scholarly journals Exercise Training Promotes Cardiac Hydrogen Sulfide Biosynthesis and Mitigates Pyroptosis to Prevent High-Fat Diet-Induced Diabetic Cardiomyopathy

Antioxidants ◽  
2019 ◽  
Vol 8 (12) ◽  
pp. 638 ◽  
Author(s):  
Sumit Kar ◽  
Hamid R. Shahshahan ◽  
Bryan T. Hackfort ◽  
Santosh K. Yadav ◽  
Roopali Yadav ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Exercise Training ◽  
Diabetic Cardiomyopathy ◽  
High Fat Diet ◽  
Inflammatory Cell ◽  
Volume Measurement ◽  
High Fat ◽  
Metabolic Remodeling ◽  
Cardioprotective Effects

Obesity increases the risk of developing diabetes and subsequently, diabetic cardiomyopathy (DMCM). Reduced cardioprotective antioxidant hydrogen sulfide (H2S) and increased inflammatory cell death via pyroptosis contribute to adverse cardiac remodeling and DMCM. Although exercise training (EX) has cardioprotective effects, it is unclear whether EX mitigates obesity-induced DMCM by increasing H₂S biosynthesis and mitigating pyroptosis in the heart. C57BL6 mice were fed a high-fat diet (HFD) while undergoing treadmill EX for 20 weeks. HFD mice developed obesity, hyperglycemia, and insulin resistance, which were reduced by EX. Left ventricle pressure-volume measurement revealed that obese mice developed reduced diastolic function with preserved ejection fraction, which was improved by EX. Cardiac dysfunction was accompanied by increased cardiac pyroptosis signaling, structural remodeling, and metabolic remodeling, indicated by accumulation of lipid droplets in the heart. Notably, EX increased cardiac H₂S concentration and expression of H₂S biosynthesis enzymes. HFD-induced obesity led to features of type 2 diabetes (T2DM), and subsequently DMCM. EX during the HFD regimen prevented the development of DMCM, possibly by promoting H₂S-mediated cardioprotection and alleviating pyroptosis. This is the first report of EX modulating H₂S and pyroptotic signaling in the heart.

Exercise restores bioavailability of hydrogen sulfide and promotes autophagy influx in livers of mice fed with high-fat diet

2017 ◽  
Vol 95 (6) ◽  
pp. 667-674 ◽  
Author(s):  
Bing Wang ◽  
Jing Zeng ◽  
Qi Gu
Keyword(s):  
Hydrogen Sulfide ◽  
Exercise Training ◽  
High Fat Diet ◽  
Mass Gain ◽  
Moderate Intensity ◽  
High Fat ◽  
Moderate Intensity Exercise ◽  
Nonalcoholic Fatty Liver ◽  
Mercaptopyruvate Sulfurtransferase ◽  
Underlying Mechanisms

In the gold standard treatment for nonalcoholic fatty liver disease (NAFLD), exercise training has been shown to effectively improve nonalcoholic steatohepatitis (NASH). However, limited data are available about the underlying mechanisms involved. This work was undertaken to investigate the mechanisms underlying the beneficial effect of exercise training on high-fat diet (HFD)-induced NAFLD in mice. Male mice were fed with HFD and given moderate-intensity exercise for 24 weeks. Exercise training lowered mass gain, attenuated systemic insulin resistance and glucose intolerance, and mitigated hepatic steatosis and fibrosis in mice fed with HFD. Exercise training improved mitochondrial function and enhanced mitochondrial β-oxidation in livers of HFD-fed mice. Exercise training enhanced hydrogen sulfide (H2S) levels in plasma and livers, and mRNA expression of cystathionine β-synthase (CBS), cystathionine γ-lyase (CES), and 3-mercaptopyruvate sulfurtransferase (3-MST) in livers of HFD-fed mice. Exercise training had no significant effect on the ratio of LC3-II/LC3-I, but decreased p62 protein expression in livers of HFD-fed mice. Additionally, exercise training reduced formation of malondialdehyde, enhanced ratio of GSH/GSSG, and down-regulated expression of TNF-α and IL-6 in livers of HFD-fed mice. Exercise training restored bioavailability of H2S and promoted autophagy influx in livers, which might contribute to its benefit on HFD-induced NAFLD.

P52 Endogenous hydrogen sulfide protects pancreatic beta-cells from a high-fat diet-induced glucotoxicity and prevents the development of type 2 diabetes

Nitric Oxide ◽  
2014 ◽  
Vol 39 ◽  
pp. S31-S32
Author(s):  
Mitsuhiro Okamoto ◽  
Mami Yamaoka ◽  
Tomomi Ando ◽  
Masahiro Takei ◽  
Shigeki Taniguchi ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Hydrogen Sulfide ◽  
Beta Cells ◽  
High Fat Diet ◽  
Pancreatic Beta Cells ◽  
High Fat

Endogenous hydrogen sulfide protects pancreatic beta-cells from a high-fat diet-induced glucotoxicity and prevents the development of type 2 diabetes

2013 ◽  
Vol 442 (3-4) ◽  
pp. 227-233 ◽  
Author(s):  
Mitsuhiro Okamoto ◽  
Mami Yamaoka ◽  
Masahiro Takei ◽  
Tomomi Ando ◽  
Shigeki Taniguchi ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Hydrogen Sulfide ◽  
Beta Cells ◽  
High Fat Diet ◽  
Pancreatic Beta Cells ◽  
High Fat

Hypoxic Exercise Training Promotes apelin/APJ Expression in Skeletal Muscles of High Fat Diet-Induced Obese Mice

2016 ◽  
Vol 24 (1) ◽  
pp. 64-70 ◽  
Author(s):  
Weixiu Ji ◽  
Lijing Gong ◽  
Jianxiong Wang ◽  
Hui He ◽  
Ying Zhang
Keyword(s):  
Exercise Training ◽  
High Fat Diet ◽  
Skeletal Muscles ◽  
Obese Mice ◽  
High Fat ◽  
Hypoxic Exercise

scholarly journals Characterizing the Retinal Phenotype in the High-Fat Diet and Western Diet Mouse Models of Prediabetes

Cells ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 464 ◽  
Author(s):  
Bright Asare-Bediako ◽  
Sunil Noothi ◽  
Sergio Li Calzi ◽  
Baskaran Athmanathan ◽  
Cristiano Vieira ◽  
...  
Keyword(s):  
Body Weight ◽  
High Fat Diet ◽  
Fundus Photography ◽  
Vascular Density ◽  
Sensitivity Index ◽  
High Fat ◽  
Permeability Studies ◽  
Induced Changes ◽  
Acellular Capillaries

We sought to delineate the retinal features associated with the high-fat diet (HFD) mouse, a widely used model of obesity. C57BL/6 mice were fed either a high-fat (60% fat; HFD) or low-fat (10% fat; LFD) diet for up to 12 months. The effect of HFD on body weight and insulin resistance were measured. The retina was assessed by electroretinogram (ERG), fundus photography, permeability studies, and trypsin digests for enumeration of acellular capillaries. The HFD cohort experienced hypercholesterolemia when compared to the LFD cohort, but not hyperglycemia. HFD mice developed a higher body weight (60.33 g vs. 30.17g, p < 0.0001) as well as a reduced insulin sensitivity index (9.418 vs. 62.01, p = 0.0002) compared to LFD controls. At 6 months, retinal functional testing demonstrated a reduction in a-wave and b-wave amplitudes. At 12 months, mice on HFD showed evidence of increased retinal nerve infarcts and vascular leakage, reduced vascular density, but no increase in number of acellular capillaries compared to LFD mice. In conclusion, the HFD mouse is a useful model for examining the effect of prediabetes and hypercholesterolemia on the retina. The HFD-induced changes appear to occur slower than those observed in type 2 diabetes (T2D) models but are consistent with other retinopathy models, showing neural damage prior to vascular changes.

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