2003
DOI: 10.1053/meta.2003.50000
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Disturbed regulation of cholesterol synthesis in monocytes of obese patients with hypercholesterolemia

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Cited by 6 publications
(3 citation statements)
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“…38 On the other hand, to an increased basal cholesterol synthesis and to a decrease in LDL-induced inhibition of endogenous cholesterol synthesis through disturbing activity of 3-hydroxy-3-methylglutarate-coenyzme A. 39 However, the latter was found only in obese subjects with hypercholesterolaemia. In individuals with simple obesity or hypercholesterolaemia, without obesity, alteration of cholesterol synthesis through this pathway was not observed.…”
Section: Resultsmentioning
confidence: 99%
“…38 On the other hand, to an increased basal cholesterol synthesis and to a decrease in LDL-induced inhibition of endogenous cholesterol synthesis through disturbing activity of 3-hydroxy-3-methylglutarate-coenyzme A. 39 However, the latter was found only in obese subjects with hypercholesterolaemia. In individuals with simple obesity or hypercholesterolaemia, without obesity, alteration of cholesterol synthesis through this pathway was not observed.…”
Section: Resultsmentioning
confidence: 99%
“…However, the reason for the presence of increased endogenous cholesterol synthesis in leptin-stimulated OW monocytes compared to control cells remained unresolved. Based on our earlier findings we concluded that the cholesterol homeostasis in monocytes of HC patients with concomitant obesity is not only disturbed in non-stimulated resting cells but is also altered after stimulation (Paragh et al 2003) Our present results raised two questions: (1) Which pathway is responsible for the 500 ng/mL leptin-mediated suppression of cholesterol synthesis in control monocytes? (2) Why is 500 ng/mL leptin-mediated suppression of cholesterol synthesis abolished in cells of OW patients?…”
Section: Discussionmentioning
confidence: 59%
“…Goldstein és Brown vizsgálataiból kiindulva vizsgáltuk az LDL és a módosult LDL szerepét hypercholesterinaemiás és diabeteses betegeken. Azt találtuk, hogy a kontroll egyénekhez képest a koleszterin szintézis gátlás csökkent a hypercholesterinaemiás betegeknél (Paragh et al, 1997). Hasonló elváltozást találtunk a diabeteses betegeknél.…”
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