Disease relevance of Lch

• SUMMARY: A low HDL-cholesterol level in humans is a risk factor for coronary heart disease [1].
• Fibrates, which increase apolipoprotein A-II synthesis, significantly decrease the incidence of major coronary artery disease events, particularly in subjects with low HDL cholesterol, high plasma triglyceride, and high body weight [2].
• CONCLUSIONS: Our results suggest that genetic variation at the eNOS locus is associated with features of metabolic syndrome, and might represent a new genetic susceptibility component for insulin resistance, hypertriglyceridemia, and low HDL-cholesterol concentrations [3].
• The phenotype of low HDL cholesterol with or without elevated triglycerides is at least as common in patients hospitalized for cardiovascular disease as is hypercholesterolemia, and it is characteristic of diabetes and the metabolic syndrome, conditions associated with increased cardiovascular risk [4].
• Low cholesterol levels produced by treating cholesterol deficient mutant mice with a cholesterol synthesis inhibitor (BM 15.766) between days 4 to 7 of pregnancy resulted in malformations consistent with those in the Smith-Lemli-Opitz syndrome (SLOS) [5].

Psychiatry related information on Lch

• Low HDL cholesterol is a significant independent predictor of coronary heart disease (CHD) and HDL raising has been associated with coronary heart disease risk reduction, but there is debate about whether CETP inhibition will reduce coronary heart disease risk [6].

High impact information on Lch

• On a low fat, low cholesterol chow diet these animals have plasma cholesterol levels of 494 mg/dl compared with 60 mg/dl in control animals, and when challenged with a high fat Western-type diet, these animals have plasma cholesterol levels of 1821 mg/dl compared with 132 mg/dl in controls [7].
• Despite the very low cholesterol levels, there was no compensatory increase in cholesterol synthesis or in lipoprotein receptor expression [8].
• The localized change in membrane fluidity due to the low cholesterol concentration could play a role in endocytosis [9].
• alpha-Lipoic acid prevents the increase in atherosclerosis induced by diabetes in apolipoprotein E-deficient mice fed high-fat/low-cholesterol diet [10].
• Saposin A Mobilizes Lipids from Low Cholesterol and High Bis(monoacylglycerol)phosphate-containing Membranes: PATIENT VARIANT SAPOSIN A LACKS LIPID EXTRACTION CAPACITY [11].

Biological context of Lch

• Hdlq10, colocalized with a mutagenesis-induced point mutation (Lch), also affecting HDL [12].
• Downregulation of ABCA1 by unsaturated fatty acids and acetoacetate may contribute to low HDL cholesterol and increased cardiovascular risk of diabetic patients [13].
• Effects of high-fat, low-cholesterol diets on hepatic lipid peroxidation and antioxidants in apolipoprotein E-deficient mice [14].
• Finally, overexpression of the dominant negative N19RhoA inhibited p38 MAPK phosphorylation and apoptosis induced by low cholesterol levels [15].

Anatomical context of Lch

• Herein, we studied the effects of C. pneumoniae infection and a diet with a low-cholesterol supplement on the development of autoantibodies to mouse Hsp60 and early lipid lesions in the aortic valve of C57BL/6JBom mice [16].
• These results indicate that administration of hydroxytyrosol in low cholesterol diets increases atherosclerotic lesion associated with the degree of monocyte activation and remodelling of plasma lipoproteins [17].
• In the aortic arch, HC+A but not LC blocked lesion progression [18].
• HC+A and LC diet reduced, significantly and to the same extent, lesion progression and complication in the aortic root, as assessed by measuring total atherosclerotic lesion area, lesion severity, and macrophage and smooth muscle cell area [18].
• It was also moderately decreased in the spleen of the low cholesterol-fed female mice and in the thyroid gland of the low cholesterol-fed male mice [19].

Associations of Lch with chemical compounds

• This observation suggests the use of RXR-selective agonists, "rexinoids," either alone or in combination with a fibrate as a new therapeutic approach to treating patients with high triglyceride and low HDL cholesterol levels [20].
• ACE activity (nmol. L His-Leu. mg protein(-1)) was measured in lung, kidney, and liver in control (receiving standard chow) and obese animals treated for 30 weeks with a high-fat, low cholesterol diet alone or in combination with LU135252, an orally active ET(A) receptor antagonist [21].
• In mice fed a low cholesterol rodent diet containing SCH 58053, cholesterol absorption was reduced by 46% and fecal neutral sterol excretion was increased 67%, but biliary lipid composition and bile acid synthesis, pool size, and pool composition were unchanged [22].
• We fed for 28 days male mice of 7 inbred strains either a low-cholesterol, commercial diet or a diet containing 2% (w/w) cholesterol, 0.5% cholic acid and 5% olive oil [23].
• Compared with the LC control, avasimibe reduced lesion area by 78% [24].

Other interactions of Lch

• PPARalpha-deficiency in mice fed a high-carbohydrate, low-cholesterol diet was associated with a decreased weight of epididymal adipose tissue and an increased concentration of adipose tissue cholesterol [25].
• The present study was designed to test the range of SR-BI effects in Sf9 insect cells that typically have very low cholesterol content and a different phospholipid profile compared with mammalian cells [26].
• Apoe-/- mice have decreased serum apolipoprotein E and exhibit lipid abnormalities and atherosclerosis even on a low-cholesterol diet [27].
• Apo A-I and LCAT are two potential targets for gene therapy of patients with atherosclerosis associated with a low HDL cholesterol level [28].

Analytical, diagnostic and therapeutic context of Lch

• A third (control) group received a low-cholesterol (LC) supplement (0.1% wt/wt; LC group) [29].

References