Hyperglycemia-Induced Cardiac Damage Is Alleviated by Heat-Inactivated Lactobacillus reuteri GMNL-263 via Activation of the IGF1R Survival Pathway
- PMID: 33527184
- DOI: 10.1007/s12602-021-09745-z
Hyperglycemia-Induced Cardiac Damage Is Alleviated by Heat-Inactivated Lactobacillus reuteri GMNL-263 via Activation of the IGF1R Survival Pathway
Abstract
Diabetes-induced cardiomyocyte apoptosis is one of the major causes of mortality in patients with diabetes. Numerous studies have indicated the beneficial effects of Lactobacillus reuteri GMNL-263. However, the protective effect of Lactobacillus reuteri GMNL-263 in cardiac damage associated with diabetes remains poorly understood. In this study, we aimed to investigate the protective effect of Lactobacillus reuteri GMNL-263 on cardiomyocytes in diabetic rats. Five-week-old male Wistar rats were categorized into normal control group, diabetes group (55 mg/kgw STZ-induced diabetes via intraperitoneal injection), and diabetic animals treated with Lactobacillus reuteri GMNL-263 (109 CFU/rat/day, oral administration for 4 weeks). The results were presented that oral administration of a high dose of Lactobacillus reuteri GMNL-263 in diabetic rats activated IGF1R cell survival pathways to decrease the Fas-dependent and mitochondrial-dependent apoptotic pathways induced by hyperglycemia. We found that GMNL-263 significantly attenuated cell apoptosis via the IGF1R survival pathway in diabetic rats. The findings of this study suggest that GMNL-263 treatment maybe an effective therapeutic approach for the prevention of cardiac apoptosis in patients with diabetes.
Keywords: Diabetes; GMNL-263; Heart; Hyperglycemia; IGF1R.
© 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC part of Springer Nature.
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