scholarly journals Mitochondrial Function, Mobility and Lifespan Are Improved in Drosophila melanogaster by Extracts of 9-cis-β-Carotene from Dunaliella salina

Marine Drugs ◽  
2019 ◽  
Vol 17 (5) ◽  
pp. 279 ◽  
Author(s):  
Tobias Weinrich ◽  
Yanan Xu ◽  
Chiziezi Wosu ◽  
Patricia J. Harvey ◽  
Glen Jeffery
Keyword(s):  
Drosophila Melanogaster ◽  
Mitochondrial Function ◽  
Dunaliella Salina ◽  
Whole Body ◽  
Biological Impact ◽  
Atp Production ◽  
Beneficial Effects ◽  
Positive Effects ◽  
Age Related ◽  
Β Carotene

Carotenoids are implicated in alleviating ageing and age-related diseases in humans. While data from different carotenoids are mixed in their outcomes, those for 9-cis-β-carotene indicate general positive effects, although basic data on its biological impact are limited. Here, we show that supplementation with 9-cis-β-carotene in ageing Drosophila melanogaster improved mitochondrial function in terms of ATP production and whole-body respiration and extended mean lifespan. It also resulted in improved mobility. These data provide a potential biological rational for the beneficial effects of dietary supplementation with 9-cis-β-carotene. These effects may be based on the maintenance of a sound mitochondrial function.

scholarly journals Loxl2 is a mediator of cardiac aging in Drosophila melanogaster; genetically examining the role of aging clock genes

2021 ◽  
Author(s):  
Mark J Bouska ◽  
Hua Bai
Keyword(s):  
Drosophila Melanogaster ◽  
Clock Genes ◽  
Turning Points ◽  
Whole Body ◽  
Specific Gene ◽  
Age Related ◽  
Human Orthologs ◽  
Age Range ◽  
Transcriptional Target

Abstract Transcriptomic, proteomic, and methylation aging clocks demonstrate that aging has a predictable preset program, while Transcriptome Trajectory Turning Points indicate that the 20 to 40 age range in humans is the likely stage at which the progressive loss of homeostatic control, and in turn aging, begins to have detrimental effects. Turning points in this age range overlapping with human aging clock genes revealed five candidates that we hypothesized could play a role in aging or age-related physiological decline. To examine these gene’s effects on lifespan and health-span, we utilized whole body and heart specific gene knockdown of human orthologs in Drosophila melanogaster. Whole body Loxl2, fz3, and Glo1 RNAi positively affected lifespan as did heart-specific Loxl2 knockdown. Loxl2 inhibition concurrently reduced age-related cardiac arrythmia and collagen (Pericardin) fiber width. Loxl2 binds several transcription factors in humans and RT-qPCR confirmed that a conserved transcriptional target CDH1 (Drosophila CadN2), has expression levels which correlate with Loxl2 reduction in Drosophila. These results point to conserved pathways and multiple mechanisms by which inhibition of Loxl2 can be beneficial to heart health and organismal aging.

scholarly journals Relevance of Whole-Body Vibration Exercises on Muscle Strength/Power and Bone of Elderly Individuals

Dose-Response ◽  
2018 ◽  
Vol 16 (4) ◽  
pp. 155932581881306 ◽  
Author(s):  
Debra Bemben ◽  
Christina Stark ◽  
Redha Taiar ◽  
Mario Bernardo-Filho
Keyword(s):  
Muscle Strength ◽  
Whole Body Vibration ◽  
Functional Independence ◽  
Whole Body ◽  
Mineral Density ◽  
Timed Up And Go ◽  
Elderly Individuals ◽  
Body Vibration ◽  
Positive Effects ◽  
Age Related

Beneficial effects are associated with whole-body vibration exercises (WBVEs). Increases in muscular strength/power, flexibility, and gait speed; improvements in bone mineral density, balance, and the quality of life; and decreased pain and risk of falls are reported. The aim is to present a review about the importance of WBVE for elderly individuals, considering clinical studies and meta-analyses, on bone and muscle strength/power. There is evidence supporting beneficial effect of WBVE in postmenopausal women (PW); however, effects in PW with osteoporosis are unclear. Age-related decrease in muscle mass and function contribute to undesirable health conditions, including death risk. The WBVEs improve muscle strength/power, functional independence measure, balance, and various fall risk factors, and mobility, measured by Timed Up and Go test, increased significantly after WBVE. An explanation for the absence of positive effects in some outcomes could be related to discrepancies in WBVE protocols as well as the populations tested. It is concluded that WBVE is effective for counteracting the loss of muscle strength associated with sarcopenia in elderly individuals. Balance and leg and plantar flexor strength improvements due to WBV indicate benefit to reduce risk and incidence of falls, frailty, and fracture risks. However, long-term feasibility of WBVE for musculoskeletal and bone health in elderly individuals needs further investigation.

scholarly journals SREBP-1c-Dependent Metabolic Remodeling of White Adipose Tissue by Caloric Restriction

2018 ◽  
Vol 19 (11) ◽  
pp. 3335 ◽  
Author(s):  
Masaki Kobayashi ◽  
Namiki Fujii ◽  
Takumi Narita ◽  
Yoshikazu Higami
Keyword(s):  
Adipose Tissue ◽  
Caloric Restriction ◽  
White Adipose Tissue ◽  
Regulatory Element ◽  
Whole Body ◽  
Peroxisome Proliferator ◽  
Master Regulator ◽  
Beneficial Effects ◽  
Age Related ◽  
Metabolic Remodeling

Caloric restriction (CR) delays the onset of many age-related pathophysiological changes and extends lifespan. White adipose tissue (WAT) is not only a major tissue for energy storage, but also an endocrine tissue that secretes various adipokines. Recent reports have demonstrated that alterations in the characteristics of WAT can impact whole-body metabolism and lifespan. Hence, we hypothesized that functional alterations in WAT may play important roles in the beneficial effects of CR. Previously, using microarray analysis of WAT from CR rats, we found that CR enhances fatty acid (FA) biosynthesis, and identified sterol regulatory element-binding protein 1c (SREBP-1c), a master regulator of FA synthesis, as a mediator of CR. These findings were validated by showing that CR failed to upregulate factors involved in FA biosynthesis and to extend longevity in SREBP-1c knockout mice. Furthermore, we revealed that SREBP-1c is implicated in CR-associated mitochondrial activation through the upregulation of peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α), a master regulator of mitochondrial biogenesis. Notably, these CR-associated phenotypes were observed only in WAT. We conclude that CR induces SREBP-1c-dependent metabolic remodeling, including the enhancement of FA biosynthesis and mitochondrial activation, via PGC-1α in WAT, resulting in beneficial effects.

scholarly journals Impact of Silibinin A on Bioenergetics in PC12APPsw Cells and Mitochondrial Membrane Properties in Murine Brain Mitochondria

Antioxidants ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 1520
Author(s):  
Carsten Esselun ◽  
Bastian Bruns ◽  
Stephanie Hagl ◽  
Rekha Grewal ◽  
Gunter P. Eckert
Keyword(s):  
Mitochondrial Dysfunction ◽  
Mitochondrial Function ◽  
Mitochondrial Membrane ◽  
Brain Mitochondria ◽  
Membrane Properties ◽  
Protective Effects ◽  
Positive Effects ◽  
Atp Levels ◽  
Age Related ◽  
Murine Brain

Introduction: Age-related multifactorial diseases, such as the neurodegenerative Alzheimer’s disease (AD), still remain a challenge to today’s society. One mechanism associated with AD and aging in general is mitochondrial dysfunction (MD). Increasing MD is suggested to trigger other pathological processes commonly associated with neurodegenerative diseases. Silibinin A (SIL) is the main bioactive compound of the Silymarin extract from the Mediterranean plant Silybum marianum (L.) (GAERTN/Compositae). It is readily available as a herbal drug and well established in the treatment of liver diseases as a potent radical scavenger reducing lipid peroxidation and stabilize membrane properties. Recent data suggest that SIL might also act on neurological changes related to MD. Methods: PC12APPsw cells produce low levels of human Aβ and thus act as a cellular model of early AD showing changed mitochondrial function. We investigated whether SIL could affect mitochondrial function by measuring ATP, MMP, as well as respiration, mitochondrial mass, cellular ROS and lactate/pyruvate concentrations. Furthermore, we investigated its effects on the mitochondrial membrane parameters of swelling and fluidity in mitochondria isolated from the brains of mice. Results: In PC12APPsw cells, SIL exhibits strong protective effects by rescuing MMP and ATP levels from SNP-induced mitochondrial damage and improving basal ATP levels. However, SIL did not affect mitochondrial respiration and mitochondrial content. SIL significantly reduced cellular ROS and pyruvate concentrations. Incubation of murine brain mitochondria with SIL significantly reduces Ca2+ induced swelling and improves membrane fluidity. Conclusions: Although OXPHOS activity was unaffected at this early stage of a developing mitochondrial dysfunction, SIL showed protective effects on MMP, ATP- after SNP-insult and ROS-levels in APPsw-transfected PC12 cells. Results from experiments with isolated mitochondria imply that positive effects possibly result from an interaction of SIL with mitochondrial membranes and/or its antioxidant activity. Thus, SIL might be a promising compound to improve cellular health when changes to mitochondrial function occur.

scholarly journals Mitochondrial Aging and Age-Related Dysfunction of Mitochondria

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Dimitry A. Chistiakov ◽  
Igor A. Sobenin ◽  
Victor V. Revin ◽  
Alexander N. Orekhov ◽  
Yuri V. Bobryshev
Keyword(s):  
Mitochondrial Function ◽  
Antioxidant Defense ◽  
Mitochondrial Dynamics ◽  
Oxidative Capacity ◽  
Ros Generation ◽  
Atp Production ◽  
Age Related ◽  
Related Phenotype ◽  
Age Dependent ◽  
Aged Subjects

Age-related changes in mitochondria are associated with decline in mitochondrial function. With advanced age, mitochondrial DNA volume, integrity and functionality decrease due to accumulation of mutations and oxidative damage induced by reactive oxygen species (ROS). In aged subjects, mitochondria are characterized by impaired function such as lowered oxidative capacity, reduced oxidative phosphorylation, decreased ATP production, significant increase in ROS generation, and diminished antioxidant defense. Mitochondrial biogenesis declines with age due to alterations in mitochondrial dynamics and inhibition of mitophagy, an autophagy process that removes dysfunctional mitochondria. Age-dependent abnormalities in mitochondrial quality control further weaken and impair mitochondrial function. In aged tissues, enhanced mitochondria-mediated apoptosis contributes to an increase in the percentage of apoptotic cells. However, implementation of strategies such as caloric restriction and regular physical training may delay mitochondrial aging and attenuate the age-related phenotype in humans.

scholarly journals Exercise rescues mitochondrial coupling in aged skeletal muscle: a comparison of different modalities in preventing sarcopenia

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Colin Harper ◽  
Venkatesh Gopalan ◽  
Jorming Goh
Keyword(s):  
Skeletal Muscle ◽  
Mitochondrial Function ◽  
Fiber Type ◽  
Skeletal Muscle Function ◽  
Atp Production ◽  
Muscle Aging ◽  
Age Related ◽  
Key Factor ◽  
Underlying Mechanisms ◽  
Skeletal Muscle Aging

AbstractSkeletal muscle aging is associated with a decline in motor function and loss of muscle mass- a condition known as sarcopenia. The underlying mechanisms that drive this pathology are associated with a failure in energy generation in skeletal muscle, either from age-related decline in mitochondrial function, or from disuse. To an extent, lifelong exercise is efficacious in preserving the energetic properties of skeletal muscle and thus may delay the onset of sarcopenia. This review discusses the cellular and molecular changes in skeletal muscle mitochondria during the aging process and how different exercise modalities work to reverse these changes. A key factor that will be described is the efficiency of mitochondrial coupling—ATP production relative to O2 uptake in myocytes and how that efficiency is a main driver for age-associated decline in skeletal muscle function. With that, we postulate the most effective exercise modality and protocol for reversing the molecular hallmarks of skeletal muscle aging and staving off sarcopenia. Two other concepts pertinent to mitochondrial efficiency in exercise-trained skeletal muscle will be integrated in this review, including- mitophagy, the removal of dysfunctional mitochondrial via autophagy, as well as the implications of muscle fiber type changes with sarcopenia on mitochondrial function.

A ketogenic diet combined with exercise alters mitochondrial function in human skeletal muscle while improving metabolic health

2020 ◽  
Vol 319 (6) ◽  
pp. E995-E1007 ◽  
Author(s):  
Vincent J. Miller ◽  
Richard A. LaFountain ◽  
Emily Barnhart ◽  
Teryn S. Sapper ◽  
Jay Short ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Ketogenic Diet ◽  
Mitochondrial Function ◽  
Metabolic Health ◽  
Whole Body ◽  
Model Assessment ◽  
Atp Production ◽  
Ketogenic Diets ◽  
Supervised Exercise

Animal data indicate that ketogenic diets are associated with improved mitochondrial function, but human data are lacking. We aimed to characterize skeletal muscle mitochondrial changes in response to a ketogenic diet combined with exercise training in healthy individuals. Twenty-nine physically active adults completed a 12-wk supervised exercise program after self-selection into a ketogenic diet (KD, n = 15) group or maintenance of their habitual mixed diet (MD, n = 14). Measures of metabolic health and muscle biopsies (vastus lateralis) were obtained before and after the intervention. Mitochondria were isolated from muscle and studied after exposure to carbohydrate (pyruvate), fat (palmitoyl-l-carnitine), and ketone (β-hydroxybutyrate+acetoacetate) substrates. Compared with MD, the KD resulted in increased whole body resting fat oxidation ( P < 0.001) and decreased fasting insulin ( P = 0.019), insulin resistance [homeostatic model assessment of insulin resistance (HOMA-IR), P = 0.022], and visceral fat ( P < 0.001). The KD altered mitochondrial function as evidenced by increases in mitochondrial respiratory control ratio (19%, P = 0.009), ATP production (36%, P = 0.028), and ATP/H2O2 (36%, P = 0.033) with the fat-based substrate. ATP production with the ketone-based substrate was four to eight times lower than with other substrates, indicating minimal oxidation. The KD resulted in a small decrease in muscle glycogen (14%, P = 0.035) and an increase in muscle triglyceride (81%, P = 0.006). These results expand our understanding of human adaptation to a ketogenic diet combined with exercise. In conjunction with weight loss, we observed altered skeletal muscle mitochondrial function and efficiency, an effect that may contribute to the therapeutic use of ketogenic diets in various clinical conditions, especially those associated with insulin resistance.

scholarly journals Does Whole-Body Vibration Treatment Make Children’s Bones Stronger?

2020 ◽  
Vol 18 (5) ◽  
pp. 471-479 ◽  
Author(s):  
Diana Swolin-Eide ◽  
Per Magnusson
Keyword(s):  
Bone Mass ◽  
Whole Body Vibration ◽  
Whole Body ◽  
Activity Levels ◽  
Body Vibration ◽  
Motor Disabilities ◽  
Beneficial Effects ◽  
Positive Effects ◽  
Severe Motor ◽  
Pediatric Populations

Abstract Purpose of Review To summarize the last 10 years of literature regarding the effects of whole-body vibration (WBV) on bone in children, and if WBV results in increased bone acquisition. Recent Findings WBV intervention appears to be a safe intervention with beneficial effects on bone mass in some diseases and syndromes, but there is still low evidence for WBV in clinical practice. The positive effects on muscle strength, balance, and walking speed are more conclusive. One of the takeaways of this review is that well-trained individuals may not further improve bone mass with WBV; thus, interventions are more beneficial in pediatric individuals with Down syndrome or severe motor disabilities with low bone mass and reduced activity levels. Summary WBV appears to be a safe non-pharmacological anabolic approach to increase bone mass in some pediatric populations; however, longer (> 6 months) and larger prospective studies are needed to elucidate the efficacy of WBV on bone health in young individuals.

Endothelial cells maintain a reduced redox environment even as mitochondrial function declines

2002 ◽  
Vol 283 (6) ◽  
pp. C1675-C1686 ◽  
Author(s):  
Ricarda Carlisle ◽  
Carol Ann Rhoads ◽  
Tak Yee Aw ◽  
Lynn Harrison
Keyword(s):  
Endothelial Cells ◽  
Oxygen Consumption ◽  
Genomic Instability ◽  
Mitochondrial Function ◽  
Replicative Senescence ◽  
Umbilical Vein ◽  
Nuclear Genome ◽  
Mitochondrial Mass ◽  
Atp Production ◽  
Age Related

Human umbilical vein endothelial cells (HUVECs) are an endothelial model of replicative senescence. Oxidative stress, possibly due to dysfunctional mitochondria, is believed to play a key role in replicative senescence and atherosclerosis, an age-related vascular disease. In this study, we determined the effect of cell division on genomic instability, mitochondrial function, and redox status in HUVECs that were able to replicate for ∼60 cumulative population doublings (CPD). After 20 CPD, the nuclear genome deteriorated and the protein content of the cell population increased. This indicated an increase in cell size, which was accompanied by an increase in oxygen consumption, ATP production, and mitochondrial genome copy number and ∼10% increase in mitochondrial mass. The antioxidant capacity increased, as seen by an increase in reduced glutathione, glutathione peroxidase, GSSG reductase, and glucose-6-phosphate dehydrogenase. However, by CPD 52, the latter two enzymes decreased, as well as the ratio of mitochondrial-to-nuclear genome copies, the mitochondrial mass, and the oxygen consumption per milligram of protein. Our results signify that HUVECs maintain a highly reducing (GSH) environment as they replicate despite genomic instability and loss of mitochondrial function.

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