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At least 1,063 records · Page 59Linked to original sources
PubMed1979

Lipoproteins and plasma cholesterol esterification in normal and diabetic subjects.

Serum lipoproteins, separated by preparative ultracentrifugation and the activity of the plasma enzyme lecithin: cholesterol acyltransferase (LCAT) have been measured in insulin-dependent diabetics, non-insulin-dependent diabetics and in age-matched non-diabetic controls. In the insulin-dependent diabetics, mean total serum cholesterol and high density lipoprotein cholesterol (HDL-C) concentrations were significantly higher than in controls. Non-insulin-dependent diabetics had significantly raised total triglycerides and cholesterol, but HDL-C levels were essentially normal. The increased low density lipoprotein cholesterol (LDL-C) in both diabetic groups was statistically significant in men. A methodological study of HDL separation techniques was carried out to facilitate interpretation of these findings. Mean LCAT activity, by a method reflecting combined enzyme and substrate effects was significantly increased in these diabetic groups. The results confirm recent reports of a raised HDL-C in those insulin-dependent diabetics who are prone to coronary heart disease.

Cholesterol↗
PubMedDate not supplied

The effect of bezofibrate and clofibrate on cholesterol accumulation, esterification and removal in cultured 3T3 fibroblasts.

3T3 mouse fibroblasts were used to determine the effect of bezafibrate and clofibrate on the cellular metabolism of cholesterol. In cells incubated in normal medium these agents decreased the incorporation of 3H-labelled oleic acid relative to 14C-labelled linoleic acid into the cholesterol ester fraction. When the 3T3 fibroblasts were incubated with cationised low density lipoprotein (LDL) the amount of esterified cholesterol which accumulated in the cells was greatly increased. This accumulation of cholesterol ester was reduced by bezafibrate and clofibrate. These agents decreased the incorporation of both 3H-labelled oleic acid and 14C-labelled linoleic acid into the cholesterol ester fraction of the cells, with a preferential effect on oleic acid as indicated by a reduction in the 3H/14C ratio. When cells which had been preincubated with cationised LDL were reincubated in normal medium, the removal of esterified cholesterol from the cells was increased by both bezafibrate and clofibrate. The mechanism of the effects of these agents on the metabolism of cellular cholesterol is discussed.

Animals↗
PubMed1996

Increased esterification of cholesterol and transfer of cholesteryl ester to apo B-containing lipoproteins in Type 2 diabetes: relationship to serum lipoproteins A-I and A-II.

This study examines the activity of two key enzymes of reverse cholesterol transport, cholesterol ester transfer protein (CETP) and lecithin:cholesterol acyl transferase (LCAT) in 21 patients with non-insulin dependent diabetes mellitus (NIDDM) and 21 control subjects. Serum CETP was assessed by measuring plasma-mediated cholesteryl ester transfer between pooled exogenous lipoprotein with endogenous LCAT inhibited--an estimate of CETP mass. CETP activity was determined as cholesteryl ester transfer in the presence of the patients' lipoproteins and LCAT (endogenous assay). LCAT activity was determined in the same assay. There was no significant difference in CETP mass between the diabetic and non-diabetic subjects and there was no correlation between CETP mass and LCAT activity. Using the endogenous lipoprotein assay, CETP was elevated in serum from diabetic patients compared to control subjects (10.05 +/- 1.89 vs. 5.50 +/- 0.53 nmol/ml/h P < 0.05). LCAT was also increased in the diabetic patients (53.63 +/- 4.70 vs. 41.22 +/- 3.40 nmol/ml/h P < 0.05). Serum free cholesterol from diabetic and control subjects correlated with CETP activity measured using endogenous lipoprotein assay (r = 0.77, P < 0.001 and r = 0.82, P < 0.001), and also with LCAT activity (r = 0.76, P < 0.01 and r = 0.79, P < 0.01). There was a negative correlation between CETP activity with the endogenous lipoprotein assay and serum high density lipoprotein (HDL) cholesterol in the diabetic patients (r = -0.38, P < 0.01), but not in control subjects. In a subgroup of 10 control subjects, there was a positive correlation between LCAT activity and apolipoprotein (apo) A-I (r = 0.49, P < 0.05) and apo A-II (r = 0.51, P < 0.05) and also between CETP activity (endogenous assay) and apo A-I (r = 0.87, P = 0.001) and apo A-II (r = 0.63, P < 0.05). No relationship was observed between CETP activity and apo A-I or apo A-II in the diabetic subjects. Thus, serum CETP mass was normal in Type 2 diabetes but CETP activity (endogenous assay) was increased and was related to free cholesterol levels and LCAT activity in both diabetic and non-diabetic subjects.

Adult↗
PubMed1995

Influence of estrogen on cholesterol esterification and fatty acid composition in serum lipoproteins of castrated rats.

Total, free and esterified cholesterol and its fatty acid composition were measured in the serum lipoproteins of castrated rats after estradiol administration. In general, castration and treatment with estradiol led to a decrease in total esterified cholesterol content. However, estradiol induced an effect opposite to that of castration on the fatty acid composition in VLDL. The effects were variable in HDL and insignificant in LDL. Similarly, the ratios of essential fatty acid to non-essential fatty acid (EFA/NEFA) and that to monoenoic acid (EFA/ME) were affected differently in castration and estradiol treatment in VLDL, but not in HDL or LDL. The pattern of lipid metabolism in castrated and estradiol-treated rats thus appears opposite to that described in human pathology.

Animals↗
PubMed1984

Structure-activity relationships of estrogens: effects of esterification of the 11 beta-hydroxyl group.

Fourteen esters (formate, acetate, propionate, butyrate, hexanoate, heptanoate, and benzoate) located at C-11 of 11 beta-hydroxyesterone and 11 beta-hydroxyestradiol-17 beta were synthesized and evaluated for uterotropic and gonadotropin release inhibition in rats, as well as their ability to displace (3H) estradiol-17 beta from the rat uterine cytosolic estrogen receptor. The most potent uterotropic agent was 11 beta-formoxyestrone which was 1,625 or 2,500 times as active as 11 beta-hydroxyesterone in the uterotropic or gonadotropin release inhibition assay, respectively. 11 beta-Formoxyestrone was 7.5 times as uterotropic as estradiol-17 beta and equal to estradiol-17 beta in inhibiting gonadotropin release. However, the most potent inhibitor of gonadotropin release was 11 beta-acetoxy-estradiol-17 beta which had 133% of the activity of estradiol-17 beta, although it had only 38% of the activity of estradiol-17 beta in the uterotropic assay. Esters larger than the acetoxy group showed sharply decreased activities in either assay. Despite the high estrogenic potency of the 11-formates or 11-acetates, they were rather weak (6% to 35% as active as estradiol-17 beta) in displacing (3H) estradiol-17 beta from the rat uterine cytosolic estrogen receptor.

Animals↗