scholarly journals Effect of Sleeve Gastrectomy, Roux-En-Y Gastric Bypass, and Ileal Transposition on Myocardial Ischaemia–Reperfusion Injury in Non-Obese Non-Diabetic Rats

Author(s):  
Oleg Kornyushin ◽  
Dmitry Sonin ◽  
Alexander Polozov ◽  
Vitaly Masley ◽  
Nika Bulavinova ◽  
...  

Abstract Bariatric surgery (BS) improves outcomes in patients with myocardial infarction (MI). Here we tested the hypothesis that BS-mediated reduction in fatal MI could be attributed to its infarct-limiting effect. Wistar rats were randomized into five groups: control (CON), sham (SHAM), Roux-en-Y gastric bypass (RYGB), sleeve gastrectomy (SG), and ileotransposition (IT). Ten weeks later, animals were subjected to 30-min myocardial ischemia plus 120-min reperfusion. Infarct size (IS) and no-reflow zone (NRZ) were determined histochemically. Fasting plasma levels of glucagon-like peptide-1 (GLP-1), leptin, ghrelin, and insulin were measured using ELISA. Compared with SHAM, RYGB and SG reduced IS by 22% (p = 0.011) and 10% (p = 0.027), and NRZ by 38% (p = 0.01) and 32% (p = 0.004), respectively. IT failed to reduce IS and NRZ. GLP1 level was increased in the SG and RYGB groups compared with CON. In both the SG and RYGB, leptin level was decreased compared with CON and SHAM. In the SG group, ghrelin level was lower than that in the CON and SHAM. Insulin levels were not different between groups. In conclusion, RYGB and SG increased myocardial tolerance to ischemia–reperfusion injury of non-obese, non-diabetic rats, and their infarct-limiting effect is associated with decreased leptin and ghrelin levels and increased GLP-1 level.

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Oleg Kornyushin ◽  
Dmitry Sonin ◽  
Alexander Polozov ◽  
Vitaly Masley ◽  
Nika Bulavinova ◽  
...  

AbstractBariatric surgery (BS) improves outcomes in patients with myocardial infarction (MI). Here we tested the hypothesis that BS-mediated reduction in fatal MI could be attributed to its infarct-limiting effect. Wistar rats were randomized into five groups: control (CON), sham (SHAM), Roux-en-Y gastric bypass (RYGB), sleeve gastrectomy (SG), and ileotransposition (IT). Ten weeks later, animals were subjected to 30-min myocardial ischemia plus 120-min reperfusion. Infarct size (IS) and no-reflow area were determined histochemically. Fasting plasma levels of glucagon-like peptide-1 (GLP-1), leptin, ghrelin, and insulin were measured using ELISA. Compared with SHAM, RYGB and SG reduced IS by 22% (p = 0.011) and 10% (p = 0.027), and no-reflow by 38% (p = 0.01) and 32% (p = 0.004), respectively. IT failed to reduce IS and no-reflow. GLP-1 level was increased in the SG and RYGB groups compared with CON. In both the SG and RYGB, leptin level was decreased compared with CON and SHAM. In the SG group, ghrelin level was lower than that in the CON and SHAM. Insulin levels were not different between groups. In conclusion, RYGB and SG increased myocardial tolerance to ischemia–reperfusion injury of non-obese, non-diabetic rats, and their infarct-limiting effect is associated with decreased leptin and ghrelin levels and increased GLP-1 level.


2015 ◽  
Vol 308 (10) ◽  
pp. H1287-H1297 ◽  
Author(s):  
Madoka Ihara ◽  
Hiroshi Asanuma ◽  
Satoru Yamazaki ◽  
Hisakazu Kato ◽  
Yoshihiro Asano ◽  
...  

Dipeptidyl peptidase 4 (DPP4) inhibitors suppress the metabolism of the potent antihyperglycemic hormone glucagon-like peptide-1 (GLP-1). DPP4 was recently shown to provide cardioprotection through a reduction of infarct size, but the mechanism for this remains elusive. Known interactions between DPP4 and adenosine deaminase (ADA) suggest an involvement of adenosine signaling in DPP4 inhibitor-mediated cardioprotection. We tested whether the protective mechanism of the DPP4 inhibitor alogliptin against myocardial ischemia-reperfusion injury involves GLP-1- and/or adenosine-dependent signaling in canine hearts. In anesthetized dogs, the coronary artery was occluded for 90 min followed by reperfusion for 6 h. A 4-day pretreatment with alogliptin reduced the infarct size from 43.1 ± 2.5% to 17.1 ± 5.0% without affecting collateral flow and hemodynamic parameters, indicating a potent antinecrotic effect. Alogliptin also suppressed apoptosis as demonstrated by the following analysis: 1) reduction in the Bax-to-Bcl2 ratio; 2) cytochrome c release, 3) an increase in Bad phosphorylation in the cytosolic fraction; and 4) terminal deoxynucleotidyl transferase dUTP nick end labeling assay. This DPP4 inhibitor did not affect blood ADA activity or adenosine concentrations. In contrast, the nonselective adenosine receptor blocker 8-( p-sulfophenyl)theophylline (8SPT) completely blunted the effect of alogliptin. Alogliptin did not affect Erk1/2 phosphorylation, but it did stimulate phosphorylation of Akt, glycogen synthase kinase-3β, and cAMP response element-binding protein (CREB). Only 8SPT prevented alogliptin-induced CREB phosphorylation. In conclusion, the DPP4 inhibitor alogliptin suppresses ischemia-reperfusion injury via adenosine receptor- and CREB-dependent signaling pathways.


Diabetes ◽  
2004 ◽  
Vol 54 (1) ◽  
pp. 146-151 ◽  
Author(s):  
A. K. Bose ◽  
M. M. Mocanu ◽  
R. D. Carr ◽  
C. L. Brand ◽  
D. M. Yellon

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