Exercise ameliorates high fat diet induced cardiac dysfunction by increasing interleukin 10

Area of Science:

• Cardiovascular Biology
• Exercise Physiology
• Metabolic Disease

Background:

• Sedentary lifestyles and high-fat diets (HFD) are linked to cardiomyopathy.
• Inflammation, driven by elevated tumor necrosis factor-alpha (TNF-α) and reduced interleukin-10 (IL-10), contributes to cardiac dysfunction in obesity and diabetes.
• The molecular mechanisms by which exercise ameliorates cardiac dysfunction remain unclear.

Purpose of the Study:

• To investigate if exercise training mitigates high-fat diet-induced cardiac dysfunction.
• To determine if exercise reduces obesity and inflammation by modulating TNF-α and IL-10 levels.
• To elucidate the molecular mechanisms underlying exercise's cardioprotective effects against HFD.

Main Methods:

• Female C57BL/6J mice were divided into four groups: normal diet (ND), HFD, HFD + exercise (HFD + Ex), and ND + Ex.
• Mice in HFD + Ex and ND + Ex groups underwent swimming exercise (1 h/day, 5 days/week for 8 weeks).
• Parameters analyzed included body weight, blood glucose, TNF-α, IL-10, cardiac fibrosis (Masson Trichrome), and cardiac function (echocardiography).

Main Results:

• HFD increased body weight and cardiac fibrosis, and impaired cardiac function (reduced ejection fraction and fractional shortening).
• Exercise in HFD + Ex mice attenuated weight gain, reduced cardiac fibrosis, and improved cardiac function compared to HFD alone.
• HFD elevated TNF-α and decreased IL-10; exercise intervention reversed these changes, increasing IL-10 and decreasing TNF-α.

Conclusions:

• Exercise training effectively mitigates high-fat diet-induced cardiomyopathy in mice.
• Exercise ameliorates cardiac dysfunction by reducing obesity and modulating inflammatory cytokines, specifically upregulating IL-10 and downregulating TNF-α.
• Moderate exercise demonstrates significant cardioprotective effects against metabolic disturbances induced by a high-fat diet.