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hyperlipidemias/triglyceride

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OBJECTIVE Elevation of postprandial lipemia characterized by a rise in triglyceride (TG)-rich lipoproteins can increase the risk of atherogenesis. The objective of this study was to investigate postprandial lipemia response to a single dietary fat/sugar load test and monitor beneficial changes

Significant Reduction of Elevated Triglycerides and Liver Fibrosis in Diabetic Dyslipidemia with Saroglitazar: A Case Report.

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Metabolic disorders are characterized by pathologies like visceral adiposity, hypertension, type 2 diabetes mellitus (T2DM), dyslipidemia, impaired glucose tolerance, fatty liver, and so on, with insulin resistance being the main contributing factor. Insulin resistance and diabetes mellitus are

Mitochondrial triglyceride transfer protein inhibition: new achievements in the treatment of dyslipidemias.

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Current lipid-lowering drugs are often unable to achieve low density lipoprotein cholesterol (LDL-C) goals. Moreover, despite LDL-C lowering mostly by statins, a considerable residual vascular risk remains. This is partly associated with atherogenic dyslipidemia where apolipoprotein (apo)
OBJECTIVE Remnant lipoproteins are atherogenic and are accumulated in patients with type III hyperlipidemia (HL). Although type III HL is diagnosed by phenotyping apolipoprotein (apo) E, this procedure is time-consuming and inconvenient for routine clinical use. Clinical indices for screening type

[Reproducibility of fasting serum cholesterol and triglycerides in ambulatory patients with mixed hyperlipidemia].

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Intraindividual variability of serum lipid concentrations in normal volunteers and in patients with hyperlipidemia is substantial. The aim of this study was to investigate prospectively the reproducibility of fasting serum triglyceride and total cholesterol concentrations in primary health care

Effects of glucose ingestion on postprandial lipemia and triglyceride clearance in humans.

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To determine whether the metabolism of diet-derived triglycerides (TG) is acutely regulated by the consumption of insulinogenic carbohydrates, we measured the effects of glucose ingestion on oral and intravenous fat tolerance, and on serum triglyceride concentrations obtained during duodenal fat

Adipocyte triglyceride turnover is independently associated with atherogenic dyslipidemia.

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BACKGROUND Inappropriate storage of fatty acids as triglycerides in adipocytes and their removal from adipocytes through lipolysis and subsequent oxidation may cause the atherogenic dyslipidemia phenotype of elevated apolipoprotein B levels and subsequent hypertriglyceridemia. We tested whether

Intestinal rather than hepatic microsomal triglyceride transfer protein as a cause of postprandial dyslipidemia in diabetes.

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Postprandial dyslipidemia may be a major cause of atherosclerosis in diabetes. Microsomal triglyceride transfer protein (MTP) is essential for the synthesis of the chylomicron particle in the intestine and very low-density lipoprotein (VLDL) in the liver. The purpose of the present study was to
Although myopathy is considered an adverse effect of treatment with 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors and fibrates in combined hyperlipidemia, the present study was performed to investigate whether combined hyperlipidemia itself is associated with skeletal muscle
Triglyceride-rich lipoproteins (TRLs), namely chylomicrons (CMs), VLDL, and their remnants, are implicated in the atherogenic features of postprandial lipemia. In human plasma, cholesteryl ester transfer protein (CETP) mediates the heteroexchange of neutral lipids, ie, triglycerides (TG) and
The effect of atorvastatin, at 10 mg or 40 mg for 6 wk, on lipid and lipoprotein metabolism during the postprandial phase in subjects (n = 11) displaying type IIB hyperlipidemia was evaluated. The postprandial increment in area under the curve above baseline concentrations in type IIB subjects was

Effects of atorvastatin on the clearance of triglyceride-rich lipoproteins in familial combined hyperlipidemia.

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Familial combined hyperlipidemia (FCHL) patients have an impaired catabolism of postprandial triglyceride (TG)-rich lipoproteins (TRLs). We investigated whether atorvastatin corrects the delayed clearance of large TRLs in FCHL by evaluating the acute clearance of Intralipid (10%) and TRLs after oral
Although editing of apolipoprotein (apo)B in the small intestine, yielding apoB-48, is thought to be nearly complete in adult humans, small amounts of intestinal apoB-100 may also be produced. We have evaluated the fraction of unedited apoB secreted from the intestine postprandially in subjects with
In the elderly, the rise in postprandial plasma triglyceride (TG) concentrations is increased, contributing to their increased risk of cardiovascular disease. We sought to determine the incorporation of ingested fat (whipping cream enriched with [1,1,1-(13)C]triolein) into plasma lipids during the

[Determinants of postprandial lipemia measured as diurnal triglyceride profile in non diabetic normolipidemic subjects].

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OBJECTIVE We decided to evaluate the clinical and biochemical predictors of postprandial lipemia, measured as daylong capillarly triglycerides (TGc) profiles, in normolipidemic non diabetic subjects. METHODS We studied 76 normolipidemic non diabetic subjects (45 premenopausal females). Accutrend was
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