scholarly journals FAHFAs Regulate the Proliferation of C2C12 Myoblasts and Induce a Shift toward a More Oxidative Phenotype in Mouse Skeletal Muscle

2020 ◽  
Vol 21 (23) ◽  
pp. 9046
Author(s):  
Melha Benlebna ◽  
Laurence Balas ◽  
Laurence Pessemesse ◽  
Béatrice Bonafos ◽  
Gilles Fouret ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acid Esters ◽  
Mitochondrial Activity ◽  
C2c12 Myoblast ◽  
C2c12 Myoblasts ◽  
Heavy Chains ◽  
Oxidative Phenotype ◽  
Species Production ◽  
First Time ◽  
Endogenous Lipids

Branched fatty acid esters of hydroxy fatty acids (FAHFAs) are endogenous lipids reported to have antidiabetic and anti-inflammatory effects. Since skeletal muscle is a major target for insulin, the aim of this study is to explore for the first time the influence of several FAHFAs in C2C12 myoblasts and in skeletal muscle phenotype in mice. Here, we show that eleven FAHFAs belonging to different families inhibit C2C12 myoblast proliferation. In addition, all FAHFAs decreased mitochondrial cytochrome c oxidase activity without affecting reactive oxygen species production and the mitochondrial network. During C2C12 myoblasts differentiation, we found that two of the most active lipids, 9-PAHPA and 9-OAHPA, did not significantly affect the fusion index and the expression of myosin heavy chains. However, we found that three months’ intake of 9-PAHPA or 9-OAHPA in mice increased the expression of more oxidative myosin in skeletal muscle without affecting skeletal muscle mass, number, and mean fiber area, mitochondrial activity, and oxidative stress parameters. In conclusion, our study indicated that the eleven FAHFAs tested decreased the proliferation rate of C2C12 myoblasts, probably through the inhibition of mitochondrial activity. In addition, we found that 9-PAHPA or 9-OAHPA supplementation in mice induced a switch toward a more oxidative contractile phenotype of skeletal muscle. These data suggest that the increase in insulin sensitivity previously described for these two FAHFAs is of muscular origin.

scholarly journals Transient Changes of Metabolism at the Pronuclear Stage in Mice Influences Skeletal Muscle Phenotype in Adulthood

2020 ◽  
Vol 21 (19) ◽  
pp. 7203
Author(s):  
Christelle Bertrand-Gaday ◽  
Martine Letheule ◽  
Emilie Blanchet ◽  
Barbara Vernus ◽  
Laurence Pessemesse ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Dependent Manner ◽  
Cell Stage ◽  
Post Translational Modifications ◽  
Stage Embryo ◽  
Skeletal Phenotype ◽  
Oxidative Phenotype ◽  
Chromatin Reprogramming ◽  
Induced Changes ◽  
First Time

Skeletal muscle has a remarkable plasticity, and its phenotype is strongly influenced by hormones, transcription factors, and physical activity. However, whether skeletal phenotype can be oriented or not during early embryonic stages has never been investigated. Here, we report that pyruvate as the only source of carbohydrate in the culture medium of mouse one cell stage embryo influenced the establishment of the muscular phenotype in adulthood. We found that pyruvate alone induced changes in the contractile phenotype of the skeletal muscle in a sexually dependent manner. For male mice, a switch to a more glycolytic phenotype was recorded, whereas, in females, the pyruvate induced a switch to a more oxidative phenotype. In addition, the influence of pyruvate on the contractile phenotypes was confirmed in two mouse models of muscle hypertrophy: the well-known myostatin deficient mouse (Mstn−/−) and a mouse carrying a specific deletion of p43, a mitochondrial triiodothyronine receptor. Finally, to understand the link between these adult phenotypes and the early embryonic period, we assessed the levels of two histone H3 post-translational modifications in presence of pyruvate alone just after the wave of chromatin reprogramming specific of the first cell cycle. We showed that H3K4 acetylation level was decreased in Mstn−/− 2-cell embryos, whereas no difference was found for H3K27 trimethylation level, whatever the genotype. These findings demonstrate for the first time that changes in the access of energy substrate during the very first embryonic stage can induce a precocious orientation of skeletal muscle phenotype in adulthood.

Skeletal muscle maximal mitochondrial activity in ambulatory children with cerebral palsy

2021 ◽  
Author(s):  
Sudarshan Dayanidhi ◽  
Elisa H Buckner ◽  
Robin S Redmond ◽  
Henry G Chambers ◽  
Simon Schenk ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cerebral Palsy ◽  
Mitochondrial Activity ◽  
Children With Cerebral Palsy

scholarly journals The MicroRNA miR-696 is Regulated by SNARK and Reduces Mitochondrial Activity in Mouse Skeletal Muscle Through Pgc1α Inhibition

2021 ◽  
pp. 101226
Author(s):  
André L. Queiroz ◽  
Sarah J. Lessard ◽  
Amanda T. Ouchida ◽  
Hygor N. Araujo ◽  
Dawit A. Gonçalves ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Mitochondrial Activity ◽  
Mouse Skeletal Muscle

scholarly journals Autophagy Deficiency by Atg4B Loss Leads to Metabolomic Alterations in Mice

Metabolites ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 481
Author(s):  
Gemma G. Martínez-García ◽  
Raúl F. Pérez ◽  
Álvaro F. Fernández ◽  
Sylvere Durand ◽  
Guido Kroemer ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Amino Acids ◽  
Mammalian Cells ◽  
Tissue Homeostasis ◽  
In Vivo Studies ◽  
Protective Mechanism ◽  
Cardiac Damage ◽  
Wide Range ◽  
First Time

Autophagy is an essential protective mechanism that allows mammalian cells to cope with a variety of stressors and contributes to maintaining cellular and tissue homeostasis. Due to these crucial roles and also to the fact that autophagy malfunction has been described in a wide range of pathologies, an increasing number of in vivo studies involving animal models targeting autophagy genes have been developed. In mammals, total autophagy inactivation is lethal, and constitutive knockout models lacking effectors of this route are not viable, which has hindered so far the analysis of the consequences of a systemic autophagy decline. Here, we take advantage of atg4b−/− mice, an autophagy-deficient model with only partial disruption of the process, to assess the effects of systemic reduction of autophagy on the metabolome. We describe for the first time the metabolic footprint of systemic autophagy decline, showing that impaired autophagy results in highly tissue-dependent alterations that are more accentuated in the skeletal muscle and plasma. These changes, which include changes in the levels of amino-acids, lipids, or nucleosides, sometimes resemble those that are frequently described in conditions like aging, obesity, or cardiac damage. We also discuss different hypotheses on how impaired autophagy may affect the metabolism of several tissues in mammals.

Effect of fluoxetine treatment on mitochondrial bioenergetics in central and peripheral rat tissues

2015 ◽  
Vol 40 (6) ◽  
pp. 565-574 ◽  
Author(s):  
Aline Isabel da Silva ◽  
Glauber Ruda Feitoza Braz ◽  
Reginaldo Silva-Filho ◽  
Anderson Apolonio Pedroza ◽  
Diorginis Soares Ferreira ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Metabolic Diseases ◽  
Mitochondrial Permeability Transition ◽  
Permeability Transition ◽  
Wistar Rat ◽  
Male Rats ◽  
Mitochondrial Activity ◽  
Rat Tissues ◽  
Transferase Activity ◽  
Mitochondrial Bioenergetics

Recent investigations have focused on the mitochondrion as a direct drug target in the treatment of metabolic diseases (obesity, metabolic syndrome). Relatively few studies, however, have explicitly investigated whether drug therapies aimed at changing behavior by altering central nervous system (CNS) function affect mitochondrial bioenergetics, and none has explored their effect during early neonatal development. The present study was designed to evaluate the effects of chronic treatment of newborn male rats with the selective serotonin reuptake inhibitor fluoxetine on the mitochondrial bioenergetics of the hypothalamus and skeletal muscle during the critical nursing period of development. Male Wistar rat pups received either fluoxetine (Fx group) or vehicle solution (Ct group) from the day of birth until 21 days of age. At 60 days of age, mitochondrial bioenergetics were evaluated. The Fx group showed increased oxygen consumption in several different respiratory states and reduced production of reactive oxygen species, but there was no change in mitochondrial permeability transition pore opening or oxidative stress in either the hypothalamus or skeletal muscle. We observed an increase in glutathione S-transferase activity only in the hypothalamus of the Fx group. Taken together, our results suggest that chronic exposure to fluoxetine during the nursing phase of early rat development results in a positive modulation of mitochondrial respiration in the hypothalamus and skeletal muscle that persists into adulthood. Such long-lasting alterations in mitochondrial activity in the CNS, especially in areas regulating appetite, may contribute to permanent changes in energy balance in treated animals.

scholarly journals Immunocytochemical localization of mitochondrial carbonic anhydrase in rat tissues.

1991 ◽  
Vol 39 (4) ◽  
pp. 451-459 ◽  
Author(s):  
H K Väänänen ◽  
N D Carter ◽  
S J Dodgson
Keyword(s):  
Skeletal Muscle ◽  
Carbonic Anhydrase ◽  
Cardiac Tissue ◽  
Polyclonal Antiserum ◽  
Heterogeneous Population ◽  
Rat Tissues ◽  
Staining Reaction ◽  
Gastric Parietal Cells ◽  
First Time ◽  
Carbonic Anhydrase Gene

We used a monospecific polyclonal antiserum against mitochondrial carbonic anhydrase (CA V) from rat liver to study tissue localization of this new member of the carbonic anhydrase gene family. Strong granular immunostaining reaction of CA V was observed in hepatocytes, myocardium, and in certain populations of skeletal muscle fibers. This is the first time that mitochondrial carbonic anhydrase is described in cardiac tissue of rat or any other species. Different epithelial cells revealed very heterogeneous staining reaction, suggesting that mitochondria are a heterogeneous population with respect to their CA V content. Many cells in different glandular epithelia did not show any CA V, whereas some cells, such as gastric parietal cells, were intensely stained with CA V antibodies. No systematic co-expression of CA V with CA I, CA II, or CA III was observed, although the distribution of CA V in skeletal muscle was somewhat similar to that of CA III. Connective tissue cells such as fibroblasts, chondroblasts, and osteoblasts were negative.

Lipopolysaccharide regulates proinflammatory cytokine expression in mouse myoblasts and skeletal muscle

2002 ◽  
Vol 283 (3) ◽  
pp. R698-R709 ◽  
Author(s):  
Robert A. Frost ◽  
Gerald J. Nystrom ◽  
Charles H. Lang
Keyword(s):  
Skeletal Muscle ◽  
Cell Wall ◽  
Mrna Expression ◽  
Nuclear Factor Κb ◽  
Cytokine Expression ◽  
Mrna Accumulation ◽  
C2c12 Myoblasts ◽  
Tnf Α ◽  
Mrna Content

The purpose of the present study was to examine the regulation of tumor necrosis factor (TNF)-α and interleukin (IL)-6 by lipopolysaccharide (LPS) in C2C12 myoblasts and mouse skeletal muscle. LPS produced dose- and time-dependent increases in TNF-α and IL-6 mRNA content in C2C12 myoblasts. The LPS-induced cytokine response could be mimicked by peptidoglycan from the cell wall of Staphylococcus aureus but not by zymosan A, a cell wall component from Saccharomyces cerevisiae. Ongoing protein synthesis was not necessary for the increase in the two cytokine mRNAs. The transcriptional inhibitor 5,6-dichloro-β-d-ribofuranosyl-benzimidazole blocked LPS-stimulated IL-6 mRNA expression without changing its mRNA half-life. The anti-inflammatory glucocorticoid dexamethasone selectively blocked LPS-stimulated IL-6 mRNA accumulation but not TNF-α. In contrast, the proteasomal inhibitor MG-132 blocked TNF-α mRNA expression but not IL-6. Exposure of myoblasts to LPS was associated with a rapid decrease in the inhibitor of nuclear factor-κB (I κB, α, and ε), and this response was also blocked by MG-132. Treatment of myocytes with IL-1 or TNF-α also increased IL-6 mRNA content, but the increase in IL-6 mRNA due to LPS could not be prevented by pretreatment with antagonists to either IL-1 or TNF. Under in vivo conditions, LPS increased the plasma concentration of TNF-α and IL-6 and stimulated the accumulation of their mRNAs in multiple tissues including skeletal muscle from wild-type mice. In contrast, the ability of LPS to stimulate the same cytokines was markedly decreased in mice that harbor a mutation in the Toll-like receptor 4. Our data suggest that LPS stimulates cytokine expression not only in classical immune tissues but also in skeletal muscle.

Sign in / Sign up

Export Citation Format

Share Document