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Related Concept Videos

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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.
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Insulin-replacement therapy usually includes both long-acting insulin (basal) and short-acting insulin (to cater to postprandial needs). In a diverse group of type 1 diabetes patients, the average daily insulin dose is typically 0.5-0.7 units/kg body weight. However, obese patients and pubertal adolescents may need more due to insulin resistance.
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Related Experiment Video

Updated: Jan 11, 2026

Combined Intravital Microscopy and Contrast-enhanced Ultrasonography of the Mouse Hindlimb to Study Insulin-induced Vasodilation and Muscle Perfusion
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Muscle Insulin Resistance Elicits Muscle Atrophy in Obesity.

Omid Razi1, Nastaran Zamani2, Ayoub Saeidi3

  • 1Department of Exercise Physiology, Faculty of Sport Sciences, Razi University, Kermanshah, Iran.

Current Obesity Reports
|November 19, 2025
PubMed
Summary

Insulin resistance (IR) drives muscle atrophy in obesity by disrupting metabolic balance and promoting muscle breakdown. Understanding these molecular pathways is key to developing interventions for muscle wasting.

Keywords:
Body fatEndocrinesMuscle atrophyProtein breakdownProtein synthesis

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Area of Science:

  • Metabolic pathways
  • Cellular biology
  • Muscle physiology

Background:

  • Skeletal muscle insulin resistance (IR) is prevalent in obesity, aging, and sedentary lifestyles.
  • IR disrupts metabolic homeostasis, impairing glucose uptake and utilization in muscle tissue.
  • This contributes to an imbalance favoring muscle protein breakdown over synthesis.

Purpose of the Study:

  • To comprehensively review the molecular and cellular pathways linking insulin resistance to muscle atrophy.
  • To elucidate the mechanisms by which IR accelerates muscle wasting in obese individuals.

Main Methods:

  • Literature review of molecular and cellular pathways.
  • Analysis of signaling cascades involved in insulin resistance and muscle atrophy.

Main Results:

  • Insulin resistance shifts skeletal muscle from anabolic to catabolic states, inhibiting protein synthesis and promoting proteolysis.
  • Key mechanisms include mitochondrial dysfunction, inflammation, oxidative stress, and impaired satellite cell function.
  • These factors contribute to progressive loss of muscle mass and function.

Conclusions:

  • Defective insulin signaling is a critical driver of muscle atrophy in obesity.
  • Understanding these interconnected mechanisms is vital for developing interventions to combat muscle wasting and improve metabolic health.