Exercise activates autophagy and regulates endoplasmic reticulum stress in muscle of high-fat diet mice to alleviate insulin resistance

Exercise Training: Demonstrated as an effective therapy for insulin resistance (IR) to relieve metabolic disorders in skeletal muscle.
Physiological Autophagy: Blocked by IR-induced severe endoplasmic reticulum (ER) stress, potentially worsening IR progression.
Study Objective: Investigate how exercise affects IR through mechanisms involving ER stress and autophagy inhibition caused by high-fat diets (HFD).
Methodology: Rodent model with HFD and an 8-week swimming exercise intervention.
Key Findings: Exercise reversed the detrimental impacts of HFD on body weight, metabolic indicators (HOMA-IR), and muscle signaling pathways (AMPK/PGC1a), indicating its role in facilitating autophagy and alleviating IR.

Insulin Resistance (IR): A leading cause of metabolic disorders, linked to excess energy intake and lack of physical activity.
Exercise as Therapy: Exercise training enhances insulin receptor activity and glucose transport, ultimately benefiting IR.
Mechanism of Exercise: The relation between exercise, autophagy imbalance, and ER stress in IR remains unclear despite documented benefits to insulin signaling.
Skeletal Muscle Role: Largest metabolic tissue influenced by ER stress, mediating glucose and lipid metabolism.
ER Stress Role: Impairs insulin signaling, promoting sugar toxicity and obesity-related complications leading to T2DM.

Mice Used: Eight-week-old male C57BL/6J mice, housed in controlled environments.
Group Division: Groups included normal diet (ND), high-fat diet (HFD), and HFD with exercise (HFD + EX).
Exercise Training Protocol: Moderate-intensity swimming training established over 8 weeks.
Data Collection: Body weights, visceral fat weights, blood samples, and muscle tissues were the main areas collected for analysis.

Body Weight Changes: HFD mice gained weight more than ND; exercise training moderated this.