Key result
Serum PGC-1 alpha levels are significantly lower in patients with diabetes and myocardial infarction.
Why the study?
The study explored the clinical significance of serum PGC-1 alpha levels in patients with diabetes mellitus and myocardial infarction and investigated the underlying mechanisms.
Does PGC-1 alpha reduce oxidative stress and myocardial damage in models of diabetes mellitus with myocardial infarction?
Observational (n=44)
No
Does PGC-1 alpha reduce oxidative stress and myocardial damage in models of diabetes mellitus with myocardial infarction?
p-value: p=<0.01
PGC-1 alpha attenuates ROS-oxidative stress via HO-1 regulation in diabetic cardiomyopathy models, suggesting it as a potential therapeutic target for diabetes mellitus with myocardial infarction.
These observations should not yet alter management; animal data leave open PGC-1α as a therapeutic target in DMMI.
BACKGROUND: In this study, we explored the clinical significance of serum peroxisome proliferator-activated receptor gamma co-activator 1 (PGC-1) alpha levels in diabetes mellitus with myocardial infarction (DMMI) patients and investigated the possible mechanism. MATERIALS AND METHODS: Serum samples were obtained from patients with DMMI or normal volunteer in Baoding First Center Hospital. C57BL/6 mice were induced by a single intraperitoneal (i.p.) injection of 100 mg/kg STZ (streptozocin) for in vivo model. Human myocardial cell lines H9C2 cells were induced with high glucose medium (33 mmol/L glucose) for in vitro model. Western blot was used to analyze the protein expressions in this study. RESULTS: Serum PGC-1 alpha levels were down-regulated in patients with DMMI. There was negative correlation between serum PGC-1 alpha levels and glycated hemoglobin, blood glucose or glucagon in DMMI patients. Recombination of PGC-1 alpha protein decreased the levels of glycated hemoglobin, blood glucose and glucagon, and inhibited oxidative stress and myocardial damage in mice of DMMI. Over-expression of PGC-1 alpha reduced reactive oxygen species (ROS)-oxidative stress, while down-regulation of PGC-1 alpha promoted ROS-oxidative stress via regulation of hemeoxygenase-1 (HO-1) expression in in vitro model of DMMI. The inhibition of HO-1 expression attenuated the anti-oxidation effects of PGC-1 alpha in vitro. CONCLUSION: PGC-1 alpha attenuated ROS-oxidative stress in diabetic cardiomyopathy model, and PGC-1 alpha served as a potential intervention to alleviate DMMI in clinical applications.
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Zhu et al. (2020) conducted an observational in Diabetes mellitus with myocardial infarction (n=44). Serum PGC-1 alpha levels vs. Normal volunteers was evaluated on Serum PGC-1 alpha level differences between groups (p=<0.01). Serum PGC-1 alpha levels were significantly down-regulated in patients with diabetes mellitus and myocardial infarction compared to normal volunteers.
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