scholarly journals A high‐fat diet impairs mitochondrial biogenesis, mitochondrial dynamics, and the respiratory chain complex in rat myocardial tissues

2018 ◽  
Vol 119 (11) ◽  
pp. 9602-9602 ◽  
Author(s):  
Dan Chen ◽  
Xia Li ◽  
LiTing Zhang ◽  
Mei Zhu ◽  
Ling Gao
Keyword(s):  
Respiratory Chain ◽  
Mitochondrial Biogenesis ◽  
High Fat Diet ◽  
Mitochondrial Dynamics ◽  
Chain Complex ◽  
Respiratory Chain Complex ◽  
High Fat

scholarly journals Low-Intensity Exercise Training Additionally Increases Mitochondrial Dynamics Caused by High-Fat Diet (HFD) but Has No Additional Effect on Mitochondrial Biogenesis in Fast-Twitch Muscle by HFD

2020 ◽  
Vol 17 (15) ◽  
pp. 5461
Author(s):  
Yun Seok Kang ◽  
Donghun Seong ◽  
Jae Cheol Kim ◽  
Sang Hyun Kim
Keyword(s):  
Endurance Exercise ◽  
Mitochondrial Biogenesis ◽  
High Fat Diet ◽  
Mitochondrial Dynamics ◽  
Chow Diet ◽  
Sprague Dawley ◽  
High Fat ◽  
Related Factors ◽  
Mitochondrial Dynamic ◽  
Low Intensity

This study examines how the high-fat diet (HFD) affects mitochondrial dynamics and biogenesis, and also whether combining it with low-intensity endurance exercise adds to these effects. Six 8-week-old male Sprague–Dawley (SD) rats were put on control (CON; standard chow diet), HF (HFD intake), and HFEx (HFD + low-intensity treadmill exercise) for 6 weeks. As a result, no change in body weight was observed among the groups. However, epididymal fat mass increased significantly in the two groups that had been given HFD. Blood free fatty acid (FFA) also increased significantly in the HF group. While HFD increased insulin resistance (IR), this was improved significantly in the HFEx group. HFD also significantly increased mitochondrial biogenesis-related factors (PPARδ, PGC-1α, and mtTFA) and mitochondrial electron transport chain proteins; however, no additional effect from exercise was observed. Mitochondrial dynamic-related factors were also affected: Mfn2 increased significantly in the HFEx group, while Drp1 and Fis-1 increased significantly in both the HF and HFEx groups. The number of mitochondria in the subsarcolemmal region, and their size in the subsarcolemmal and intermyofibrillar regions, also increased significantly in the HFEx group. Taken overall, these results show that HFD in combination with low-intensity endurance exercise has no additive effect on mitochondrial biogenesis, although it does have such an effect on mitochondrial dynamics by improving IR.

scholarly journals Identification of novel genes involved in apoptosis of HIV-infected macrophages using unbiased genome-wide screening

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Simon X. M. Dong ◽  
Frederick S. Vizeacoumar ◽  
Kalpana K. Bhanumathy ◽  
Nezeka Alli ◽  
Cristina Gonzalez-Lopez ◽  
...  
Keyword(s):  
T Cells ◽  
Hiv Infection ◽  
Respiratory Chain ◽  
Cd4 T Cells ◽  
Chain Complex ◽  
Respiratory Chain Complex ◽  
Complex Ii ◽  
Genome Wide ◽  
Latently Infected ◽  
Induced Apoptosis

Abstract Background Macrophages, besides resting latently infected CD4+ T cells, constitute the predominant stable, major non-T cell HIV reservoirs. Therefore, it is essential to eliminate both latently infected CD4+ T cells and tissue macrophages to completely eradicate HIV in patients. Until now, most of the research focus is directed towards eliminating latently infected CD4+ T cells. However, few approaches have been directed at killing of HIV-infected macrophages either in vitro or in vivo. HIV infection dysregulates the expression of many host genes essential for the survival of infected cells. We postulated that exploiting this alteration may yield novel targets for the selective killing of infected macrophages. Methods We applied a pooled shRNA-based genome-wide approach by employing a lentivirus-based library of shRNAs to screen novel gene targets whose inhibition should selectively induce apoptosis in HIV-infected macrophages. Primary human MDMs were infected with HIV-eGFP and HIV-HSA viruses. Infected MDMs were transfected with siRNAs specific for the promising genes followed by analysis of apoptosis by flow cytometry using labelled Annexin-V in HIV-infected, HIV-exposed but uninfected bystander MDMs and uninfected MDMs. The results were analyzed using student’s t-test from at least four independent experiments. Results We validated 28 top hits in two independent HIV infection models. This culminated in the identification of four target genes, Cox7a2, Znf484, Cstf2t, and Cdk2, whose loss-of-function induced apoptosis preferentially in HIV-infected macrophages. Silencing these single genes killed significantly higher number of HIV-HSA-infected MDMs compared to the HIV-HSA-exposed, uninfected bystander macrophages, indicating the specificity in the killing of HIV-infected macrophages. The mechanism governing Cox7a2-mediated apoptosis of HIV-infected macrophages revealed that targeting respiratory chain complex II and IV genes also selectively induced apoptosis of HIV-infected macrophages possibly through enhanced ROS production. Conclusions We have identified above-mentioned novel genes and specifically the respiratory chain complex II and IV genes whose silencing may cause selective elimination of HIV-infected macrophages and eventually the HIV-macrophage reservoirs. The results highlight the potential of the identified genes as targets for eliminating HIV-infected macrophages in physiological environment as part of an HIV cure strategy.

scholarly journals NAD + repletion produces no therapeutic effect in mice with respiratory chain complex III deficiency and chronic energy deprivation

2018 ◽  
Vol 32 (11) ◽  
pp. 5913-5926 ◽  
Author(s):  
Janne Purhonen ◽  
Jayasimman Rajendran ◽  
Saara Tegelberg ◽  
Olli-Pekka Smolander ◽  
Eija Pirinen ◽  
...  
Keyword(s):  
Therapeutic Effect ◽  
Respiratory Chain ◽  
Chain Complex ◽  
Complex Iii ◽  
Respiratory Chain Complex ◽  
Energy Deprivation

scholarly journals Dietary supplementation with fish oil alters the expression levels of proteins governing mitochondrial dynamics and prevents high-fat diet-induced endothelial dysfunction

2014 ◽  
Vol 112 (2) ◽  
pp. 145-153 ◽  
Author(s):  
Ruifang Sun ◽  
Xiaoming Wang ◽  
Yan Liu ◽  
Min Xia
Keyword(s):  
Endothelial Cell ◽  
Fish Oil ◽  
High Fat Diet ◽  
Mitochondrial Dynamics ◽  
Atherosclerotic Lesion ◽  
Partial Replacement ◽  
Lesion Volume ◽  
High Fat ◽  
Endothelial Cell Function ◽  
Expression Levels

Diets supplemented with fish oil (FO), which is rich in n-3 PUFA, have been shown to modify several key risk factors for CVD. The purpose of the present study was to determine the effect of FO supplementation on mitochondrial dynamic protein expression in the endothelium and on endothelial cell function. Male apoE-deficient (apoE− / −) mice (8 weeks old, n 12 per group) were fed a high-fat diet containing 45 % fat (HFD group) or a HFD with partial replacement of lard with 10 % (w/w) FO (FO group) (total EPA and DHA content 64·1 g/kg) for 8 weeks. ApoE− / − mice in the FO group had a greater endothelium-dependent vasorelaxation response to acetylcholine (Ach) than those in the HFD group. The atherosclerotic lesion volume in the aortic sinus of mice in the FO group was 54 % lower than that in the HFD group (P< 0·01). In addition, the aortas isolated from mice in the FO group had higher expression levels of Mfn2 and Opa1 but lower expression levels of Fis1 than those from the HFD group. Compared with mice fed the HFD, those fed the FO diet showed significantly lower levels of mitochondrial oxidative stress, cytochrome c release and caspase-3 activity (each P< 0·05). Furthermore, FO-fed mice displayed increased NO release and availability and enhanced endothelial NO synthase activity compared with HFD-fed mice. Taken together, these results reveal a novel mechanism by which FO protects against endothelial cell dysfunction, which may result in improved mitochondrial dynamics.

scholarly journals The NADH-binding subunit of respiratory chain complex I is nuclear-encoded in plants and identified only in mitochondria

1996 ◽  
Vol 10 (5) ◽  
pp. 793-803 ◽  
Author(s):  
Lutz Grohmann ◽  
Allan G. Rasmusson ◽  
Volker Heiser ◽  
Oliver Thieck ◽  
Axel Brennicke
Keyword(s):  
Respiratory Chain ◽  
Complex I ◽  
Chain Complex ◽  
Respiratory Chain Complex ◽  
Binding Subunit
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