Hyperglycemia-Induced Cardiac Damage Is Alleviated by Heat-Inactivated Lactobacillus reuteri GMNL-263 via Activation of the IGF1R Survival Pathway

Ker Ping Koay; Bruce Chi Kang Tsai; Chia Hua Kuo; Wei Wen Kuo; Hsiang Ning Luk; Cecilia Hsuan Day; Ray Jade Chen; Michael Yu Chih Chen; V. Vijaya Padma; Chih Yang Huang

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

Ker Ping Koay, Bruce Chi Kang Tsai, Chia Hua Kuo, Wei Wen Kuo, Hsiang Ning Luk, Cecilia Hsuan Day, Ray Jade Chen, Michael Yu Chih Chen, V. Vijaya Padma, Chih Yang Huang

Department of Surgery

Research output: Contribution to journal › Article › peer-review

19 Citations (Scopus)

Abstract

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. Graphical abstract: [Figure not available: see fulltext.]

Original language	English
Pages (from-to)	1044-1053
Number of pages	10
Journal	Probiotics and Antimicrobial Proteins
Volume	13
Issue number	4
DOIs	https://doi.org/10.1007/s12602-021-09745-z
Publication status	Published - Aug 2021

Keywords

Diabetes
GMNL-263
Heart
Hyperglycemia
IGF1R

ASJC Scopus subject areas

Microbiology
Molecular Medicine
Molecular Biology

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1007/s12602-021-09745-z

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Koay, K. P., Tsai, B. C. K., Kuo, C. H., Kuo, W. W., Luk, H. N., Day, C. H., Chen, R. J., Chen, M. Y. C., Padma, V. V., & Huang, C. Y. (2021). Hyperglycemia-Induced Cardiac Damage Is Alleviated by Heat-Inactivated Lactobacillus reuteri GMNL-263 via Activation of the IGF1R Survival Pathway. Probiotics and Antimicrobial Proteins, 13(4), 1044-1053. https://doi.org/10.1007/s12602-021-09745-z

@article{e7d13ba001284803826d28cdb2a93141,

title = "Hyperglycemia-Induced Cardiac Damage Is Alleviated by Heat-Inactivated Lactobacillus reuteri GMNL-263 via Activation of the IGF1R Survival Pathway",

abstract = "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. Graphical abstract: [Figure not available: see fulltext.]",

keywords = "Diabetes, GMNL-263, Heart, Hyperglycemia, IGF1R",

author = "Koay, \{Ker Ping\} and Tsai, \{Bruce Chi Kang\} and Kuo, \{Chia Hua\} and Kuo, \{Wei Wen\} and Luk, \{Hsiang Ning\} and Day, \{Cecilia Hsuan\} and Chen, \{Ray Jade\} and Chen, \{Michael Yu Chih\} and Padma, \{V. Vijaya\} and Huang, \{Chih Yang\}",

note = "Funding Information: This work is supported grant CMU-103-ASIA-13 from China Medical University and Asia University. We would like to acknowledge Dr. Hao-Chin Wang and Dr. B. Mahalakshmi, who provided suggestions during the writing of this manuscript draft. Publisher Copyright: {\textcopyright} 2021, The Author(s), under exclusive licence to Springer Science+Business Media, LLC part of Springer Nature.",

year = "2021",

month = aug,

doi = "10.1007/s12602-021-09745-z",

language = "English",

volume = "13",

pages = "1044--1053",

journal = "Probiotics and Antimicrobial Proteins",

issn = "1867-1306",

publisher = "Springer",

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TY - JOUR

T1 - Hyperglycemia-Induced Cardiac Damage Is Alleviated by Heat-Inactivated Lactobacillus reuteri GMNL-263 via Activation of the IGF1R Survival Pathway

AU - Koay, Ker Ping

AU - Tsai, Bruce Chi Kang

AU - Kuo, Chia Hua

AU - Kuo, Wei Wen

AU - Luk, Hsiang Ning

AU - Day, Cecilia Hsuan

AU - Chen, Ray Jade

AU - Chen, Michael Yu Chih

AU - Padma, V. Vijaya

AU - Huang, Chih Yang

N1 - Funding Information: This work is supported grant CMU-103-ASIA-13 from China Medical University and Asia University. We would like to acknowledge Dr. Hao-Chin Wang and Dr. B. Mahalakshmi, who provided suggestions during the writing of this manuscript draft. Publisher Copyright: © 2021, The Author(s), under exclusive licence to Springer Science+Business Media, LLC part of Springer Nature.

PY - 2021/8

Y1 - 2021/8

N2 - 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. Graphical abstract: [Figure not available: see fulltext.]

AB - 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. Graphical abstract: [Figure not available: see fulltext.]

KW - Diabetes

KW - GMNL-263

KW - Heart

KW - Hyperglycemia

KW - IGF1R

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U2 - 10.1007/s12602-021-09745-z

DO - 10.1007/s12602-021-09745-z

M3 - Article

C2 - 33527184

AN - SCOPUS:85100097184

SN - 1867-1306

VL - 13

SP - 1044

EP - 1053

JO - Probiotics and Antimicrobial Proteins

JF - Probiotics and Antimicrobial Proteins

IS - 4

ER -

Hyperglycemia-Induced Cardiac Damage Is Alleviated by Heat-Inactivated Lactobacillus reuteri GMNL-263 via Activation of the IGF1R Survival Pathway

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

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