The combination of high dietary methionine plus cholesterol induces myocardial fibrosis in rabbits

Zulli, Anthony; Hare, David; Buxton, Brian F.; Black, M. Jane

doi:10.1016/j.atherosclerosis.2005.06.036

Cited by 10 publications

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References 11 publications

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“…The experiments were carried out according to the National Health and Medical Research Council 'Australian Code of Practice for the Care and Use of Animals for Scientific Purposes' (6th Edition, 1997). The animals were then euthanized by an overdose intravenous injection of ketamine and xylazine via the main ear vein, as previously described elsewhere (Zulli et al 2003(Zulli et al , 2004(Zulli et al , 2006a. The aorta was then excised, cleaned of connective tissue and fat and used for isometric tension studies (Zulli et al 2003).…”

Section: Methodsmentioning

confidence: 99%

“…Hyperhomocysteinemia induces endothelial dysfunction, is pro-atherogenic and is associated with cardiovascular disease (Guthikonda & Haynes 2006). We have previously used a diet consisting of 1% methionine in rabbits to induce endothelial dysfunction, hyperhomocysteinemia and intimal thickening, (Zulli et al 2003) and when coupled with high dietary cholesterol, this abolishes endothelial function and exacerbates atherosclerosis formation (Zulli et al 2003(Zulli et al , 2004, and also induces myocardial fibrosis (Zulli et al 2006a).…”

Section: )mentioning

confidence: 99%

“…2003) and when coupled with high dietary cholesterol, this abolishes endothelial function and exacerbates atherosclerosis formation (Zulli et al. 2003, 2004), and also induces myocardial fibrosis (Zulli et al. 2006a).…”

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A physiologically relevant atherogenic diet causes severe endothelial dysfunction within 4 weeks in rabbit

Rai

Hare

Zulli

2009

Int J Experimental Path

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A physiological atherogenic human diet consists of 0.1% cholesterol, fat, as well as high levels of methionine, which is the precursor to homocysteine. The pathological effects of a diet enriched with physiologically high levels of cholesterol, methionine and fat over a short period on the aorta are unknown. In this regard, we sought to determine the effects of a 0.1% cholesterol diet in combination with a 1% methionine over a 4-week period on endothelial function and artery pathology and the expression of endothelial nitric oxide synthase as well as nitrosative stress by nitrotyrosine (NT), oxidative stress by heat shock protein 70 (HSP70) and endoplasmic reticulum stress by glucose regulated protein 78 (GRP78). Rabbits were fed for 4 weeks a diet supplemented with 1% methionine + 0.1% cholesterol + 5% peanut oil (MC). The endothelial function of the abdominal aorta was examined using organ bath techniques, atherosclerosis determined in each artery by microscopy and eNOS, NT, GRP78 and HSP70 by standard immunohistochemistry. Endothelium dependent relaxation in response to acetylcholine significantly decreased by 63% at 1 muM acetylcholine (P < 0.001) compared with control arteries. There was no evidence of atherosclerosis formation in any artery studied, however, eNOS, NT and GRP78 was clearly present in all arteries studied but HSP70 was not easily detectable. Severe endothelial dysfunction is present in the abdominal aorta of rabbits within 4 weeks of physiological dietary manipulation, possibly due to NT formation and endoplasmic reticulum stress. This model could be used to study the early onset of endothelial dysfunction prior to the initiation of atherosclerosis.

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Section: Methodsmentioning

confidence: 99%

Section: )mentioning

confidence: 99%

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A physiologically relevant atherogenic diet causes severe endothelial dysfunction within 4 weeks in rabbit

Rai

Hare

Zulli

2009

Int J Experimental Path

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“…The myocardium responds to physiological and pathological stress by remodeling with increased deposition of interstitial collagen [ 7 ]. The presence of diffuse myocardial fibrosis has been known to confer risk for various types of CVD [ 8 ], and common traditional cardiovascular risk factors are known to be associated with myocardial fibrosis [ 9 - 12 ]. One noninvasive method to assess diffuse myocardial fibrosis is by measuring the T 1 relaxivity of myocardial tissue before and/or after administration of a gadolinium based contrast agent using cardiovascular magnetic resonance (CMR) [ 13 , 14 ].…”

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confidence: 99%

The association between cardiovascular risk and cardiovascular magnetic resonance measures of fibrosis: the Multi-Ethnic Study of Atherosclerosis (MESA)

Tee

et al. 2015

Journal of Cardiovascular Magnetic Resonance

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BackgroundRisk scores for cardiovascular disease (CVD) are in common use to integrate multiple cardiovascular risk factors in order to identify individuals at greatest risk for disease. The purpose of this study was to determine if individuals at greater cardiovascular risk have T1 mapping indices by cardiovascular magnetic resonance (CMR) indicative of greater myocardial fibrosis.MethodsCVD risk scores for 1208 subjects (men, 50.8%) ages 55–94 years old were evaluated in the Multiethnic Study of Atherosclerosis (MESA) at six centers. T1 times were determined at 1.5Tesla before and after gadolinium administration (0.15 mmol/kg) using a modified Look-Locker pulse sequence. The relationship between CMR measures (native T1, 12 and 25 minute post-gadolinium T1, partition coefficient and extracellular volume fraction) and 14 established different cardiovascular risk scores were determined using regression analysis. Bootstrapping analysis with analysis of variance was used to compare different CMR measures. CVD risk scores were significantly different for men and women (p < 0.001).Results25 minute post gadolinium T1 time showed more statistically significant associations with risk scores (10/14 scores, 71%) compared to other CMR indices (e.g. native T1 (7/14 scores, 50%) and partition coefficient (7/14, 50%) in men. Risk scores, particularly the new 2013 AHA/ASCVD risk score, did not correlate with any CMR fibrosis index.ConclusionsMen with greater CVD risk had greater CMR indices of myocardial fibrosis. T1 times at greater delay time (25 minutes) showed better agreement with commonly used risk score indices compared to ECV and native T1 time.Clinical trial registrationhttp://www.mesa-nhlbi.org/, NCT00005487.

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“…6 However, coronary atherosclerosis induced by dietary hypercholesterolemia was exacerbated by dietary methionine in rabbits, 6 and this combination also induced cardiac fibrosis. 7 In this issue of Hypertension, Zulli et al 8 present data showing in this model that dietary taurine, a downstream metabolite of methionine and cysteine, can ameliorate coronary atherosclerosis and also prevent hyperhomocysteinemia and ameliorated hypermethionemia. This observation raises a number of questions: (1) is there negative feedback by taurine on its own metabolic pathway; (2) if so, is the protective effect of taurine dependent on a reduction in homocysteine; (3) does taurine have antiatherosclerotic effects that are not related to its metabolic pathway; and (4) is dietary taurine supplementation always safe.…”

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Taurine

2009

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The combination of high dietary methionine plus cholesterol induces myocardial fibrosis in rabbits

Cited by 10 publications

References 11 publications

A physiologically relevant atherogenic diet causes severe endothelial dysfunction within 4 weeks in rabbit

A physiologically relevant atherogenic diet causes severe endothelial dysfunction within 4 weeks in rabbit

The association between cardiovascular risk and cardiovascular magnetic resonance measures of fibrosis: the Multi-Ethnic Study of Atherosclerosis (MESA)

Taurine

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