Table 2.
Cardiovascular Benefits and Mechanisms Associated With Exercise-Regulated Microbiome Metabolites
| Metabolite | Disease or Model | Mechanisms | Ref. # | |
|---|---|---|---|---|
| Short-chain fatty acids | Propionate | Hypertensive | Propionate affected immune homeostasis and beneficially modulated effector T cells. | 201 |
| Akt2 knockout–induced cardiac contractile and mitochondrial dysfunction | Propionate attenuated the decrease in G protein–coupled receptor GPR41 in this model. | 202 | ||
| Myocardial infarction | Propionate promoted macrophages reduction and inhibited JNK/P38/NFκB. | 203 | ||
| Butyrate | Diabetic cardiomyopathy mice (streptozotocin) | Butyrate inhibited HDAC4 and increased GLUT1 and GLUT4, as well as GLUT1 acetylation in the myocardium. | 204 | |
| Diabetic rats (HFD and low dose streptozotocin) | Sodium butyrate and exercise increased VEGF-A and VEGFR2. | 205 | ||
| Doxorubicin-induced cardiotoxicity | Butyrate derivative phenylalanine-butyramide inhibited oxidative and nitrosative stress and counteracted mitochondrial dysfunction. | 206 | ||
| 3-HPA | Myocardial infarction | 3-HPA and 4-HBA increased the expression of NRF2 in oxygen glucose deprivation/reoxygenation-induced neonatal rat cardiomyocytes. | 165 | |
| 4-HBA | ||||
HFD = high-fat diet; VEGF = vascular endothelial growth factor; VEGFR = vascular endothelial growth factor receptor.