Sleeve Gastrectomy Ameliorates Diabetes-Induced Cardiac Hypertrophy Correlates With the MAPK Signaling Pathway

被引:7
作者
Xu, Qian [1 ]
Ding, Huanxin [1 ]
Li, Songhan [1 ]
Dong, Shuohui [1 ]
Li, Linchuan [2 ]
Shi, Bowen [1 ]
Zhong, Mingwei [2 ]
Zhang, Guangyong [1 ]
机构
[1] Shandong Univ, Shandong Prov Qianfoshan Hosp, Dept Gen Surg, Jinan, Peoples R China
[2] Shandong First Med Univ, Dept Gen Surg, Affiliated Hosp 1, Jinan, Peoples R China
来源
FRONTIERS IN PHYSIOLOGY | 2021年 / 12卷
基金
中国国家自然科学基金;
关键词
diabetes-induced cardiac hypertrophy; sleeve gastrectomy; MAPK; ERK1; 2; DUSP6; HEART-FAILURE; CARDIOMYOPATHY; METABOLISM; ACTIVATION; INHIBITORS; MELLITUS;
D O I
10.3389/fphys.2021.785799
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Background: Cardiac hypertrophy as a main pathological manifestation of diabetic cardiomyopathy (DCM), is a significant complication of diabetes. Bariatric surgery has been proven to relieve DCM; however, whether it can alleviate diabetes-induced cardiac hypertrophy is undefined.Methods: Diabetic and obese rats were performed sleeve gastrectomy (SG) after having diabetes for 16weeks. The rats were euthanized 8weeks after SG. Metabolic parameters, heart function parameters, myocardial glucose uptake, morphometric and histological changes, and the expression level of mitogen-activated protein kinases (MAPKs) were determined and compared among the control group (CON group), diabetes mellitus group (DM group), sham operation group (SHAM group), and SG group.Results: Compared with the SHAM group, the blood glucose, body weight, insulin resistance, and other metabolic parameters were significantly improved in the SG group. There was also a marked improvement in myocardial morphometric and histological parameters after SG. Furthermore, the myocardial glucose uptake and heart function were reversed after SG. Additionally, the phosphorylation of MAPKs was inhibited after SG, including p38 MAPKs, c-Jun N-terminal kinases (JNKs), and extracellular signal-regulated kinases 1/2 (ERK1/2). The expression of DUSP6, which dephosphorylates ERK1/2, was upregulated after SG. These findings suggest that SG ameliorated diabetes-induced cardiac hypertrophy correlates with the MAPK signaling pathway.Conclusion: These results showed that diabetes-induced cardiac hypertrophy was ameliorated after SG was closely related to the inhibition of the MAPK signaling pathway and upregulation of DUSP6. Therefore, this study provides a novel strategy for treating diabetes-induced cardiac hypertrophy.
引用
收藏
页数:14
相关论文
共 50 条
  • [41] Bawei Chenxiang Wan Ameliorates Cardiac Hypertrophy by Activating AMPK/PPAR-α Signaling Pathway Improving Energy Metabolism
    Zhang, Xiaoying
    Zhang, Zhiying
    Wang, Pengxiang
    Han, Yiwei
    Liu, Lijun
    Li, Jie
    Chen, Yichun
    Liu, Duxia
    Wang, Jinying
    Tian, Xiaoying
    Zhao, Qin
    Yan, Fengxia
    FRONTIERS IN PHARMACOLOGY, 2021, 12
  • [42] Dapagliflozin attenuates diabetes-induced diastolic dysfunction and cardiac fibrosis by regulating SGK1 signaling
    Lee, Seul-Gee
    Kim, Darae
    Lee, Jung-Jae
    Lee, Hyun-Ju
    Moon, Ro-Kyung
    Lee, Yong-Joon
    Lee, Seung-Jun
    Lee, Oh-Hyun
    Kim, Choongki
    Oh, Jaewon
    Lee, Chan Joo
    Lee, Yong-Ho
    Park, Seil
    Jeon, Ok-Hee
    Choi, Donghoon
    Hong, Geu-Ru
    Kim, Jung-Sun
    BMC MEDICINE, 2022, 20 (01)
  • [43] Dapagliflozin attenuates diabetes-induced diastolic dysfunction and cardiac fibrosis by regulating SGK1 signaling
    Seul-Gee Lee
    Darae Kim
    Jung-Jae Lee
    Hyun-Ju Lee
    Ro-kyung Moon
    Yong-Joon Lee
    Seung-Jun Lee
    Oh-Hyun Lee
    Choongki Kim
    Jaewon Oh
    Chan Joo Lee
    Yong-ho Lee
    Seil Park
    Ok-Hee Jeon
    Donghoon Choi
    Geu-Ru Hong
    Jung-Sun Kim
    BMC Medicine, 20
  • [44] QiShenYiQi Pill Ameliorates Cardiac Fibrosis After Pressure Overload-Induced Cardiac Hypertrophy by Regulating FHL2 and the Macrophage RP S19/TGF-β1 Signaling Pathway
    Anwaier, Gulinigaer
    Xie, Ting-Ting
    Pan, Chun-Shui
    Li, An-Qing
    Yan, Li
    Wang, Di
    Chen, Fan-Kai
    Weng, Ding-Zhou
    Sun, Kai
    Chang, Xin
    Fan, Jing-Yu
    Han, Jing-Yan
    Liu, Jian
    FRONTIERS IN PHARMACOLOGY, 2022, 13
  • [45] Caloric Restriction Ameliorates Angiotensin II-Induced Mitochondrial Remodeling and Cardiac Hypertrophy
    Finckenberg, Piet
    Eriksson, Ove
    Baumann, Marc
    Merasto, Saara
    Lalowski, Maciej M.
    Levijoki, Jouko
    Haasio, Kristiina
    Kyto, Ville
    Muller, Dominik N.
    Luft, Friedrich C.
    Oresic, Matej
    Mervaala, Eero
    HYPERTENSION, 2012, 59 (01) : 76 - U209
  • [46] Liraglutide ameliorates TAC-induced cardiac hypertrophy and heart failure by upregulating expression level of ANP expression
    Li, Ruisha
    Zhang, Keyin
    Xu, Zhenjun
    Yu, Yanrong
    Wang, Dongjin
    Li, Kai
    Liu, Wenxue
    Pan, Jun
    HELIYON, 2024, 10 (11)
  • [47] Darbepoetin-α ameliorates diabetes-induced mesangial cell damage In Vitro and In Vivo
    Xu, Jian Wei
    Lee, Eun Seong
    Chin, Ho Jun
    INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL MEDICINE, 2017, 10 (11): : 15080 - +
  • [48] Downregulation of p38 MAPK Signaling Pathway Ameliorates Tissue-Engineered Corneal Epithelium
    Mao, Yi
    Ou, Shangkun
    Zhu, Chengfang
    Lin, Sijie
    Liu, Xiaodong
    Liang, Minghui
    Yu, Jingwen
    Wu, Yiming
    He, Hui
    Zong, Rongrong
    Lin, Zhirong
    Liu, Zuguo
    Li, Wei
    TISSUE ENGINEERING PART A, 2022, 28 (23-24) : 977 - 989
  • [49] Antioxidant treatment with edaravone or taurine ameliorates diabetes-induced testicular dysfunction in the rat
    Tsounapi, Panagiota
    Saito, Motoaki
    Dimitriadis, Fotios
    Koukos, Sotirios
    Shimizu, Shogo
    Satoh, Keisuke
    Takenaka, Atsushi
    Sofikitis, Nikolaos
    MOLECULAR AND CELLULAR BIOCHEMISTRY, 2012, 369 (1-2) : 195 - 204
  • [50] Novel therapeutic effects of sesamin on diabetes-induced cardiac dysfunction
    Tran Duong Thuy
    Nam Nhut Phan
    Wang, Chih-Yang
    Yu, Han-Gang
    Wang, Shu-Yin
    Huang, Pung-Ling
    Do, Yi-Yin
    Lin, Yen-Chang
    MOLECULAR MEDICINE REPORTS, 2017, 15 (05) : 2949 - 2956