Prediabetes Induced by Fructose-Enriched Diet Influences Cardiac Lipidome and Proteome and Leads to Deterioration of Cardiac Function prior to the Development of Excessive Oxidative Stress and Cell Damage.


Journal

Oxidative medicine and cellular longevity
ISSN: 1942-0994
Titre abrégé: Oxid Med Cell Longev
Pays: United States
ID NLM: 101479826

Informations de publication

Date de publication:
2019
Historique:
received: 21 06 2019
revised: 03 10 2019
accepted: 16 10 2019
entrez: 31 12 2019
pubmed: 31 12 2019
medline: 12 6 2020
Statut: epublish

Résumé

Prediabetes is a condition affecting more than 35% of the population. In some forms, excessive carbohydrate intake (primarily refined sugar) plays a prominent role. Prediabetes is a symptomless, mostly unrecognized disease which increases cardiovascular risk. In our work, we examined the effect of a fructose-enriched diet on cardiac function and lipidome as well as proteome of cardiac muscle. Male Wistar rats were divided into two groups. The control group received a normal diet while the fructose-fed group received 60% fructose-supplemented chow for 24 weeks. Fasting blood glucose measurement and oral glucose tolerance test (OGTT) showed slightly but significantly elevated values due to fructose feeding indicating development of a prediabetic condition. Both echocardiography and isolated working heart perfusion performed at the end of the feeding protocol demonstrated diastolic cardiac dysfunction in the fructose-fed group. Mass spectrometry-based, high-performance lipidomic and proteomic analyses were executed from cardiac tissue. The lipidomic analysis revealed complex rearrangement of the whole lipidome with special emphasis on defects in cardiolipin remodeling. The proteomic analysis showed significant changes in 75 cardiac proteins due to fructose feeding including mitochondria-, apoptosis-, and oxidative stress-related proteins. Nevertheless, just very weak or no signs of apoptosis induction and oxidative stress were detected in the hearts of fructose-fed rats. Our results suggest that fructose feeding induces marked alterations in the cardiac lipidome, especially in cardiolipin remodeling, which leads to mitochondrial dysfunction and impaired cardiac function. However, at the same time, several adaptive responses are induced at the proteome level in order to maintain a homeostatic balance. These findings demonstrate that even very early stages of prediabetes can impair cardiac function and can result in significant changes in the lipidome and proteome of the heart prior to the development of excessive oxidative stress and cell damage.

Identifiants

pubmed: 31885782
doi: 10.1155/2019/3218275
pmc: PMC6925817
doi:

Substances chimiques

Fructose 30237-26-4

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

3218275

Informations de copyright

Copyright © 2019 Gergő Szűcs et al.

Déclaration de conflit d'intérêts

The authors declare that there is no conflict of interest regarding the publication of this paper.

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Auteurs

Gergő Szűcs (G)

Metabolic Diseases and Cell Signaling Group, Department of Biochemistry, Faculty of Medicine, University of Szeged, Szeged H-6720, Hungary.
Interdisciplinary Centre of Excellence, University of Szeged, Szeged H-6720, Hungary.

Andrea Sója (A)

Metabolic Diseases and Cell Signaling Group, Department of Biochemistry, Faculty of Medicine, University of Szeged, Szeged H-6720, Hungary.
Interdisciplinary Centre of Excellence, University of Szeged, Szeged H-6720, Hungary.

Mária Péter (M)

Institute of Biochemistry, Biological Research Center of the Hungarian Academy of Sciences, Szeged H-6726, Hungary.

Márta Sárközy (M)

Metabolic Diseases and Cell Signaling Group, Department of Biochemistry, Faculty of Medicine, University of Szeged, Szeged H-6720, Hungary.
Interdisciplinary Centre of Excellence, University of Szeged, Szeged H-6720, Hungary.

Bella Bruszel (B)

Interdisciplinary Centre of Excellence, University of Szeged, Szeged H-6720, Hungary.
Institute of Medical Chemistry, Faculty of Medicine, University of Szeged, Szeged H-6720, Hungary.

Andrea Siska (A)

Department of Laboratory Medicine, Faculty of Medicine, University of Szeged, Szeged H-6720, Hungary.

Imre Földesi (I)

Department of Laboratory Medicine, Faculty of Medicine, University of Szeged, Szeged H-6720, Hungary.

Zoltán Szabó (Z)

Interdisciplinary Centre of Excellence, University of Szeged, Szeged H-6720, Hungary.
Institute of Medical Chemistry, Faculty of Medicine, University of Szeged, Szeged H-6720, Hungary.

Tamás Janáky (T)

Interdisciplinary Centre of Excellence, University of Szeged, Szeged H-6720, Hungary.
Institute of Medical Chemistry, Faculty of Medicine, University of Szeged, Szeged H-6720, Hungary.

László Vígh (L)

Institute of Biochemistry, Biological Research Center of the Hungarian Academy of Sciences, Szeged H-6726, Hungary.

Gábor Balogh (G)

Institute of Biochemistry, Biological Research Center of the Hungarian Academy of Sciences, Szeged H-6726, Hungary.

Tamás Csont (T)

Metabolic Diseases and Cell Signaling Group, Department of Biochemistry, Faculty of Medicine, University of Szeged, Szeged H-6720, Hungary.
Interdisciplinary Centre of Excellence, University of Szeged, Szeged H-6720, Hungary.

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