Sleeve gastrectomy in obese Wistar rats improves diastolic function and promotes cardiac recovery independent of weight loss.
Bariatric surgery
Diastolic function
Heart failure with preserved ejection fraction
Obesity
Journal
Surgery for obesity and related diseases : official journal of the American Society for Bariatric Surgery
ISSN: 1878-7533
Titre abrégé: Surg Obes Relat Dis
Pays: United States
ID NLM: 101233161
Informations de publication
Date de publication:
Jun 2019
Jun 2019
Historique:
received:
01
10
2018
accepted:
20
02
2019
pubmed:
19
5
2019
medline:
7
7
2020
entrez:
19
5
2019
Statut:
ppublish
Résumé
Heart failure with preserved ejection fraction is the most common cause of heart failure and is characterized by impaired diastolic relaxation. Bariatric surgery significantly improves diastolic relaxation, but a mechanism beyond weight loss remains unknown. We tested the hypothesis that a sleeve gastrectomy (SG) will improve diastolic dysfunction independent of weight loss due to postoperative alterations in the enterocardiac axis. University research laboratory. Male Wistar rats were fed a high-fat diet (HFD) or low-fat diet (LFD) for 10 weeks and then divided into SG-HFD, pair-fed sham HFD, ad-lib sham HFD, or ad-lib sham LFD groups (n = 9-14 per group). At least 2 months postoperatively, cardiac function, meal tolerance, glucose tolerance, and cardiac gene expression were compared between groups. Only the SG cohort showed significant improvements in postoperative diastolic relaxation (isovolumetric relaxation time pre-SG: 14.7 ± 2.3 msec, post-SG: 11.2 ± 1.8 msec, P < .001). SG significantly increased active glucagon-like peptide-1 (P = .03). Compared to pair-fed sham HFD rats, SG-HFD rats had significantly altered mRNA cardiac gene expression, including sarco/endoplasmic reticulum Ca2+-ATPase 2 a (SERCA2 a) (P < .001). SG improves diastolic function independent of weight loss in a rat model of obesity with beneficial alterations in cardiac gene expression of multiple known targets related to cardiac failure, including SERCA2 a. These data support that a greater curve gastrectomy induces beneficial intracellular cardiac signaling for diastolic function mediated by the enterocardiac axis that is independent of weight loss. These findings could translate to offering metabolic surgery to patients with heart failure with preserved ejection fraction.
Sections du résumé
BACKGROUND
BACKGROUND
Heart failure with preserved ejection fraction is the most common cause of heart failure and is characterized by impaired diastolic relaxation. Bariatric surgery significantly improves diastolic relaxation, but a mechanism beyond weight loss remains unknown.
OBJECTIVES
OBJECTIVE
We tested the hypothesis that a sleeve gastrectomy (SG) will improve diastolic dysfunction independent of weight loss due to postoperative alterations in the enterocardiac axis.
SETTING
METHODS
University research laboratory.
METHODS
METHODS
Male Wistar rats were fed a high-fat diet (HFD) or low-fat diet (LFD) for 10 weeks and then divided into SG-HFD, pair-fed sham HFD, ad-lib sham HFD, or ad-lib sham LFD groups (n = 9-14 per group). At least 2 months postoperatively, cardiac function, meal tolerance, glucose tolerance, and cardiac gene expression were compared between groups.
RESULTS
RESULTS
Only the SG cohort showed significant improvements in postoperative diastolic relaxation (isovolumetric relaxation time pre-SG: 14.7 ± 2.3 msec, post-SG: 11.2 ± 1.8 msec, P < .001). SG significantly increased active glucagon-like peptide-1 (P = .03). Compared to pair-fed sham HFD rats, SG-HFD rats had significantly altered mRNA cardiac gene expression, including sarco/endoplasmic reticulum Ca2+-ATPase 2 a (SERCA2 a) (P < .001).
CONCLUSIONS
CONCLUSIONS
SG improves diastolic function independent of weight loss in a rat model of obesity with beneficial alterations in cardiac gene expression of multiple known targets related to cardiac failure, including SERCA2 a. These data support that a greater curve gastrectomy induces beneficial intracellular cardiac signaling for diastolic function mediated by the enterocardiac axis that is independent of weight loss. These findings could translate to offering metabolic surgery to patients with heart failure with preserved ejection fraction.
Identifiants
pubmed: 31101567
pii: S1550-7289(19)30102-9
doi: 10.1016/j.soard.2019.03.036
pmc: PMC6682432
mid: NIHMS1529797
pii:
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
837-842Subventions
Organisme : NCATS NIH HHS
ID : KL2 TR001438
Pays : United States
Informations de copyright
Copyright © 2019 American Society for Bariatric Surgery. Published by Elsevier Inc. All rights reserved.
Références
N Engl J Med. 2000 Apr 13;342(15):1077-84
pubmed: 10760308
Am J Pathol. 2002 Jun;160(6):2035-43
pubmed: 12057908
Physiol Genomics. 2002 Jul 12;10(1):31-44
pubmed: 12118103
Am J Transplant. 2006 Apr;6(4):775-82
pubmed: 16539635
J Bioenerg Biomembr. 2005 Dec;37(6):375-80
pubmed: 16691468
J Clin Endocrinol Metab. 2008 Jul;93(7):2479-85
pubmed: 18430778
J Am Coll Cardiol. 2009 Dec 15;54(25):2376-81
pubmed: 20082927
Circ Res. 2010 Nov 12;107(10):1198-208
pubmed: 21071717
Eur Heart J. 2011 Mar;32(6):670-9
pubmed: 21138935
Gastroenterology. 2011 Sep;141(3):950-8
pubmed: 21699789
Hypertension. 2012 Jan;59(1):70-5
pubmed: 22068866
Endocr Rev. 2012 Apr;33(2):187-215
pubmed: 22323472
Can J Cardiol. 2013 Aug;29(8):969-75
pubmed: 23380297
Circ Res. 2014 Jan 3;114(1):101-8
pubmed: 24065463
Circ Heart Fail. 2013 Nov;6(6):1112-5
pubmed: 24255055
Obes Res Clin Pract. 2012 Jul-Sep;6(3):e175-262
pubmed: 24331521
Nature. 2014 May 8;509(7499):183-8
pubmed: 24670636
Circ Heart Fail. 2015 Mar;8(2):362-72
pubmed: 25669938
Obes Surg. 2016 May;26(5):1030-40
pubmed: 26328532
NCHS Data Brief. 2015 Nov;(219):1-8
pubmed: 26633046
Circulation. 2017 Apr 25;135(17):1577-1585
pubmed: 28258170
Obes Surg. 2017 Sep;27(9):2370-2377
pubmed: 28299572
Surg Endosc. 2018 Feb;32(2):805-812
pubmed: 28779240
Surg Obes Relat Dis. 2018 Jan;14(1):117-122
pubmed: 29108893
J Am Coll Cardiol. 2017 Nov 14;70(20):2476-2486
pubmed: 29141781
J Cardiovasc Transl Res. 2018 Jun;11(3):259-267
pubmed: 29464655