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Effects of medium-chain triglyceride (MCT) application to SHR on cardiac function, hypertrophy and expression of endothelin-1 mRNA and other genes.

Abstract
In spontaneously hypertensive rats a decrease occurs in myocardial energy supply from long-chain triglyceride (LCT) by CD36 gene mutation-induced dysfunction. We investigated whether long-term intake of medium-chain triglyceride, which enters into cells without CD36, upregulates fatty acid metabolic capacity in the heart of spontaneously hypertensive rats, and whether this upregulation improves cardiac hypertrophy and molecular markers. Male 4-week-old spontaneously hypertensive rats were given medium-chain triglyceride (SHR-MCT) or LCT (SHR-LCT) for 16 weeks. After hemodynamic measurement, we determined myocardial fatty acid metabolic enzyme activity and mRNA expression of molecular markers (endothelin-1, alpha-skeletal actin, angiotensin-converting enzyme and brain natriuretic peptide) for cardiac hypertrophy. We used Wistar-Kyoto rats (WKY-MCT and WKY-LCT) as controls. When compared with SHR-LCT rats, SHRMCT rats showed an increase in myocardial fatty acid metabolic enzyme activity and improvement in cardiac function (left ventricular end-diastolic pressure and +dP/dt/P) and cardiac hypertrophy. Blood pressure did not differ between them. The mRNA expression of endothelin-1, alpha-skeletal actin, angiotensin-converting enzyme and brain natriuretic peptide in the heart was significantly higher in SHR-LCT than in WKY-MCT and WKYLCT rats, and there was no significant difference between SHRLCT and SHR-MCT. These findings suggest that medium-chain triglyceride application to spontaneously hypertensive rats improves decreased cardiac function and cardiac hypertrophy without affecting blood pressure and myocardial mRNA expression of molecular markers. Because mechanical stress to the heart is similar between SHR-LCT and SHR-MCT, this may be a reason for the lack of difference in expression of molecular markers.
AuthorsNobutake Shimojo, Takashi Miyauchi, Motoyuki Iemitsu, Yoko Irukayama-Tomobe, Seiji Maeda, Takeshi Ohkubo, Yukihisa Tanaka, Katsutoshi Goto, Iwao Yamaguchi
JournalJournal of cardiovascular pharmacology (J Cardiovasc Pharmacol) Vol. 44 Suppl 1 Pg. S181-5 (Nov 2004) ISSN: 1533-4023 [Electronic] United States
PMID15838274 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Actins
  • Endothelin-1
  • RNA, Messenger
  • Triglycerides
  • Natriuretic Peptide, Brain
  • 3-Hydroxyacyl CoA Dehydrogenases
  • Peptidyl-Dipeptidase A
Topics
  • 3-Hydroxyacyl CoA Dehydrogenases (metabolism)
  • Actins (metabolism)
  • Animals
  • Blood Pressure
  • Cardiomegaly (genetics, metabolism, physiopathology, prevention & control)
  • Disease Models, Animal
  • Endothelin-1 (genetics, metabolism)
  • Energy Metabolism
  • Heart Rate
  • Hypertension (complications, genetics, metabolism, physiopathology)
  • Male
  • Myocardium (enzymology, metabolism, pathology)
  • Natriuretic Peptide, Brain (metabolism)
  • Peptidyl-Dipeptidase A (metabolism)
  • RNA, Messenger (metabolism)
  • Rats
  • Rats, Inbred SHR
  • Rats, Inbred WKY
  • Time Factors
  • Triglycerides (metabolism)
  • Ventricular Function, Left
  • Ventricular Pressure

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