still unclear if fat or CHO is the main inducer. Therefore, we are currently investigating the effect of different CHO-types on AT-inflammation.During 15 weeks, male C57BL/6JRj mice were kept on several diets, consisting of high-fructose (HFRD), high-sucrose-high-fructose (HCFD), high-starch (HSTD) or a WD (n = 10 per group). Weekly monitoring of body weight and food intake was followed by analyses of visceral AT-inflammation. Kruskal-wallis tests were used for statistical analysis.Mice on HSTD and HCD had gained significantly less body weight compared to mice on WD after 15 weeks of diet. Mice on HSTD also gained significantly less body weight compared to mice on HFRD and HCFD. Moreover, mice on HSTD and HCD also had significantly smaller AT-depots as compared to mice on WD. Total plasma cholesterol as well as HDL and LDL levels were significantly lower in mice on HSTD and on HCD as compared to mice on WD. Gene expression analysis revealed a significantly lower expression of several pro-inflammatory markers (F4/80, Arg1, Mannose receptor, TNF, MCP1 and Saa3) in AT of mice on HSTD and on HCD compared to a WD. A HSTD also induced lower AT-expression of MCP1 and Saa3 than a HCFD and Saa3 expression was also significantly lower in the HSTD-group compared to the HFRD-group. Furthermore, Foxp3 expression, a marker for anti-inflammatory Treg cells, was significantly increased in AT of all CHO-diet fed mice as compared to the WD-group.In conclusion, these data suggest that certain dietary carbohydrates, in contrast to a WD, do not induce obesity or AT-inflammation, including lower gene expression of Saa3. It is stated that a WD induces Saa3 expression not only in AT, but also in the colon. Furthermore, since Saa3 is able to bind bacteria and is associated with inflammation, further research is necessary to investigate Saa3 as a possible link between disturbances in the gut microbiota and AT-inflammation.

Adrenergic induction of bimodal myocardial protection: signal transduction and cardiac gene reprogramming

1999 ◽  
Vol 276 (5) ◽  
pp. R1525-R1533 ◽  
Author(s):  
Xianzhong Meng ◽  
Brian D. Shames ◽  
Edward J. Pulido ◽  
Daniel R. Meldrum ◽  
Lihua Ao ◽  
...  
Keyword(s):  
Gene Expression ◽  
Signal Transduction ◽  
Adaptive Response ◽  
Ischemia Reperfusion ◽  
Functional Adaptation ◽  
Immunofluorescent Staining ◽  
Northern Analysis ◽  
Cardiac Gene Expression ◽  
Cardiac Gene

This study tested the hypothesis that in vivo norepinephrine (NE) treatment induces bimodal cardiac functional protection against ischemia and examined the roles of α1-adrenoceptors, protein kinase C (PKC), and cardiac gene expression in cardiac protection. Rats were treated with NE (25 μg/kg iv). Cardiac functional resistance to ischemia-reperfusion (25/40 min) injury was examined 30 min and 1, 4, and 24 h after NE treatment with the Langendorff technique, and effects of α1-adrenoceptor antagonism and PKC inhibition on the protection were determined. Northern analysis was performed to examine cardiac expression of mRNAs encoding α-actin and myosin heavy chain (MHC) isoforms. Immunofluorescent staining was performed to localize PKC-βI in the ventricular myocardium. NE treatment improved postischemic functional recovery at 30 min, 4 h, and 24 h but not at 1 h. Pretreatment with prazosin or chelerythrine abolished both the early adaptive response at 30 min and the delayed adaptive response at 24 h. NE treatment induced intranuclear translocation of PKC-βI in cardiac myocytes at 10 min and increased skeletal α-actin and β-MHC mRNAs in the myocardium at 4–24 h. These results demonstrate that in vivo NE treatment induces bimodal myocardial functional adaptation to ischemia in a rat model. α1-Adrenoceptors and PKC appear to be involved in signal transduction for inducing both the early and delayed adaptive responses. The delayed adaptive response is associated with the expression of cardiac genes encoding fetal contractile proteins, and PKC-βI may transduce the signal for reprogramming of cardiac gene expression.

scholarly journals Phosphorylcholine Phosphatase: A Peculiar Enzyme of Pseudomonas aeruginosa

2011 ◽  
Vol 2011 ◽  
pp. 1-12 ◽  
Author(s):  
Carlos Eduardo Domenech ◽  
Lisandro Horacio Otero ◽  
Paola Rita Beassoni ◽  
Angela Teresita Lisa
Keyword(s):  
Gene Expression ◽  
Pseudomonas Aeruginosa ◽  
Adaptive Response ◽  
Metal Ion ◽  
Coordination Geometry ◽  
Choline Metabolism ◽  
Inhibitory Site ◽  
Closed Structure ◽  
Phosphorylcholine Phosphatase ◽  
Hydrolysis Of

Pseudomonas aeruginosa synthesizes phosphorylcholine phosphatase (PchP) when grown on choline, betaine, dimethylglycine or carnitine. In the presence of Mg2+ or Zn2+, PchP catalyzes the hydrolysis of p-nitrophenylphosphate (p-NPP) or phosphorylcholine (Pcho). The regulation of pchP gene expression is under the control of GbdR and NtrC; dimethylglycine is likely the metabolite directly involved in the induction of PchP. Therefore, the regulation of choline metabolism and consequently PchP synthesis may reflect an adaptive response of P. aeruginosa to environmental conditions. Bioinformatic and biochemistry studies shown that PchP contains two sites for alkylammonium compounds (AACs): one in the catalytic site near the metal ion-phosphoester pocket, and another in an inhibitory site responsible for the binding of the alkylammonium moiety. Both sites could be close to each other and interact through the residues 42E, 43E and 82YYY84. Zn2+ is better activator than Mg2+ at pH 5.0 and it is more effective at alleviating the inhibition produced by the entry of Pcho or different AACs in the inhibitory site. We postulate that Zn2+ induces at pH 5.0 a conformational change in the active center that is communicated to the inhibitory site, producing a compact or closed structure. However, at pH 7.4, this effect is not observed because to the hydrolysis of the [Zn2+L2−1L20(H2O)2] complex, which causes a change from octahedral to tetrahedral in the metal coordination geometry. This enzyme is also present in P. fluorescens, P. putida, P. syringae, and other organisms. We have recently crystallized PchP and solved its structure.

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