hypertrophy/triglyceride

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Myocardial triglyceride content in patients with left ventricular hypertrophy: comparison between hypertensive heart disease and hypertrophic cardiomyopathy.

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Proton magnetic resonance spectroscopy (1H-MRS) enables the assessment of myocardial triglyceride (TG) content, which is reported to be associated with cardiac dysfunction and morphology accompanied by metabolic disorder and cardiac hemodynamic status. The clinical usefulness of myocardial TG

Alpha-syntrophin deficient mice are protected from adipocyte hypertrophy and ectopic triglyceride deposition in obesity.

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Alpha-syntrophin (SNTA) is a molecular adapter protein which is expressed in adipocytes. Knock-down of SNTA in 3T3-L1 preadipocytes increases cell proliferation, and differentiated adipocytes display small lipid droplets. These effects are both characteristics of healthy adipose tissue growth which

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

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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

Metabolic Modulation by Medium-Chain Triglycerides Reduces Oxidative Stress and Ameliorates CD36-Mediated Cardiac Remodeling in Spontaneously Hypertensive Rat in the Initial and Established Stages of Hypertrophy.

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BACKGROUND Left ventricular hypertrophy (LVH) is characterized by a decrease in oxidation of long-chain fatty acids, possibly mediated by reduced expression of the cell-surface protein cluster of differentiation 36 (CD36). Spontaneously hypertensive rats (SHRs) were therefore supplemented with

Insulin resistance and plasma triglyceride level are differently related to cardiac hypertrophy and arterial stiffening in hypertensive subjects.

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OBJECTIVE The frequent association between the type 2 diabetes mellitus and cardio-vascular diseases suggests that metabolic factors may contribute to cardio-vascular remodeling. The aim of our study was to examine the relationships between left ventricular posterior wall thickness (LVPWT), pulse

Potential new cardiovascular risk factors: left ventricular hypertrophy, homocysteine, lipoprotein(a), triglycerides, oxidative stress, and fibrinogen.

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The 1996 Bethesda Conference acknowledged left ventricular hypertrophy, hyperhomocysteinemia, lipoprotein(a) excess, hypertriglyceridemia, oxidative stress, and hyperfibrinogenemia as possible new cardiac risk factors. This review summarizes the current literature that supports these conditions as

Downregulation of adipose triglyceride lipase promotes cardiomyocyte hypertrophy by triggering the accumulation of ceramides.

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Adipose triglyceride lipase (ATGL), the rate-limiting enzyme of triglyceride (TG) hydrolysis, plays an important role in TG metabolism. ATGL knockout mice suffer from TG accumulation and die from heart failure. However, the mechanisms underlying cardiac hypertrophy caused by ATGL dysfunction remain

Blood pressure, cholesterol and triglyceride lowering effects of portacaval anastomosis. Efficacy in the rat, associated with hepatic weight reduction and cardiac and renal hypertrophy.

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Left ventricular hypertrophy and ambulatory blood pressure monitoring in chronic renal failure.

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BACKGROUND Left ventricular hypertrophy (LVH) is both common and an important predictor of risk of death in end-stage renal failure (ESRF). In mild to moderate chronic renal failure (CRF), the timing of onset of LVH and the factors involved in its initial development have not been fully elucidated.

IL-1β directly inhibits milk lipid production in lactating mammary epithelial cells concurrently with enlargement of cytoplasmic lipid droplets.

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Mammary epithelial cells (MECs) in lactating mammary glands produce milk lipid, which provides a large percentage of calories and bioactive lipids for appropriate infant growth. However, secreted milk lipid is often reduced concurrently with increases in IL-1β, IL-6, and TNF-α in mammary glands with

Proteomic analysis of 3T3-L1 adipocyte mitochondria during differentiation and enlargement.

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The increase in adipose tissue mass arises in part from progressive lipid loading and triglyceride accumulation in adipocytes. Enlarged adipocytes produce the highest levels of pro-inflammatory molecules and reactive oxygen species (ROS). Since mitochondria are the site for major metabolic processes

Suppression of adipocyte hypertrophy by polymethoxyflavonoids isolated from Kaempferia parviflora.

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We previously demonstrated that ethyl acetate extracts of Kaempferia parviflora Wall. Ex Baker (KPE) improve insulin resistance in TSOD mice and showed that its components induce differentiation and adipogenesis in 3T3-L1 preadipocytes. The present study was undertaken to examine whether KPE and its

Selenium significantly inhibits adipocyte hypertrophy and abdominal fat accumulation in OLETF rats via induction of fatty acid β-oxidation.

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A combination of selenium (Se) with other trace element is associated with partially modulate fatty acid distribution as well as reduction of the body weight and feed efficiency. To investigate whether or not Se treatment has an impact on lipid metabolism, we examined the levels of lipid

Fenofibrate inhibits adipocyte hypertrophy and insulin resistance by activating adipose PPARalpha in high fat diet-induced obese mice.

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Peroxisome proliferator-activated receptor alpha (PPARalpha) activation in rodents is thought to improve insulin sensitivity by decreasing ectopic lipids in non-adipose tissues. Fenofibrate, a lipid-modifying agent that acts as a PPARalpha agonist, may prevent adipocyte hypertrophy and insulin

Fast-twitch muscle hypertrophy partly induces lipid accumulation inhibition with Alaska pollack protein intake in rats.

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Fish protein is a source of animal protein that is consumed worldwide. Although it has been reported that the intake of Alaska pollack protein (APP) reduces serum triglyceride and body fat accumulation in rats, the mechanisms underlying these effects are poorly understood. In the present study, we

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