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sitosterol/insultas

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The lymphatic recovery of radiolabeled sitosterol administered in various amounts to the stomach was almost the same between stroke-prone spontaneously hypertensive rats (SHRSPs), a strain having a missense mutation in ATP binding cassette transporter g5 (Abcg5), and Wistar rats, a normal strain.
ATP binding cassette transporter G5 (ABCG5) and ATP binding cassette transporter G8 (ABCG8) have been suggested to transport absorbed plant sterols and cholesterol from enterocytes to the intestinal lumen and from hepatocytes to bile. It has been thought that mutations of ABCG5 or ABCG8 cause the

Mechanisms of phytosterolemia in stroke-prone spontaneously hypertensive and WKY rats.

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Analysis of sterol composition in serum, liver, adipose tissue, adrenals, and abdominal aorta demonstrated that the contents of plant sterols, campesterol and sitosterol, were evidently higher in WKY and stroke-prone spontaneously hypertensive (SHRSP) rats than in Wistar and WKA rats fed a diet
Stroke-prone spontaneously hypertensive rats (SHRSP) deposit plant sterols in their bodies and have a mutation in ATP binding cassette transporter G5 (Abcg5). Lymphatic recovery rates of campesterol and sitosterol in SHRSP rats were comparable to those in Wistar rats, a strain that does not deposit
BACKGROUND Available data are inconsistent regarding factors influencing plasma cholesterol homeostasis marker concentrations and their value in predicting subsequent cardiovascular disease (CVD) events. RESULTS To address this issue, the relationship between markers of cholesterol absorption
OBJECTIVE Hypercholesterolemia is a major risk factor for cardiovascular disease (CVD), and diabetes mellitus and statin treatment affect cholesterol metabolism. The aim of the present study was to evaluate markers of cholesterol metabolism and determine their relationship with CVD in patients
UNASSIGNED To elucidate the effects of intensive LDL-C lowering treatment with a standard dose of statin and ezetimibe in patients with dyslipidaemia and high risk of coronary events, targeting LDL-C less than 70 mg/dL (1.8 mmol/L), compared with standard LDL-C lowering lipid monotherapy targeting
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