The novel inflammatory biomarker GlycA and triglyceride-rich lipoproteins are associated with the presence of subclinical myocardial dysfunction in subjects with type 1 diabetes mellitus.


Journal

Cardiovascular diabetology
ISSN: 1475-2840
Titre abrégé: Cardiovasc Diabetol
Pays: England
ID NLM: 101147637

Informations de publication

Date de publication:
24 11 2022
Historique:
received: 23 01 2022
accepted: 23 09 2022
entrez: 26 11 2022
pubmed: 27 11 2022
medline: 30 11 2022
Statut: epublish

Résumé

Subjects with Type 1 diabetes mellitus (T1DM) have an increased incidence of heart failure (HF). Several pathophysiological mechanisms have been involved in its development. The aim of this study was to analyze the potential contribution of the advanced lipoprotein profile and plasma glycosylation (GlycA) to the presence of subclinical myocardial dysfunction in subjects with T1DM. We included subjects from a Danish cohort of T1DM subjects (Thousand & 1 study) with either diastolic and/or systolic subclinical myocardial dysfunction, and a control group without myocardial dysfunction, matched by age, sex and HbA1c. All underwent a transthoracic echocardiogram and an advanced lipoprotein profile obtained by using the NMR-based Liposcale® test. GlycA NMR signal was also analyzed. Systolic dysfunction was defined as left ventricular ejection fraction ≤ 45% and diastolic dysfunction was considered as E/e'≥12 or E/e' 8-12 + volume of the left atrium > 34 ml/m2. To identify a metabolic profile associated with the presence of subclinical myocardial dysfunction, a multivariate supervised model of classification based on least squares regression (PLS-DA regression) was performed. One-hundred forty-six subjects had diastolic dysfunction and 18 systolic dysfunction. Compared to the control group, patients with myocardial dysfunction had longer duration of diabetes (p = 0.005), and higher BMI (p = 0.013), serum NTproBNP concentration (p = 0.001), systolic blood pressure (p < 0.001), albuminuria (p < 0.001), and incidence of advanced retinopathy (p < 0.001). The supervised classification model identified a specific pattern associated with myocardial dysfunction, with a capacity to discriminate patients with myocardial dysfunction from controls. PLS-DA showed that triglyceride-rich lipoproteins (TGRLs), such as VLDL (total VLDL particles, large VLDL subclass and VLDL-TG content) and IDL (IDL cholesterol content), as well as the plasma concentration of GlycA, were associated with the presence of subclinical myocardial dysfunction. Proatherogenic TGRLs and the proinflammatory biomarker Glyc A are strongly associated to myocardial dysfunction in T1DM. These findings suggest a pivotal role of TGRLs and systemic inflammation in the development of subclinical myocardial dysfunction in T1DM.

Sections du résumé

BACKGROUND
Subjects with Type 1 diabetes mellitus (T1DM) have an increased incidence of heart failure (HF). Several pathophysiological mechanisms have been involved in its development. The aim of this study was to analyze the potential contribution of the advanced lipoprotein profile and plasma glycosylation (GlycA) to the presence of subclinical myocardial dysfunction in subjects with T1DM.
METHODS
We included subjects from a Danish cohort of T1DM subjects (Thousand & 1 study) with either diastolic and/or systolic subclinical myocardial dysfunction, and a control group without myocardial dysfunction, matched by age, sex and HbA1c. All underwent a transthoracic echocardiogram and an advanced lipoprotein profile obtained by using the NMR-based Liposcale® test. GlycA NMR signal was also analyzed. Systolic dysfunction was defined as left ventricular ejection fraction ≤ 45% and diastolic dysfunction was considered as E/e'≥12 or E/e' 8-12 + volume of the left atrium > 34 ml/m2. To identify a metabolic profile associated with the presence of subclinical myocardial dysfunction, a multivariate supervised model of classification based on least squares regression (PLS-DA regression) was performed.
RESULTS
One-hundred forty-six subjects had diastolic dysfunction and 18 systolic dysfunction. Compared to the control group, patients with myocardial dysfunction had longer duration of diabetes (p = 0.005), and higher BMI (p = 0.013), serum NTproBNP concentration (p = 0.001), systolic blood pressure (p < 0.001), albuminuria (p < 0.001), and incidence of advanced retinopathy (p < 0.001). The supervised classification model identified a specific pattern associated with myocardial dysfunction, with a capacity to discriminate patients with myocardial dysfunction from controls. PLS-DA showed that triglyceride-rich lipoproteins (TGRLs), such as VLDL (total VLDL particles, large VLDL subclass and VLDL-TG content) and IDL (IDL cholesterol content), as well as the plasma concentration of GlycA, were associated with the presence of subclinical myocardial dysfunction.
CONCLUSION
Proatherogenic TGRLs and the proinflammatory biomarker Glyc A are strongly associated to myocardial dysfunction in T1DM. These findings suggest a pivotal role of TGRLs and systemic inflammation in the development of subclinical myocardial dysfunction in T1DM.

Identifiants

pubmed: 36434633
doi: 10.1186/s12933-022-01652-z
pii: 10.1186/s12933-022-01652-z
pmc: PMC9700974
doi:

Substances chimiques

Triglycerides 0
Lipoproteins 0
Biomarkers 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

257

Informations de copyright

© 2022. The Author(s).

Références

Endocr Metab Immune Disord Drug Targets. 2012 Jun;12(2):132-47
pubmed: 22236025
J Clin Med. 2020 Aug 01;9(8):
pubmed: 32752190
J Proteome Res. 2019 Nov 1;18(11):4038-4045
pubmed: 31503497
J Am Coll Cardiol. 2019 Feb 12;73(5):602-611
pubmed: 30732715
Nat Rev Cardiol. 2020 Sep;17(9):585-607
pubmed: 32080423
Front Physiol. 2018 Oct 30;9:1514
pubmed: 30425649
J Pharm Biomed Anal. 2020 Oct 25;190:113525
pubmed: 32827999
Eur Heart J. 2013 Oct;34(39):3035-87
pubmed: 23996285
Diabet Med. 1996 Sep;13(9):834-40
pubmed: 8891459
J Am Coll Cardiol. 2014 Aug 12;64(6):541-9
pubmed: 25104521
Int J Mol Sci. 2020 Jan 30;21(3):
pubmed: 32019138
J Lab Precis Med. 2020 Apr;5:
pubmed: 32363327
Diabetes Metab Res Rev. 2021 Jan;37(1):e3362
pubmed: 32515046
J Clin Invest. 2011 Jul;121(7):2625-40
pubmed: 21670500
Clin Chem. 2015 May;61(5):714-23
pubmed: 25779987
Basic Res Cardiol. 2018 Nov 15;114(1):2
pubmed: 30443826
Am J Prev Cardiol. 2020 Nov 07;4:100120
pubmed: 34327480
Diabetologia. 2014 Apr;57(4):660-71
pubmed: 24477973
J Am Heart Assoc. 2014 Sep 23;3(5):e001221
pubmed: 25249300
Rev Clin Esp (Barc). 2020 Mar;220(2):135-138
pubmed: 30878139
Am J Med. 2006 Jul;119(7):591-9
pubmed: 16828631
Curr Atheroscler Rep. 2017 Jun;19(6):27
pubmed: 28432635
Lancet. 2015 Feb 26;385 Suppl 1:S86
pubmed: 26312908
Clin Nutr. 2021 Mar;40(3):1241-1246
pubmed: 32847693
J Clin Med. 2020 Jan 27;9(2):
pubmed: 32012794
J Endocrinol Invest. 2021 Apr;44(4):745-753
pubmed: 32734319
J Proteome Res. 2018 Nov 2;17(11):3730-3739
pubmed: 30353728
Curr Opin Lipidol. 2014 Aug;25(4):266-73
pubmed: 24977981
J Am Soc Echocardiogr. 2005 Dec;18(12):1440-63
pubmed: 16376782
Lancet Diabetes Endocrinol. 2015 Nov;3(11):876-85
pubmed: 26388415
J Clin Med. 2019 Nov 05;8(11):
pubmed: 31694246
Lancet Diabetes Endocrinol. 2017 Oct;5(10):799-807
pubmed: 28838683
J Am Coll Cardiol. 2007 Aug 21;50(8):768-77
pubmed: 17707182
Diabetologia. 2014 Apr;57(4):672-80
pubmed: 24449393
Clin Chem. 2016 Jul;62(7):1020-31
pubmed: 27173011
J Am Coll Cardiol. 2006 Feb 7;47(3):598-604
pubmed: 16458143
J Lipid Res. 2015 Mar;56(3):737-746
pubmed: 25568061
Clin Chim Acta. 2019 Aug;495:382-393
pubmed: 31078566
Herz. 2019 Apr;44(2):96-106
pubmed: 30715565
Eur J Clin Invest. 2020 Nov;50(11):e13320
pubmed: 32535887
Diabetes Care. 2001 Sep;24(9):1614-9
pubmed: 11522708
Circ Heart Fail. 2020 Aug;13(8):e007067
pubmed: 32762458
Int J Mol Sci. 2019 Jul 02;20(13):
pubmed: 31269778
Analyst. 2018 Jul 23;143(15):3526-3539
pubmed: 29947623
J Transl Med. 2017 Oct 27;15(1):219
pubmed: 29078787
J Am Coll Cardiol. 2020 Mar 24;75(11):1324-1340
pubmed: 32192660
J Mol Endocrinol. 2017 May;58(4):R225-R240
pubmed: 28373293
Arterioscler Thromb Vasc Biol. 2018 Feb;38(2):464-472
pubmed: 29097364

Auteurs

Carlos Puig-Jové (C)

Department of Endocrinology & Nutrition, University Hospital Mútua de Terrassa, Terrassa, Spain.
Department of Medicine, Autonomous University of Barcelona (UAB), Barcelona, Spain.

Josep Julve (J)

Center for Biomedical Research on Diabetes and Associated Metabolic Diseases (CIBERDEM), Instituto de Salud Carlos III, Barcelona, Spain.
Sant Pau Biomedical Research Institute (IIB Sant Pau), Barcelona, Spain.

Esmeralda Castelblanco (E)

Division of Endocrinology, Metabolism and Lipid Research, Washington University School of Medicine in St. Louis, St Louis, MO, USA.

M Teresa Julián (MT)

Center for Biomedical Research on Diabetes and Associated Metabolic Diseases (CIBERDEM), Instituto de Salud Carlos III, Barcelona, Spain.
Department of Endocrinology & Nutrition, University Hospital and Health Sciences Research Institute Germans Trias i Pujol, Badalona, Spain.

Núria Amigó (N)

Center for Biomedical Research on Diabetes and Associated Metabolic Diseases (CIBERDEM), Instituto de Salud Carlos III, Barcelona, Spain.
Biosfer Teslab SL, Reus, Spain.
Department of Basic Medical Sciences, Universitat Rovira i Virgili (URV), Reus, Spain.

Henrik U Andersen (HU)

Steno Diabetes Center Copenhagen, Herlev, Denmark.

Tarunveer S Ahluwalia (TS)

Steno Diabetes Center Copenhagen, Herlev, Denmark.
Department of Biology, University of Copenhagen, Copenhagen, Denmark.

Peter Rossing (P)

Steno Diabetes Center Copenhagen, Herlev, Denmark.
Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark.

Dídac Mauricio (D)

Center for Biomedical Research on Diabetes and Associated Metabolic Diseases (CIBERDEM), Instituto de Salud Carlos III, Barcelona, Spain.
Faculty of Medicine, University of Vic - Central University of Catalonia (UVic/UCC), Vic, Spain.
Department of Endocrinology & Nutrition, Hospital de la Santa Creu i Sant Pau & Sant Pau Biomedical Research Institute (IIB Sant Pau), Barcelona, Spain.

Magnus T Jensen (MT)

Department of Cardiology, Copenhagen University Hospital Amager Hvidovre, Copenhagen, Denmark.

Núria Alonso (N)

Department of Medicine, Autonomous University of Barcelona (UAB), Barcelona, Spain. nalonso32416@yahoo.es.
Center for Biomedical Research on Diabetes and Associated Metabolic Diseases (CIBERDEM), Instituto de Salud Carlos III, Barcelona, Spain. nalonso32416@yahoo.es.
Department of Endocrinology & Nutrition, University Hospital and Health Sciences Research Institute Germans Trias i Pujol, Badalona, Spain. nalonso32416@yahoo.es.

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