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Metformin Ingestion Rejuvenates Myoblasts from Older Adult Donors

ABSTRACT: We tested the hypothesis that 2-weeks of metformin ingestion in healthy older adults would improve intrinsic age-related deficits in myoblast (activated satellite cell) function as tested by a series of in vitro functional assays to determine proliferation, fusion index, and myoblast-endothelial cell homing.

ORGANISM(S): Homo sapiens

PROVIDER: GSE153953 | GEO | 2021/09/15

REPOSITORIES: GEO

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Metformin Ingestion Rejuvenates Myoblasts from Older Adult Donors

Project description:Metformin Ingestion Rejuvenates Myoblasts from Older Adult Donors

| PRJNA644603 | ENA

Metformin Alters Skeletal Muscle Transcriptome Adaptations to Resistance Training in Older Adults

Project description:Evidence from clinical trials and observational studies suggests that both progressive resistance training (PRT) and metformin delay a variety of age-related morbidities. Previously, we completed a clinical trial testing the effects of 14 weeks of PRT + metformin (metPRT) compared to PRT with placebo (plaPRT) on muscle hypertrophy in older adults. We found that metformin blunted PRT-induced muscle hypertrophic response. To understand potential mechanisms underlying the inhibitory effect of metformin on PRT, we analyzed the muscle transcriptome in 23 metPRT and 24 plaPRT participants. PRT significantly increased expression of genes involved in extracellular matrix remodeling pathways, and downregulated RNA processing pathways in both groups, however, metformin blunted the number of differentially expressed genes within these pathways compared to plaPRT. Pathway analysis showed that genes unique to metPRT modulated aging-relevant pathways, such as cellular senescence and autophagy. Differentially expressed genes from baseline biopsies in older adults compared to resting muscle from young volunteers were reduced following PRT in plaPRT and were further reduced in metPRT. We suggest that although metformin may blunt pathways induced by PRT to promote muscle hypertrophy, adjunctive metformin during PRT may have beneficial effects on aging-associated pathways in muscle from older adults.

2020-09-08 | GSE157585 | GEO

Influence of metformin treatment during five days of bed rest and recovery in older adults

Project description:The primary goal of this study was to determine the effect of metformin treatment during 5 days of bed rest in older adults and observe any residual effects of metformin treatment during recovery from this disuse period.

2023-11-22 | GSE224900 | GEO

Metformin Regulates Metabolic and Non-Metabolic Pathways in Skeletal Muscle and Subcutaneous Adipose Tissues of Older Adults

Project description:Administration of metformin increases healthspan and lifespan in model systems and evidence from clinical trials and observational studies suggests that metformin delays a variety of age-related morbidities. Although metformin has been shown to modulate multiple biological pathways at the cellular level, these pleiotropic effects of metformin on the biology of human aging have not been studied. We studied ~70-year-old participants (n=14), in a randomized, double-blind, placebo-controlled, crossover trial in which they were treated with 6 weeks each of metformin and placebo. Following each treatment period, skeletal muscle and subcutaneous adipose tissue biopsies were obtained, and a mixed-meal challenge test was performed. As expected, metformin therapy lowered 2-hour glucose, insulin AUC, and insulin secretion compared to placebo. Using FDR<0.05, 647 genes were differentially expressed in muscle and 146 genes were differentially expressed in adipose tissue. Both metabolic and non-metabolic pathways were significantly influenced, including pyruvate metabolism and DNA repair in muscle and PPAR & SREBP signaling, mitochondrial fatty acid oxidation and collagen trimerization in adipose. While each tissue had, a signature reflecting its own function, we identified a cascade of predictive upstream transcriptional regulators, including mTORC1, MYC, TNF, TGFß1 and miRNA-29b, that may explain tissue-specific transcriptomic changes in response to metformin treatment. This study provides the first evidence that, in older adults, metformin has metabolic and non-metabolic effects linked to aging. These data can inform the development of biomarkers for the effects of metformin, and potentially other drugs, on key aging pathways. Key words: Aging, biguanides, gene expression, metabolism, upstream regulators

2017-12-12 | GSE107894 | GEO

RNAseq of C. elegans cultured on metformin sensitive and resistant E. coli strains with and without 50mM metformin treatment.

Project description:Metformin is the therapy of choice for treating type 2 diabetes and is currently repurposed for a wide range of diseases including aging. Recent evidence implicates the gut microbiota as a site of metformin action. Combining two tractable genetic models, the bacterium E. coli and the nematode C. elegans, we performed C. elegans RNAseq to investigate the role of the metformin sensitive OP50 and metformin resistant OP50-MR E. coli microbiota in the drug effects on the host. Our data suggest an evolutionarily conserved bacterial mediation of metformin effects on host lipid metabolism and lifespan.

2019-07-13 | E-MTAB-7272 | biostudies-arrayexpress

Pleiotropic effects of metformin on inflammation, oxidative and dicarbonyl stress in transgenic spontaneously hypertensive rats expressing human C-reactive protein.

Project description:Inflammation, oxidative and dicarbonyl stress play important roles in the pathophysiology of type 2 diabetes. Metformin is the first-line drug of choice for the treatment of type 2 diabetes because it effectively suppresses gluconeogenesis in the liver, however, its “pleiotropic“ effects remain controversial. In the current study, we tested the effects of metformin on inflammation, oxidative and dicarbonyl stress in an animal model of inflammation and metabolic syndrome, the spontaneously hypertensive rat transgenically expressing human C-reactive protein (SHR-CRP). In the SHR-CRP transgenic strain, we found that metformin treatment decreased circulating levels of inflammatory response marker IL6 while levels of human CRP remained unchanged and metformin also significantly reduced oxidative stress (levels of conjugated dienes and TBARS) in the liver while no significant effects were observed in SHR control rats. In addition, in the presence of high human CRP, metformin reduced methylglyoxal levels in left ventricles but not in kidneys. Finally, metformin treatment reduced adipose tissue lipolysis. Possible molecular mechanisms of metformin action studied by gene expression profiling in the liver revealed deregulated genes from inflammatory, insulin signaling, AMP-activated protein kinase (AMPK) signaling and gluconeogenesis pathways. It can be concluded that in the presence of high levels of human CRP metformin protects against inflammation, oxidative and dicarbonyl stress in the heart and ameliorates insulin resistance and dyslipidemia.

2016-07-03 | E-MTAB-3791 | biostudies-arrayexpress

Metformin on human macrophages

Project description:Metformin on human macrophages Human blood derived macrophages were treated with 10micromolar Metformin (Sigma-Aldrich) for 4h

2020-06-27 | GSE153318 | GEO

Genome-wide analysis of gene expression in M. bovis BCG infected THP-1 cells subjected to Metformin treatement

Project description:Analysis of Metfromin induced changes in mycobacteria infected cell at gene expression level. The hypothesis tested in the present study was whether metformin has any effect on the host immune response in mycobacteria infected cells? Results provide important information on the effect of metformin on the inflammatory response and immune activation associated with mycobacterial infection. In conclusion, Metfromin normalizes the effect of infection in THP1 cells.

2014-12-01 | GSE51803 | GEO

Genome-wide analysis of gene expression in lung cells from metformin treated Mycobacterium tuberculosis infected mice

Project description:Analysis of Metfromin induced changes in the lung cells of Mycobacterium tuberculosis infected mouse at gene expression level. The hypothesis tested in the present study was whether metformin has any effect on the host immune response in Mycobacterium tuberculosis infected mice? Results provide important information on the effect of metformin on the inflammatory response and immune activation associated with mycobacterial infection. In conclusion, Metfromin normalizes the chronic inflammation associated with Mycobacterium tuberculosis infection.

2014-12-02 | GSE57275 | GEO

Distinct perturbation of the translatome by the anti-diabetic drug metformin

Project description:Reduced cancer incidence has been reported among type II diabetics treated with metformin. Metformin exhibits anti-proliferative and anti-neoplastic effects associated with inhibition of mTORC1, but the mechanisms are poorly understood. We provide the first genome-wide analysis of translational targets of canonical mTOR inhibitors (rapamycin and PP242) and metformin, revealing that metformin controls gene expression at the level of mRNA translation to an extent comparable to that of canonical mTOR inhibitors. Importantly, metformin's anti-proliferative activity can be explained by selective translational suppression of mRNAs encoding cell cycle regulators via the mTORC1/4E-BP pathway. Thus, metformin selectively inhibits mRNA translation of encoded proteins that promote neoplastic proliferation, motivating further studies of this compound and related biguanides in cancer prevention and treatment. MCF7 cells were treated with rapamycin, metformin or PP242 at concentrations that inhibited proliferation to 50% of control. Both cytoplasmic and polysome-associated mRNA was extracted from treatments and a vehicle treated control and probed with microarrays.

2012-05-20 | E-GEOD-36847 | biostudies-arrayexpress

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