title: 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.
authors.affiliation: Cardiovascular Division, Department of Internal Medicine, University of Tsukuba, Tsukuba, Japan.
authors.forename: Nobutake
authors.initials: N
authors.lastname: Shimojo
authors.forename: Takashi
authors.initials: T
authors.lastname: Miyauchi
authors.forename: Motoyuki
authors.initials: M
authors.lastname: Iemitsu
authors.forename: Yoko
authors.initials: Y
authors.lastname: Irukayama-Tomobe
authors.forename: Seiji
authors.initials: S
authors.lastname: Maeda
authors.forename: Takeshi
authors.initials: T
authors.lastname: Ohkubo
authors.forename: Yukihisa
authors.initials: Y
authors.lastname: Tanaka
authors.forename: Katsutoshi
authors.initials: K
authors.lastname: Goto
authors.forename: Iwao
authors.initials: I
authors.lastname: Yamaguchi
mesh_terms: D015094:3-Hydroxyacyl CoA Dehydrogenases / Q000378:metabolism; D000199:Actins / Q000378:metabolism; D000818:Animals; D001794:Blood Pressure; D006332:Cardiomegaly / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D004195:Disease Models, Animal; D019332:Endothelin-1 / Q000235:genetics / Q000378:metabolism*; D004734:Energy Metabolism; D006339:Heart Rate; D006973:Hypertension / Q000150:complications / Q000235:genetics / Q000378:metabolism* / Q000503:physiopathology; D008297:Male; D009206:Myocardium / Q000201:enzymology / Q000378:metabolism* / Q000473:pathology; D020097:Natriuretic Peptide, Brain / Q000378:metabolism; D007703:Peptidyl-Dipeptidase A / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism*; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D013997:Time Factors; D014280:Triglycerides / Q000378:metabolism*; D016277:Ventricular Function, Left; D017725:Ventricular Pressure
chemical_list: D000199:Actins; D019332:Endothelin-1; D012333:RNA, Messenger; D014280:Triglycerides; D020097:Natriuretic Peptide, Brain; D015094:3-Hydroxyacyl CoA Dehydrogenases; D007703:Peptidyl-Dipeptidase A