Publikasi Scopus FKUI 2021 per tanggal 4 Januari 2021 (879 artikel)

Authors_(Last_Name)

Umbarawan Y., Kawakami R., Syamsunarno M.R.A.A., Obinata H., Yamaguchi A., Hanaoka H., Hishiki T., Hayakawa N., Koitabashi N., Sunaga H., Matsui H., Kurabayashi M., Iso T.

Author S Id

57196077830;57210447153;36142388300;6506181723;23394341400;56020036100;7004072867;57221461061;6603109711;55061468300;57212330485;7103371684;7003498756;

Title

Reduced fatty acid use from cd36 deficiency deteriorates streptozotocin-induced diabetic cardiomyopathy in mice

Year

2021

Source Title

Metabolites

Volume

Issue

Art No

881

Page Start

Page End

Page Count

Cited By

Link

https://www.scopus.com/inward/record.uri?eid=2-s2.0-85121605641&doi=10.3390%2fmetabo11120881&partnerID=40&md5=50b9a38996d07912da5741dbe717f2f0

Affiliations

Department of Cardiovascular Medicine, Gunma University Graduate School of Medicine, 3-39-22 Showa-Machi, Maebashi, 371-8511, Japan; Department of Internal Medicine, Faculty of Medicine, Universitas Indonesia, Jl. Salemba Raya no. 6, Jakarta, 10430, Indonesia; Department of Biomedical Sciences, Universitas Padjadjaran, Jl. Raya Bandung Sumedang KM 21, Jatinangor, 45363, Indonesia; Education and Research Support Center, Gunma University Graduate School of Medicine, 3-39-22 Showa-Machi, Maebashi, 371-8511, Japan; Department of Bioimaging Information Analysis, Gunma University Graduate School of Medicine, 3-39-22 Showa-Machi, Maebashi, 371-8511, Japan; Department of Biochemistry, Keio University School of Medicine, 35 Shinano-Machi, Shinjuku-Ku, Tokyo, 160-8582, Japan; Clinical and Translational Research Center, Keio University School of Medicine, 35 Shinano-Machi, Shinjuku-Ku, Tokyo, 160-8582, Japan; Center for Liberal Arts and Sciences, Ashikaga University, 268-1 Omae-Machi, Ashikaga, 326-8558, Japan; Department of Laboratory Sciences, Gunma University Graduate School of Health Sciences, 3-39-22 Showa-Machi, Maebashi, 371-8511, Japan; Department of Medical Technology and Clinical Engineering, Gunma University of Health and Welfare, 191-1 Kawamagari-Machi, Maebashi, 371-0823, Japan

Authors With Affiliations

Umbarawan, Y., Department of Cardiovascular Medicine, Gunma University Graduate School of Medicine, 3-39-22 Showa-Machi, Maebashi, 371-8511, Japan, Department of Internal Medicine, Faculty of Medicine, Universitas Indonesia, Jl. Salemba Raya no. 6, Jakarta, 10430, Indonesia; Kawakami, R., Department of Cardiovascular Medicine, Gunma University Graduate School of Medicine, 3-39-22 Showa-Machi, Maebashi, 371-8511, Japan; Syamsunarno, M.R.A.A., Department of Cardiovascular Medicine, Gunma University Graduate School of Medicine, 3-39-22 Showa-Machi, Maebashi, 371-8511, Japan, Department of Biomedical Sciences, Universitas Padjadjaran, Jl. Raya Bandung Sumedang KM 21, Jatinangor, 45363, Indonesia; Obinata, H., Education and Research Support Center, Gunma University Graduate School of Medicine, 3-39-22 Showa-Machi, Maebashi, 371-8511, Japan; Yamaguchi, A., Department of Bioimaging Information Analysis, Gunma University Graduate School of Medicine, 3-39-22 Showa-Machi, Maebashi, 371-8511, Japan; Hanaoka, H., Department of Bioimaging Information Analysis, Gunma University Graduate School of Medicine, 3-39-22 Showa-Machi, Maebashi, 371-8511, Japan; Hishiki, T., Department of Biochemistry, Keio University School of Medicine, 35 Shinano-Machi, Shinjuku-Ku, Tokyo, 160-8582, Japan, Clinical and Translational Research Center, Keio University School of Medicine, 35 Shinano-Machi, Shinjuku-Ku, Tokyo, 160-8582, Japan; Hayakawa, N., Department of Biochemistry, Keio University School of Medicine, 35 Shinano-Machi, Shinjuku-Ku, Tokyo, 160-8582, Japan, Clinical and Translational Research Center, Keio University School of Medicine, 35 Shinano-Machi, Shinjuku-Ku, Tokyo, 160-8582, Japan; Koitabashi, N., Department of Cardiovascular Medicine, Gunma University Graduate School of Medicine, 3-39-22 Showa-Machi, Maebashi, 371-8511, Japan; Sunaga, H., Department of Cardiovascular Medicine, Gunma University Graduate School of Medicine, 3-39-22 Showa-Machi, Maebashi, 371-8511, Japan, Center for Liberal Arts and Sciences, Ashikaga University, 268-1 Omae-Machi, Ashikaga, 326-8558, Japan; Matsui, H., Department of Laboratory Sciences, Gunma University Graduate School of Health Sciences, 3-39-22 Showa-Machi, Maebashi, 371-8511, Japan; Kurabayashi, M., Department of Cardiovascular Medicine, Gunma University Graduate School of Medicine, 3-39-22 Showa-Machi, Maebashi, 371-8511, Japan; Iso, T., Department of Cardiovascular Medicine, Gunma University Graduate School of Medicine, 3-39-22 Showa-Machi, Maebashi, 371-8511, Japan, Department of Medical Technology and Clinical Engineering, Gunma University of Health and Welfare, 191-1 Kawamagari-Machi, Maebashi, 371-0823, Japan

Abstract

Cardiac dysfunction is induced by multifactorial mechanisms in diabetes. Deranged fatty acid (FA) utilization, known as lipotoxicity, has long been postulated as one of the upstream events in the development of diabetic cardiomyopathy. CD36, a transmembrane glycoprotein, plays a major role in FA uptake in the heart. CD36 knockout (CD36KO) hearts exhibit reduced rates of FA transport with marked enhancement of glucose use. In this study, we explore whether reduced FA use by CD36 ablation suppresses the development of streptozotocin (STZ)-induced diabetic cardiomyopathy. We found that cardiac contractile dysfunction had deteriorated 16 weeks after STZ treatment in CD36KO mice. Although accelerated glucose uptake was not reduced in CD36KO-STZ hearts, the total energy supply, estimated by the pool size in the TCA cycle, was significantly reduced. The isotopomer analysis with13 C6-glucose revealed that accelerated glycolysis, estimated by enrichment of13 C2-citrate and13 C2-malate, was markedly suppressed in CD36KO-STZ hearts. Levels of ceramides, which are cardiotoxic lipids, were not elevated in CD36KO-STZ hearts compared to wild-type-STZ ones. Furthermore, increased energy demand by transverse aortic constriction resulted in synergistic exacerbation of contractile dysfunction in CD36KO-STZ mice. These findings suggest that CD36KO-STZ hearts are energetically compromised by reduced FA use and suppressed glycolysis; therefore, the limitation of FA utilization is detrimental to cardiac energetics in this model of diabetic cardiomyopathy. © 2021 by the authors. Licensee MDPI, Basel, Switzerland.

Author Keywords

CD36; Ceramide; Diabetic cardiomyopathy; Fatty acid; Glucose; Metabolomics; Streptozotocin

Index Keywords

Publisher

MDPI

Issn

22181989

Isbn

Pubmed Id

Document Type

Article

Sjr Best Quartile

Sjr

1109

Sjr Rank

3744