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

Abstract

Increasing evidence suggests that a sedentary lifestyle and a high fat diet (HFD) leads to cardiomyopathy. Moderate exercise ameliorates cardiac dysfunction, however underlying molecular mechanisms are poorly understood. Increased inflammation due to induction of pro-inflammatory cytokine such as tumor necrosis factor-alpha (TNF-α) and attenuation of anti-inflammatory cytokine such as interleukin 10 (IL-10) contributes to cardiac dysfunction in obese and diabetics. We hypothesized that exercise training ameliorates HFD- induced cardiac dysfunction by mitigating obesity and inflammation through upregulation of IL-10 and downregulation of TNF-α. To test this hypothesis, 8 week old, female C57BL/6J mice were fed with HFD and exercised (swimming 1 h/day for 5 days/week for 8 weeks). The four treatment groups: normal diet (ND), HFD, HFD + exercise (HFD + Ex) and ND + Ex were analyzed for mean body weight, blood glucose level, TNF-α, IL-10, cardiac fibrosis by Masson Trichrome, and cardiac dysfunction by echocardiography. Mean body weights were increased in HFD but comparatively less in HFD + Ex. The level of TNF-α was elevated and IL-10 was downregulated in HFD but ameliorated in HFD + Ex. Cardiac fibrosis increased in HFD and was attenuated by exercise in the HFD + Ex group. The percentage ejection fraction and fractional shortening were decreased in HFD but comparatively increased in HFD + Ex. There was no difference between ND and ND + Ex for the above parameters except an increase in IL-10 level following exercise. Based on these results, we conclude that exercise mitigates HFD- induced cardiomyopathy by decreasing obesity, inducing IL-10, and reducing TNF-α in mice.

Effects of exercise training on brain‐derived neurotrophic factor in skeletal muscle and heart of rats post myocardial infarction

“…) and increases IL‐10 (Kesherwani et al . ) in the LV, it is possible that the increase in mBDNF is mediated by a decrease in these pro‐inflammatory cytokines and an increase in anti‐inflammatory cytokines. Finally, as cardiac BDNF mRNA did not increase in parallel with protein, one cannot exclude the possibility that uptake from the circulation might play a role (Knaepen et al .…”

Shining LIGHT on the metabolic role of the cytokine TNFSF14 and the implications on hepatic IL‐6 production

“…We were also interested in the potential association of IL‐10 and TNFSF14 as studies have previously reported that IL‐10 is involved in the protection against diet‐induced metabolic dysfunction including hyperinsulinemia . Interestingly, mice fed a HFD and lacking TNFSF14 exhibited both hyperinsulinemia and significantly elevated expression of hepatic IL‐10 compared with HFD fed WT mice.…”

“…We were also interested in the potential association of IL-10 and TNFSF14 as studies have previously reported that IL-10 is involved in the protection against dietinduced metabolic dysfunction including hyperinsulinemia. 43,44 Interestingly, mice fed a HFD and lacking TNFSF14 exhibited both hyperinsulinemia and significantly elevated expression of hepatic IL-10 compared with HFD fed WT mice. This increased hepatic IL-10 expression in the Tnfsf14 KO mice on a HFD may be a compensatory mechanism to attempt to reduce hepatic inflammation as evidenced by the vast infiltration of inflammatory cells in the H&E stained liver sections of the Tnfsf14 KO mice on a HFD.…”

Exercise Preconditioning Protects against Acute Cardiac Injury Induced by Lipopolysaccharide Through General Control Nonderepressible 2 Kinase

“…22) In our study, the exercise protocol followed that of Kesherwani Varun and Jeong-sun Ju. 15,16) Kesherwani Varun found that the EF value of the swimming group was slightly higher than that of the sedentary group, but there was no significant difference. 16) We think that when the exercise intensity is relatively low, this will not cause changes in the structure and function of the heart but may affect the cardiac reserve function.…”

“…Sedentary control animals were handled and immersed for a few minutes in the warm water (a depth of 3 cm) to subject them to stress similar to that of the trained mice. 15,16) LPS administration: Escherichia coli LPS (026: B6, 200 μg; Sigma-Aldrich, St. Louis, MO, USA) was diluted in prepared sterile saline at a concentration of 4 mg/mL. As shown in Figure 1, 24 hours after the last swimming training, we immediately started injecting LPS at a dose of 10 ug/g in the abdominal cavity of the mice.…”