Related Experiment Video

Updated: Aug 8, 2026

Behavioral and Locomotor Measurements Using an Open Field Activity Monitoring System for Skeletal Muscle Diseases
06:52

Behavioral and Locomotor Measurements Using an Open Field Activity Monitoring System for Skeletal Muscle Diseases

Published on: September 29, 2014

Glucocorticoid-induced muscle atrophy: mechanisms and therapeutic strategies

B Salehian1, K Kejriwal

  • 1Department of Medicine, Division of Endocrinology, Charles R. Drew University of Medicine and Science, Los Angeles, California, USA.

Endocrine Practice : Official Journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists
|July 15, 2004
PubMed
Abstract

Insights

Glucocorticoids cause muscle atrophy by breaking down myosin. Testosterone and glutamine show promise in counteracting this effect, with further human research needed.

Area of Science:

  • Endocrinology
  • Muscle Physiology
  • Pharmacology

Background:

  • Glucocorticoids are potent anti-inflammatory drugs with significant catabolic side effects.
  • Muscle atrophy is a serious adverse effect of long-term glucocorticoid therapy.
  • Understanding the mechanisms of glucocorticoid-induced muscle atrophy is crucial for developing effective countermeasures.

Purpose of the Study:

  • To elucidate the mechanisms by which glucocorticoids induce muscle atrophy.
  • To evaluate the potential of testosterone and other therapeutic interventions to mitigate glucocorticoid-induced muscle atrophy.

Main Methods:

  • Systematic review of existing literature on glucocorticoid-induced muscle atrophy.
  • Analysis of animal models and human studies.
  • Assessment of pathophysiologic features, including glucocorticoid-induced hypogonadism.
  • Review of testosterone's effects on muscle in hypogonadal and eugonadal men.
  • Examination of exercise and glutamine as potential therapeutic agents.

Main Results:

  • Glucocorticoids promote rapid muscle breakdown via myosin heavy chain degradation and reduced synthesis.
  • Glucocorticoid-induced hypogonadism is a contributing factor to muscle atrophy.
  • Androgens demonstrate anabolic and anticatabolic effects, counteracting cortisol's catabolic impact.
  • Exercise and glutamine show promise in preclinical models of glucocorticoid-induced muscle atrophy.

Conclusions:

  • Testosterone and glutamine may be effective in combating glucocorticoid-induced muscle atrophy.
  • These natural products possess favorable safety profiles, warranting further clinical investigation in humans.

More Related Videos

In Situ Immunofluorescent Staining of Autophagy in Muscle Stem Cells08:35

In Situ Immunofluorescent Staining of Autophagy in Muscle Stem Cells

Published on: June 12, 2017

Freezing Injury in Mouse Masseter Muscle to Establish an Orofacial Muscle Fibrosis Model06:33

Freezing Injury in Mouse Masseter Muscle to Establish an Orofacial Muscle Fibrosis Model

Published on: December 29, 2023

Related Concept Videos

Cross-bridge Cycle01:26

Cross-bridge Cycle

As muscle contracts, the overlap between the thin and thick filaments increases, decreasing the length of the sarcomere—the contractile unit of the muscle—using energy in the form of ATP. At the molecular level, this is a cyclic, multistep process that involves binding and hydrolysis of ATP, and movement of actin by myosin.
Myasthenia Gravis: Overview and Treatment01:20

Myasthenia Gravis: Overview and Treatment

Myasthenia gravis is a neuromuscular transmission disorder characterized by weakness and increased fatigability of skeletal muscles. It is an autoimmune disease affecting approximately one in 2000 people, where antibodies against the α1 subunit of nicotinic acetylcholine receptors are produced.
These antibodies interfere with the function of the nicotinic receptors in three ways: by binding to the receptor and disrupting acetylcholine binding; by causing cross-linking of receptors which leads...
Skeletal Muscle Relaxants: Adverse Effects01:21

Skeletal Muscle Relaxants: Adverse Effects

Skeletal muscle relaxants are widely used for muscle paralysis and relieving pain following any muscle injury or stiffness. However, depending on the drug type, they can have adverse effects that range from mild to severe. Usually, nondepolarizing neuromuscular blockers have minimal side effects. For example, drugs like d-tubocurarine, cisatracurium, and rocuronium cause hypotension, whereas drugs like baclofen, when stopped abruptly, can lead to the recurrence of spastic conditions.
Unlike...
Disorders of the Skeletal Muscle01:28

Disorders of the Skeletal Muscle

The clinical conditions affecting the skeletal muscle tissue are broadly categorized as musculoskeletal and neuromuscular disorders.
Musculoskeletal disorders
Musculoskeletal disorders involve injuries and conditions affecting the skeletal muscles and associated connective tissues. These disorders can arise from acute biomechanical stresses or chronic overuse and can occur across different age groups. Common injuries include sprains, fractures, and muscular strains, often resulting from...
Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents01:29

Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents

Crohn's disease is an inflammatory bowel disorder marked by chronic inflammation of the GI tract. Various treatment strategies for Crohn's disease are employed, such as immunomodulatory agents, glucocorticoids, and biologics or anti-TNF therapy. Azathioprine (Imuran), a commonly used immunomodulatory drug for Crohn's disease, is converted in the body to mercaptopurine, which inhibits purine biosynthesis and cell proliferation. Both are utilized in severe cases of Inflammatory Bowel Disease...
Drugs for Treatment of Crohn's Disease in IBD Using Glucocorticoids01:21

Drugs for Treatment of Crohn's Disease in IBD Using Glucocorticoids

Glucocorticoids, a class of anti-inflammatory drugs, are pivotal in treating moderate to severe Crohn's disease by inducing remission. They exhibit their anti-inflammatory action by inhibiting the production of inflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-1, and chemokines like IL-8. In addition, they reduce the expression of inflammatory cell adhesion molecules and inhibit gene transcription of nitric oxide synthase, phospholipase A2, cyclooxygenase-2 (COX-2),...