Testosterone improves muscle function of the extensor digitorum longus in rats with sepsis

Jinlong, W.; Wu, Tong

doi:10.1101/850636

Cited by 2 publications

(3 citation statements)

References 21 publications

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“…Longterm inhibition of mTORC1 signaling can cause myopathy [70]. A study showed that testosterone propionate promoted the phosphorylation of the mTOR signaling pathway, improving the strength, endurance, and volume of the skeletal muscle in septic rats [76]. Protein degradation in the skeletal muscle is similar to that of the mammalian cells and is under the control of two main proteolytic systems, including ubiquitin-proteasome and autophagy-lysosome [77].…”

Section: Discussionmentioning

confidence: 99%

Exploring the Muscle Metabolomics in the Mouse Model of Sepsis-Induced Acquired Weakness

Jiang

Wei

Liu

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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Background/Aim. We aimed to identify the differentially expressing metabolites (DEMs) in the muscles of the mouse model of sepsis-induced acquired weakness (sepsis-AW) using liquid chromatography-mass spectrometry (LC-MS). Materials and Methods. Sepsis by cecal ligation puncture (CLP) with lower limb immobilization was used to produce a sepsis-AW model. After this, the grip strength of the C57BL/6 male mice was investigated. The transmission electron microscopy was utilized to determine the pathological model. LC-MS was used to detect the metabolic profiles within the mouse muscles. Additionally, a statistically diversified analysis was carried out. Results. Compared to the sepsis group, 30 DEMs, including 17 upregulated and 13 down-regulated metabolites, were found in the sepsis-AW group. The enriched metabolic pathways including purine metabolism, valine/leucine/isoleucine biosynthesis, cGMP-PKG pathway, mTOR pathway, FoxO pathway, and PI3K-Akt pathway were found to differ between the two groups. The targeted metabolomics analysis explored significant differences between four amino acid metabolites (leucine, cysteine, tyrosine, and serine) and two energy metabolites (AMP and cAMP) in the muscles of the sepsis-AW experimental model group, which was comparable to the sepsis group. Conclusion. The present work identified DEMs and metabolism-related pathways within the muscles of the sepsis-AW mice, which offered valuable experimental data for diagnosis and identification of the pathogenic mechanism underlying sepsis-AW.

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Section: Discussionmentioning

confidence: 99%

Exploring the Muscle Metabolomics in the Mouse Model of Sepsis-Induced Acquired Weakness

Jiang

Wei

Liu

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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“…As testosterone signals via the mTOR pathway and androgen receptors leading to skeletal muscle hypertrophy [ 184 ], hypotestosteronemia may contribute to a net catabolic state resulting in ICUAW. In a septic rat model, short term treatment with testosterone propionate significantly improved maximum contractile force, and CSA of extensor digitorum longus muscle fibers without onset of testicular atrophy [ 185 ]. Importantly, testosterone treatment significantly increased protein levels of fast MyHC suggesting that testosterone may be a beneficial treatment to ameliorate ICUAW [ 185 ].…”

Section: Mechanisms and The Potential For Intervention During And mentioning

confidence: 99%

“…In a septic rat model, short term treatment with testosterone propionate significantly improved maximum contractile force, and CSA of extensor digitorum longus muscle fibers without onset of testicular atrophy [ 185 ]. Importantly, testosterone treatment significantly increased protein levels of fast MyHC suggesting that testosterone may be a beneficial treatment to ameliorate ICUAW [ 185 ]. Overall, hormone therapy for ICUAW has been met with encouraging pre-clinical data but limited clinical success.…”

Section: Mechanisms and The Potential For Intervention During And mentioning

confidence: 99%

Intensive Care Unit-Acquired Weakness: Not Just Another Muscle Atrophying Condition

Lad

Saumur

Herridge

et al. 2020

IJMS

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Intensive care unit-acquired weakness (ICUAW) occurs in critically ill patients stemming from the critical illness itself, and results in sustained disability long after the ICU stay. Weakness can be attributed to muscle wasting, impaired contractility, neuropathy, and major pathways associated with muscle protein degradation such as the ubiquitin proteasome system and dysregulated autophagy. Furthermore, it is characterized by the preferential loss of myosin, a distinct feature of the condition. While many risk factors for ICUAW have been identified, effective interventions to offset these changes remain elusive. In addition, our understanding of the mechanisms underlying the long-term, sustained weakness observed in a subset of patients after discharge is minimal. Herein, we discuss the various proposed pathways involved in the pathophysiology of ICUAW, with a focus on the mechanisms underpinning skeletal muscle wasting and impaired contractility, and the animal models used to study them. Furthermore, we will explore the contributions of inflammation, steroid use, and paralysis to the development of ICUAW and how it pertains to those with the corona virus disease of 2019 (COVID-19). We then elaborate on interventions tested as a means to offset these decrements in muscle function that occur as a result of critical illness, and we propose new strategies to explore the molecular mechanisms of ICUAW, including serum-related biomarkers and 3D human skeletal muscle culture models.

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Testosterone improves muscle function of the extensor digitorum longus in rats with sepsis

Cited by 2 publications

References 21 publications

Exploring the Muscle Metabolomics in the Mouse Model of Sepsis-Induced Acquired Weakness

Exploring the Muscle Metabolomics in the Mouse Model of Sepsis-Induced Acquired Weakness

Intensive Care Unit-Acquired Weakness: Not Just Another Muscle Atrophying Condition

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