scholarly journals Lactobacillus paracasei PS23 decelerated age-related muscle loss by ensuring mitochondrial function in SAMP8 mice

Aging ◽  
2019 ◽  
Vol 11 (2) ◽  
pp. 756-770 ◽  
Author(s):  
Li-Han Chen ◽  
Shih-Yi Huang ◽  
Kuo-Chin Huang ◽  
Chih-Chieh Hsu ◽  
Kuen-Cheh Yang ◽  
...  
Keyword(s):  
Mitochondrial Function ◽  
Lactobacillus Paracasei ◽  
Muscle Loss ◽  
Age Related ◽  
Samp8 Mice

scholarly journals Lactobacillus paracasei PS23 Delays Progression of Age-Related Cognitive Decline in Senescence Accelerated Mouse Prone 8 (SAMP8) Mice

Nutrients ◽  
2018 ◽  
Vol 10 (7) ◽  
pp. 894 ◽  
Author(s):  
Shih-Yi Huang ◽  
Li-Han Chen ◽  
Ming-Fu Wang ◽  
Chih-Chieh Hsu ◽  
Ching-Hung Chan ◽  
...  
Keyword(s):  
Cognitive Decline ◽  
Brain Dysfunction ◽  
Lactobacillus Paracasei ◽  
Oxidative Enzymes ◽  
Control Group ◽  
Age Related ◽  
Chemotactic Protein ◽  
Age Related Cognitive Decline ◽  
Samp8 Mice ◽  
Senescence Accelerated Mouse

Probiotic supplements are potential therapeutic agents for age-related disorders due to their antioxidant and anti-inflammatory properties. However, the effect of probiotics on age-related brain dysfunction remains unclear. To investigate the effects of Lactobacillus paracasei PS23 (LPPS23) on the progression of age-related cognitive decline, male and female senescence-accelerated mouse prone 8 (SAMP8) mice were divided into two groups (n = 6 each): the control and PS23 groups. From the age of 16 weeks, these groups were given saline and LPPS23, respectively, because SAMP8 mice start aging rapidly after four months of age. After 12 weeks of treatment, we evaluated the effect of LPPS23 by analyzing their appearance, behavior, neural monoamines, anti-oxidative enzymes, and inflammatory cytokines. The PS23 group showed lower scores of senescence and less serious anxiety-like behaviors and memory impairment compared to the control group. The control mice also showed lower levels of neural monoamines in the striatum, hippocampus, and serum. Moreover, LPPS23 induced the anti-oxidative enzymes superoxide dismutase (SOD) and glutathione peroxidase (GPx). Higher levels of tumor necrosis factor (TNF)-α and monocyte chemotactic protein-1 (MCP1) and lower levels of interleukin (IL)-10 indicated that LPPS23 modulated the inflammation. Our results suggest that LPPS23 supplements could delay age-related cognitive decline, possibly by preventing oxidation and inflammation and modulating gut–brain axis communication.

scholarly journals Lactobacillus paracasei PS23 modulated the age‐related inflammation in Senescence Accelerated Mouse Prone 8 (SAMP8) mice

2019 ◽  
Vol 33 (S1) ◽  
Author(s):  
Hui‐Yu Huang ◽  
Ying‐Xu Huang ◽  
Yi‐Wen Chen ◽  
Nien‐Wei Chou ◽  
Yi‐Rong Chen ◽  
...  
Keyword(s):  
Lactobacillus Paracasei ◽  
Age Related ◽  
Samp8 Mice ◽  
Senescence Accelerated Mouse

scholarly journals An Examination of Lactobacillus paracasei GKS6 and Bifidobacterium lactis GKK2 Isolated from Infant Feces in an Aged Mouse Model

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Shih-Wei Lin ◽  
You-Shan Tsai ◽  
Yen-Lien Chen ◽  
Ming-Fu Wang ◽  
Chin-Chu Chen ◽  
...  
Keyword(s):  
Population Aging ◽  
Thiobarbituric Acid ◽  
Lactobacillus Paracasei ◽  
Aged Mouse ◽  
Bifidobacterium Lactis ◽  
Age Related ◽  
Fiber Number ◽  
Infant Feces ◽  
Muscle Fiber Number ◽  
Samp8 Mice

Supplementary which could maintain normal physiological mechanisms and functions while aging has drawn our attention due to the population aging in recent years. Probiotics have been believed with desirable properties such as antioxidation and anti-inflammatory for delaying the aging process. However, the age-related experiments conducted in the mammalian models with probiotics were few. In this study, we demonstrated the effects of administration of probiotics Lactobacillus paracasei GKS6 (GKS6) and Bifidobacterium lactis GKK2 (GKK2), respectively, at the dosage of 5.0 × 109 cfu/kg BW/day for fourteen weeks in senescence-accelerated mouse prone 8 (SAMP8) mice. The three-month-old SAMP8 mice were divided into three groups: control, mice fed with GKS6, and mice fed with GKK2. There were ten females and ten males in each group. The SAMP8 mice fed with probiotics GKS6 and GKK2 showed a significantly lower degree of aging followed by Takeda’s grading method on the eleventh week of the experiment. The GKK2 group showed significantly increased forelimb grip strength in male SAMP8 mice and muscle fiber number in both genders. Compared to the control, both GKS6 and GKK2 presented a significant increase in liver superoxide dismutase and catalase activities. In addition, a significant decrease in the levels of liver thiobarbituric acid-reactive substances was observed in the probiotics group. These results suggested that probiotics GKS6 and GKK2 could act as antioxidants in delaying the process of aging and preventing age-related muscle loss.

scholarly journals Age-­related muscle loss of the anterior and posterior thigh assessed by means of MRI/CT and ultrasound

2014 ◽  
Vol 3 (2) ◽  
pp. 47-52
Author(s):  
Takashi Abe ◽  
Jeremy P Loenneke ◽  
Robert S Thiebaud ◽  
Mark Loftin
Keyword(s):  
Muscle Loss ◽  
Posterior Thigh ◽  
Age Related

Abstract 13946: Sleep Problems on Simvastatin Differentially Predict Weight Change in Men

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Beatrice A Golomb ◽  
Hayley J Koslik ◽  
Alexis K Bui
Keyword(s):  
Young Adults ◽  
Weight Gain ◽  
Weight Change ◽  
Sleep Problems ◽  
Metabolic Effects ◽  
Muscle Loss ◽  
Relative Contribution ◽  
Age Related ◽  
Baseline Weight ◽  
Interaction Term

Background and Goal: Sleep problems were significantly increased on simvastatin ( simva ) (but not pravastatin) vs placebo in the UCSD Statin Study. Sleep problems on simva predicted glucose rise. Weight gain has also been reported as a statin side effect. We sought to capitalize on existing data to assess whether sleep problems on simva related to weight gain in men. Method: 442 men without known diabetes or CVD were randomized to simva 20mg or placebo for 6 mon. One hundred eighty and 186 completed single-item self-rating of change in sleep problems vs baseline ( Δslpprob ). Weight (lb) was measured at baseline and 6 mon. Missing 6 mon values were imputed. Analyses: A. Regressions stratified by treatment assessed prediction of weight change by Δslpprob, adjusted for baseline weight. B. Regressions assessed prediction of weight change by the interaction term of simva (vs placebo) x Δslpprob, adjusted for the components of the interaction and baseline weight. Since age-related muscle loss may complicate weight change in elderly; and young adults have low vulnerability to metabolic problems, analyses were repeated excluding these groups. Results: A. Increased sleep problems on simva predicted weight gain (significant), but on placebo predicted weight loss (nonsignificant). B. The Δslpprob x simva interaction term significantly predicted weight gain. When that was parceled out, simva, outside of the sleep relationship, negatively predicted weight change. Exclusion of young adults and elderly strengthened significance of findings (Table). Discussion: Sleep problems, which differentially arise on simva, differentially predict weight gain on simva. This expands the metabolic effects to which sleep problems on simva may contribute and might possibly favor mediation by sleep apnea (a reported complication of simva). Once the sleep problem effect is considered, simva use predicted weight loss . The relative contribution of fat vs muscle loss (vs other) requires exploration.

Exercise and Mitochondrial Function: Importance and InferenceA Mini Review

2021 ◽  
Vol 21 ◽  
Author(s):  
Vaishali K. ◽  
Nitesh Kumar ◽  
Vanishree Rao ◽  
Rakesh Krishna Kovela ◽  
Mukesh Kumar Sinha
Keyword(s):  
Skeletal Muscle ◽  
Mitochondrial Function ◽  
Skeletal Muscles ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Present Review ◽  
Age Related ◽  
Exercise Induced ◽  
Mitochondrial Adaptations

: Skeletal muscles must generate and distribute energy properly in order to function perfectly. Mitochondria in skeletal muscle cells form vast networks to meet this need, and their functions may improve as a result of exercise. In the present review, we discussed exercise-induced mitochondrial adaptations, age-related mitochondrial decline, and a biomarker as a mitochondrial function indicator and exercise interference.

The Intersection of Metformin and Inflammation

2021 ◽  
Author(s):  
Leena P. Bharath ◽  
Barbara S. Nikolajczyk
Keyword(s):  
Mitochondrial Function ◽  
Immune Cells ◽  
Immune Cell ◽  
Cell Types ◽  
Remarkable Effect ◽  
Tumor Onset ◽  
Age Related ◽  
Immune Mediated ◽  
Autoimmune Conditions ◽  
Near Term

The biguanide metformin is the most commonly used antidiabetic drug. Recent studies show that metformin not only improves chronic inflammation by improving metabolic parameters but also has a direct anti-inflammatory effect. In light of these findings, it is essential to identify the inflammatory pathways targeted by metformin to develop a comprehensive understanding of the mechanisms of action of this drug. Commonly accepted mechanisms of metformin action include AMPK activation and inhibition of mTOR pathways, which are evaluated in multiple diseases. Additionally, metformin's action on mitochondrial function and cellular homeostasis processes such as autophagy, is of particular interest because of the importance of these mechanisms in maintaining cellular health. Both dysregulated mitochondria and failure of the autophagy pathways, the latter of which impair clearance of dysfunctional, damaged, or excess organelles, affect cellular health drastically and can trigger the onset of metabolic and age-related diseases. Immune cells are the fundamental cell types that govern the health of an organism. Thus, dysregulation of autophagy or mitochondrial function in immune cells has a remarkable effect on susceptibility to infections, response to vaccination, tumor onset, and the development of inflammatory and autoimmune conditions. Here we summarize the latest research on metformin's regulation of immune cell mitochondrial function and autophagy as evidence that new clinical trials on metformin with primary outcomes related to the immune system should be considered to treat immune-mediated diseases over the near term.

scholarly journals Inhibition of 11β-HSD1 Ameliorates Cognition and Molecular Detrimental Changes after Chronic Mild Stress in SAMP8 Mice

2021 ◽  
Vol 14 (10) ◽  
pp. 1040
Author(s):  
Dolors Puigoriol-Illamola ◽  
Júlia Companys-Alemany ◽  
Kris McGuire ◽  
Natalie Z. M. Homer ◽  
Rosana Leiva ◽  
...  
Keyword(s):  
Stress Responses ◽  
Healthy Aging ◽  
Molecular Mechanisms ◽  
Chronic Mild Stress ◽  
Mild Stress ◽  
Cognitive Improvement ◽  
Age Related ◽  
Mtorc1 Signaling ◽  
Cognitive Disturbances ◽  
Samp8 Mice

Impaired glucocorticoid (GC) signaling is a significant factor in aging, stress, and neurodegenerative diseases such as Alzheimer’s disease. Therefore, the study of GC-mediated stress responses to chronic moderately stressful situations, which occur in daily life, is of huge interest for the design of pharmacological strategies toward the prevention of neurodegeneration. To address this issue, SAMP8 mice were exposed to the chronic mild stress (CMS) paradigm for 4 weeks and treated with RL-118, an 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) inhibitor. The inhibition of this enzyme is linked with a reduction in GC levels and cognitive improvement, while CMS exposure has been associated with reduced cognitive performance. The aim of this project was to assess whether RL-118 treatment could reverse the deleterious effects of CMS on cognition and behavioral abilities and to evaluate the molecular mechanisms that compromise healthy aging in SAMP8 mice. First, we confirmed the target engagement between RL-118 and 11β-HSD1. Additionally, we showed that DNA methylation, hydroxymethylation, and histone phosphorylation were decreased by CMS induction, and increased by RL-118 treatment. In addition, CMS exposure caused the accumulation of reactive oxygen species (ROS)-induced damage and increased pro-oxidant enzymes—as well as pro-inflammatory mediators—through the NF-κB pathway and astrogliosis markers, such as GFAP. Of note, these modifications were reversed by 11β-HSD1 inhibition. Remarkably, although CMS altered mTORC1 signaling, autophagy was increased in the SAMP8 RL-118-treated mice. We also showed an increase in amyloidogenic processes and a decrease in synaptic plasticity and neuronal remodeling markers in mice under CMS, which were consequently modified by RL-118 treatment. In conclusion, 11β-HSD1 inhibition through RL-118 ameliorated the detrimental effects induced by CMS, including epigenetic and cognitive disturbances, indicating that GC-excess attenuation shows potential as a therapeutic strategy for age-related cognitive decline and AD.

scholarly journals Senescent Accelerated Prone 8 (SAMP8) Mice as A Model of Age Dependent Neuroinflammation

2020 ◽  
Author(s):  
Andrés Fernández ◽  
Elena Quintana ◽  
Patricia Velasco ◽  
Belén de Andrés ◽  
Maria Luisa Gaspar ◽  
...  
Keyword(s):  
Choroid Plexus ◽  
Inflammatory Cytokines ◽  
Hippocampal Formation ◽  
Morphological Changes ◽  
Interleukin 1 ◽  
Brain Parenchyma ◽  
Age Related ◽  
Inflammatory Changes ◽  
Samp8 Mice ◽  
The Brain

Abstract Background: Aging and age related diseases are strong risk factors for the development of neurodegenerative diseases. Neuroinflammation (NIF), as the brain's immune response, plays an important role in aged associated degeneration of central nervous system (CNS). The need of animal models that will allow us to understand and modulate this process is required for the scientific community. Methods: We have analyzed aging-phenotypical and inflammatory changes of brain myeloid cells (bMyC) in a senescent accelerated prone aged (SAMP8) mouse model, and compared with their resistant to senescence control (SAMR1). We have performed morphometric methods to evaluate the architecture of cellular prolongations and analyzed Iba1+ clustered cells with aging. To analyse specific constant brain areas we have performed stereology measurements of Iba1+ cells in the hippocampal formation. We have isolated bMyC from brain parenchyma (BP) and choroid plexus and meningeal membranes (m/Ch), and analyzed their response to systemic LPS- driven inflammation.Results: Aged 10 month old SAMP8 mice presents many of the hallmarks of aging-dependent neuroinflammation when compared with their senescence resistant control (SAMR1); ie, increase of protein aggregates, presence of Iba1+ clusters, but not increase in the number of Iba1+ cells. We have further observed and increased of main inflammatory mediator IL-1β, and augment of border MHCII+Iba1+ cells. Isolated CD45+ bMyC from brain parenchyma (BP) and choroid plexus and meningeal membranes (m/Ch) have been analyzed showing that there is not significant increase of CD45+ from the periphery. Our data support that aged-driven pro-inflammatory cytokine interleukin 1 beta (IL1β) transcription is mainly enhanced in CD45+BP cells. Furthermore, we are showing that LPS-driven systemic inflammation produces inflammatory cytokines mainly in the border bMyC, sensed to a lesser extent by the BP bMyC, and is enhanced in aged SAMP8 compared to control SAMR1.Conclusion: Our data validate the SAMP8 model to study age-associated neuroinflammatory events, but careful controls for age and strain are required. These animals show morphological changes in their bMyC cell repertoires associated to age, corresponding to an increase in the production of main pro inflammatory cytokines such as IL-1β, which predispose the brain to an enhanced inflammatory response after LPS-systemic challenge.

scholarly journals Screening for Sarcopenia (Physical Frailty) in the COVID-19 Era

2021 ◽  
Vol 2021 ◽  
pp. 1-16
Author(s):  
Amira Mohammed Ali ◽  
Hiroshi Kunugi
Keyword(s):  
Physical Activity ◽  
Older Adults ◽  
Muscle Strength ◽  
Radiation Risk ◽  
Protective Measure ◽  
Considerable Proportion ◽  
Muscle Loss ◽  
Related Disorder ◽  
Age Related ◽  
Obesity And Diabetes

Although the numbers of aged populations have risen considerably in the last few decades, the current coronavirus disease 2019 (COVID-19) has revealed an extensive vulnerability among these populations. Sarcopenia is an age-related disorder that increases hospitalization, dependencies, and mortality in older adults. It starts to develop in midlife or even earlier as a result of unbalanced diet/poor nutrition and low levels of physical activity, in addition to chronic disorders such as obesity and diabetes mellitus. Given that social isolation is adopted as the most protective measure against COVID-19, the level of physical activity and the intake of adequate diet have considerably declined, especially among older adults—denoting an increased possibility for developing sarcopenia. Research also shows a higher vulnerability of sarcopenic people to COVID-19 as well as the development of wasting disorders such as sarcopenia and cachexia in a considerable proportion of symptomatic and recovering COVID-19 patients. Muscular wasting in COVID-19 is associated with poor prognosis. Accordingly, early detection and proper management of sarcopenia and wasting conditions in older adults and COVID-19 patients may minimize morbidity and mortality during the current COVID-19 crisis. This review explored different aspects of screening for sarcopenia, stressing their relevance to the detection of altered muscular structure and performance in patients with COVID-19. Current guidelines recommend prior evaluation of muscle strength by simple measures such as grip strength to identify individuals with proven weakness who then would be screened for muscle mass loss. The latter is best measured by MRI and CT. However, due to the high cost and radiation risk entailed by these techniques, other simpler and cheaper techniques such as DXA and ultrasound are given preference. Muscle loss in COVID-19 patients was measured during the acute phase by CT scanning of the pectoralis muscle simultaneously during a routine check for lung fibrosis, which seems to be an efficient evaluation of sarcopenia among those patients with no additional cost. In recovering patients, muscle strength and physical performance have been evaluated by electromyography and traditional tests such as the six-minute walk test. Effective preventive and therapeutic interventions are necessary in order to prevent muscle loss and associated physical decline in COVID-19 patients.

Sign in / Sign up

Export Citation Format

Share Document