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hyperlipidemias/albumine

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Postprandial lipemia is associated with elevated risk of cardiovascular disease. Very little data exists regarding postprandial response in subjects with metabolic syndrome (MetS). The current study was conducted within the LIPGENE EU Integrated Project. Patients were randomized to one of the four

Diagnostic Utility of Serum Glycated Albumin for Diabetes Mellitus and Its Correlation With Hyperlipidemia.

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BACKGROUND Glycated albumin (GA) is a better marker of short-term glycemic control than glycated hemoglobin (A1c). Dyslipidemia is the main cause of cardiovascular complications in diabetes mellitus (DM). Studies on the correlation of GA with lipid indices are sparse. We investigated the diagnostic

Proteinuria, not altered albumin metabolism, affects hyperlipidemia in the nephrotic rat.

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It has been established previously that nephrotic hyperlipidemia is characterized by both an increase in lipid synthesis and a defect in removal of lipoproteins. The relationship between these defects and altered albumin metabolism is uncertain. One hypothesis is that hepatic lipogenesis increases

Albumin synthesis, albuminuria and hyperlipemia in nephrotic patients.

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Hyperlipemia is a common manifestation of the nephrotic syndrome. Serum lipid concentrations have been observed by others to be negatively correlated with serum protein concentration. Hyperlipemia has been postulated to result from a coordinate increase in the synthesis of both albumin and

[Role of lipolytic enzymes in the development of hyperlipidemia induced by administration of heterologous albumin in rabbits].

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Experiments on rabbits have shown hyperlipidemia to develop within the first 48 h after a single intravenous injection of bovine serum albumin (BSA, fraction V). The mean concentration of blood plasma triglycerides (TG) was considerably higher than normal (by 262% after 24 and by 625% after 48 h).
OBJECTIVE To determine whether cerivastatin, a newly developed novel synthetic potent statin, exerts a renoprotective effect, we assessed urinary albumin excretion (UAE) and plasma and urinary endothelin (ET)-1 concentrations in normotensive microalbuminuric type 2 diabetes patients with

The hyperlipidemia of the nephrotic syndrome. Relation to plasma albumin concentration, oncotic pressure, and viscosity.

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Although hyperlipidemia is a common feature of the nephrotic syndrome, the distribution of cholesterol among the plasma lipoproteins and the mechanism of the enhanced hepatic synthesis of lipoprotein lipids are not well understood. We studied the distribution of cholesterol among the plasma
Urinary albumin-creatinine ratio is a marker of diabetic nephropathy and microvascular damage. Metabolic-related traits are observationally associated with ACR but their causal role is uncertain. Here, we confirmed ACR as a marker of microvascular damage and tested whether metabolic-related traits

The causal role of plasma albumin deficiency in experimental nephrotic hyperlipemia and hypercholesteremia.

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In vivo studies of the role of albumin in endogenous and heparin-activated lipemia-clearing in nephrotic rats.

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Effect of alimentary lipaemia on the glycoproteins and the congo red-binding capacity of albumin in healthy and atherosclerotic individuals.

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Role of serum albumin in lipemia clearing reaction.

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Therapeutic Plasma-albumin Exchange for Hyperlipidemia Induced Acute Pancreatitis.

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Associations between glycated albumin or hemoglobin A1c and the presence of coronary artery disease.

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OBJECTIVE We investigated the associations between serum levels of glycated albumin (GA) or hemoglobin A1c (HbA1c) and the presence of coronary artery disease (CAD) in patients who underwent coronary computed tomography angiography (CTA). RESULTS The study consisted of 244 consecutive patients who

Combination of alcohol and fructose exacerbates metabolic imbalance in terms of hepatic damage, dyslipidemia, and insulin resistance in rats.

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Although both alcohol and fructose are particularly steatogenic, their long-term effect in the development of a metabolic syndrome has not been studied in vivo. Consumption of fructose generally leads to obesity, whereas ethanol can induce liver damage in the absence of overweight. Here,
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