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Biomedical subjects

M Abbey

Publications and source records attributed to M Abbey.

43 records · Page 3Linked to original sources

Influence of various therapies on hyperlipidemia in diabetes mellitus.

The relationship between diabetes mellitus and the factors involved in its treatment, and plasma lipoprotein concentrations, is far from clear. The prognostic value of plasma HDL cholesterol measurements is also unclear, as none of the published data relating to this are concerned with diabetes mellitus. The plasma concentration of HDL at any particular time is the result of a combination of factors. The production of nascent HDL particles by the liver and intestine, and small HDL particles from unknown sources (which may include triglyceride-rich particles undergoing catabolism in the circulation), and the production of HDL esterified cholesterol by LCAT, are balanced by the still poorly understood mechanisms of HDL catabolism outlined above. Until these mechanisms are better understood, we are unlikely to understand the implications of plasma HDL and HDL cholesterol concentrations in diabetes mellitus, and the effects of treatment of diabetes.

Cholesterol, HDL↗

Changes in lipid and apolipoprotein composition of pig lipoproteins facilitated by rabbit lipid transfer protein.

A lipid transfer protein has been purified from the lipoprotein-free fraction of rabbit plasma. Rabbit lipid transfer protein, which was purified 600-700-fold with a 4% recovery, has an apparent Mr of 68 000 and facilitates the transfer of isotopically labelled cholesteryl ester, triacylglycerol and phosphatidylcholine between low-density lipoprotein (LDL) and high-density lipoprotein (HDL). Rabbit lipid transfer protein, which appears to be very similar to the cholesteryl ester exchange protein previously purified from human plasma, was incubated with pig plasma at 37 degrees C for up to 6 h. Analysis of very-low-density lipoprotein (VLDL, d less than 1.006 g/ml), LDL (d 1.019-1.063 g/ml) and HDL (d 1.090-1.21 g/ml) after incubation showed that lipid transfer protein had a marked effect on the composition of the lipoprotein classes. The VLDL became enriched with cholesteryl ester and depleted of triacylglycerol. The LDL and HDL became enriched with triacylglycerol. In addition to these changes in lipid composition there were also changes in apolipoprotein composition. The most prominent change in apolipoprotein distribution was a marked increase in the apolipoprotein E content of LDL which was observed only after incubation in the presence of lipid transfer protein.

Animals↗

Detection of lipid transfer protein activity in rabbit liver perfusate.

Cholesteryl ester, triacylglycerol and phospholipid transfer activity was detected in rabbit liver perfusate after 2 h perfusions in situ. Lipoproteins were removed from the perfusate plasma by ultracentrifugation prior to hydrophobic interaction chromatography of the lipoprotein-free perfusate. The hydrophobic protein, eluted with water from a Phenyl-Sepharose column, facilitated the transfer of radiolabelled cholesteryl ester, triacylglycerol and phosphatidylcholine from low-density lipoprotein to high-density lipoprotein during 3 h incubations at 37 degrees C. These results suggest that rabbit plasma lipid transfer protein is produced by the liver.

Animals↗

Effect of fish oil on lipoproteins, lecithin:cholesterol acyltransferase, and lipid transfer protein activity in humans.

A group of 33 mildly hypercholesterolemic men were stratified into three groups on diets closely matched except for the polyunsaturated fatty acid supplement. The first group received 14 g/day of linoleic acid (safflower oil); the second group, 9 g of alpha-linolenic acid (linseed oil); and the third group, 3.8 g of n-3 fatty acids (fish oil). Only fish oil lowered plasma triglycerides (by 24% at 6 weeks, p less than 0.05 compared to safflower oil). Very low density lipoprotein (VLDL) apoprotein (apo) B, triglyceride, and cholesterol all fell significantly with the fish-oil diet (p less than 0.01). Low density lipoprotein (LDL) cholesterol fell by 0.18 and 0.10 mmol/l, respectively, with the safflower-oil and linseed-oil diets, but rose by 0.24 mmol/l with the fish-oil diet (p less than 0.05). There was a strong correlation between the changes in VLDL triglyceride and LDL cholesterol with the fish-oil diet (r = -0.84, p less than 0.002). High density lipoprotein (HDL) cholesterol fell slightly in all three groups (p less than 0.02 with the linseed-oil diet only). However, the apo A-I/A-II ratio rose by 5% (p less than 0.05), and the HDL2/HDL3 protein ratio increased by 28% with the fish-oil diet (p less than 0.005). Fish oil reduced the capacity for transfer of cholesteryl ester between LDL and HDL by 23% (p less than 0.02 compared to baseline), reduced plasma lecithin:cholesterol acyltransferase activity by 21% (p less than 0.05), and reduced maximal stimulated thromboxane production by 9% (p less than 0.05). Thus fish oil produced three potentially beneficial changes: significant decreases in VLDL concentration and in thromboxane production and an increase in the HDL2/HDL3 ratio. The increase in the average HDL particle size probably reflected reduced cholesteryl ester acceptor capacity within the smaller pool of VLDL, as well as the decline in lipid transfer activity in plasma involving transfer protein itself, LDL, and HDL.

Apolipoproteins↗

Relationship between sensitivity to dietary fat and dietary cholesterol.

A group of 56 hypercholesterolemic and normocholesterolemic men and women were given approximately 700 mg a day of egg yolk cholesterol in a double-blind, crossover study while they were on a background diet containing approximately 30% of energy as fat. Overall there was a 0.23 mmol/l rise in plasma cholesterol (3.7%, p less than 0.001) after 4 weeks, a 0.19 mmol/l rise in low density lipoprotein (LDL) cholesterol (4.9%, p = 0.002), and a 0.07 mmol/l rise in high density lipoprotein (HDL) cholesterol (5.4%, p less than 0.001). Plasma triglycerides fell by 0.07 mmol/l (5.1%). Normocholesterolemic individuals (plasma cholesterol less than 5.2 mmol/l) experienced small, nonsignificant rises of 0.06, 0.02, and 0.05 mmol/l in total, LDL, and HDL cholesterol, respectively. Hypercholesterolemic subjects were classified on the basis of their response to a low fat diet. Diet-sensitive subjects were defined by a greater than 10% fall in plasma cholesterol on a 25% fat, low cholesterol (less than 200 mg/day) diet. These individuals were found to be more responsive to the effect of dietary cholesterol than were diet-insensitive subjects; the respective changes in the two groups were rises of 0.36 mmol/l versus 0.19 mmol/l in plasma cholesterol (p = 0.06) and rises of 0.30 versus 0.15 mmol/l in LDL cholesterol (p = 0.06). In addition to elevating HDL cholesterol by 0.09 mmol/l and 0.07 mmol/l, respectively, dietary cholesterol also produced an increase in the proportion of HDL2, from 40% to 44% of HDL protein (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Apolipoproteins E↗

Surviving cancer: a review of the impact and consequences.

In this critical review of the literature, the author examines articles assessing the effects on patients of cancer survival. Implications for nursing practice, education and research are also discussed.

Health Services Needs and Demand↗