cardiomegaly/triacylglycerol

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Cold acclimation induces physiological cardiac hypertrophy and increases assimilation of triacylglycerol metabolism through lipoprotein lipase.

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The contribution of triacylglycerol to energy provision in the hypertrophied heart, mediated through lipoprotein lipase (LPL) is largely unknown and the contribution of very-low-density lipoprotein (VLDL) receptor to control of LPL presentation at the endothelium is unclear. For isolated perfused

Triacylglycerol molecular species are depleted to different extents in the myocardium of spontaneously hypertensive rats fed two oleic acid-rich oils.

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BACKGROUND During the development of hypertension, glucose replaces triacylglycerols (TG) as the main energy source for the myocardium. However, there are no available studies investigating the TG molecular species composition of the myocardium in the spontaneously hypertensive rat (SHR). The

Perturbation of phospholipid and triacylglycerol fatty acid positional location in the heart of rats depleted of n-3 long-chain polyunsaturates.

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Rats depleted of long-chain polyunsaturated n-3 fatty acids (n-3-D) display several features of the metabolic syndrome, including obesity, liver steatosis, insulin resistance, hypertension, and cardiac hypertrophy. In this study, the heart phospholipid (PL) and triacylglycerol (TG) fatty acid

Phospholipid and triacylglycerol fatty acid content and pattern in the cardiac endothelium of rats depleted in long-chain polyunsaturated omega 3 fatty acids.

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Rats depleted in long-chain polyunsaturated omega3 fatty acids (omega3-depleted rats) display several features of the metabolic syndrome including hypertension and cardiac hypertrophy. This coincides with alteration of the cardiac muscle phospholipid and triacylglycerol fatty acid content and/or

Reduction of rat cardiac hypertrophy by osthol is related to regulation of cardiac oxidative stress and lipid metabolism.

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The objective of this study was to examine the therapeutic effect of osthol, a coumarin compound isolated from the fruit of Cnidium monnieri (L.) Cusson, on cardiac hypertrophy in rats and investigate its potential mechanisms. The rats with cardiac hypertrophy induced by renovascular hypertension

LXRα improves myocardial glucose tolerance and reduces cardiac hypertrophy in a mouse model of obesity-induced type 2 diabetes.

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OBJECTIVE Diabetic cardiomyopathy is a myocardial disease triggered by impaired insulin signalling, increased fatty acid uptake and diminished glucose utilisation. Liver X receptors (LXRs) are key transcriptional regulators of metabolic homeostasis. However, their effect in the diabetic heart is

Comprehensive plasma and tissue profiling reveals systemic metabolic alterations in cardiac hypertrophy and failure.

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UNASSIGNED Heart failure is characterized by structural and metabolic cardiac remodelling. The aim of the present study is to expand our understanding of the complex metabolic alterations in the transition from pathological hypertrophy to heart failure and exploit the results from a translational

Long-term programming of blood pressure by maternal dietary iron restriction in the rat.

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We have reported that blood pressure was elevated in 3-month-old rats whose mothers were Fe-restricted during pregnancy. These animals also had improved glucose tolerance and decreased serum triacylglycerol. The aim of the present study was to determine whether these effects of maternal nutritional

Western diet increases cardiac ceramide content in healthy and hypertrophied hearts.

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OBJECTIVE Obesity and cardiac left ventricular hypertrophy (LVH) are recognised independent risk factors in the development of heart failure (HF). However, the combination of these factors may exacerbate the onset of cardiovascular disease by mechanisms as yet unclear. LVH leads to significant

Cardiac lipoprotein lipase activity in the hypertrophied heart may be regulated by fatty acid flux.

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Cardiac hypertrophy is characterised by an imbalance between lipid uptake and fatty acid β-oxidation leading to an accumulation of lipids, particularly triacylglycerol (TAG). It is unclear whether uptake mechanisms such as lipoprotein lipase (LPL) can be attenuated to diminish this uptake. Rats were

Lipid and fatty acid composition of organs from copper-deficient mice.

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Experiments were conducted to study the total lipid and fatty acid composition of liver, kidney, brain and heart of 7-wk-old male C57BL mice. Dietary copper deficiency was initiated at birth by feeding dams a purified diet containing 0.5 mg/kg copper. Offspring were fed the copper-deficient diet 4

Green tea (Cammellia sinensis) attenuates ventricular remodeling after experimental myocardial infarction.

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BACKGROUND Considering the high morbidity and mortality after myocardial infarction (MI), the study of compounds with potential benefits for cardiac remodeling is reasonable. Green tea (GT) (Cammellia sinensis) is the most consumed beverage in the world. The potential action mechanisms of GT include

Obesity-associated cardiac pathogenesis in broiler breeder hens: Development of metabolic cardiomyopathy.

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Feed intake is typically restricted (R) in broiler hens to avoid obesity and improve egg production and livability. To determine whether improved heart health contributes to improved livability, fully adult 45-week-old R hens were allowed to consume feed to appetite (ad libitum; AL) up to 10 wk (70

Dietary Supplementation of 25-Hydroxycholecalciferol Improves Livability in Broiler Breeder Hens-Amelioration of Cardiac Pathogenesis and Hepatopathology.

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A supplement of 69 μg 25-hydroxycholecalciferol (25-OH-D3)/kg feed increased livability in feed restricted (R-hens) broiler breeder hens by 9.9% and by 65.6% in hens allowed ad libitum feed intake (Ad-hens) in a feeding trial from age 26-60 weeks. Hens with higher bodyweight and/or adiposity

Effect of metformin therapy on cardiac function and survival in a volume-overload model of heart failure in rats.

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Advanced HF (heart failure) is associated with altered substrate metabolism. Whether modification of substrate use improves the course of HF remains unknown. The antihyperglycaemic drug MET (metformin) affects substrate metabolism, and its use might be associated with improved outcome in diabetic

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