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B Belling

Publications and source records attributed to B Belling.

5 recordsLinked to original sources
PubMed1995

Restriction fragment length polymorphism of the apolipoprotein B gene and response to dietary fat and cholesterol.

OBJECTIVE: The relationship between response to dietary fat and cholesterol, and the EcoRI restriction fragment length polymorphism (RFLP) of the apolipoprotein B(apoB) gene was examined. DESIGN: Forty-nine free-living subjects took part in a prospective double-blind crossover dietary intervention study. The apoB EcoRI cutting site was present in five women and 18 men (E+) and absent in 15 women and 11 men (E-). INTERVENTION: Subjects consumed a low fat (25% energy), low cholesterol (less than 200 mg/day) diet. After two weeks on this background diet (baseline) subjects were randomly assigned to consume a liquid supplement for three weeks which was either fat and cholesterol free or which contained fat (30 to 36 g) and cholesterol (650 to 780 mg). After the first three-week period subjects switched to the other supplement. Blood samples were collected for plasma lipid analysis after an overnight fast on two consecutive days at the end of baseline and on three consecutive days after each three-week supplement period. RESULTS: There was no significant difference in response to diet between the RFLP groups. Changes in plasma total, low density lipoprotein (LDL), high density lipoprotein(HDL), HDL2 and HDL3 cholesterol or plasma triglyceride were not different between the two RFLP groups. There was a significant difference between RFLP groups for baseline HDL2-cholesterol (0.31 +/- 0.04 and 0.16 +/- 0.02 mmol/L for E- and E+ subjects, respectively) which was independent of sex and apoE genotype (P = 0.032). CONCLUSIONS: These results indicate that the EcoRI RFLP of the apoB gene is not associated with response to dietary fat and cholesterol.

Apolipoproteins B↗
PubMed1992

Plasma lipoprotein lipid and Lp[a] changes with substitution of elaidic acid for oleic acid in the diet.

The effect of additional dietary trans fatty acids (7% energy) on plasma lipids was assessed in a double-blind comparison of four separate diets: 1, enriched with butter fat (lauric-myristic-palmitic); 2, oleic acid-rich; 3, elaidic acid-rich; 4, palmitic acid-rich. The total dietary period was 11 weeks and comprised normal foods plus specific fat supplements. In 27 mildly hypercholesterolemic men, total and LDL cholesterol were significantly lower during the 3-week oleic acid-rich diet, and were similar during the other three diets. For the four diets LDL cholesterol levels were in mg/dl: 1, 163; 2, 151; 3, 165; 4, 161. HDL cholesterol was significantly higher with the palmitic acid-rich diet, 42 mg/dl, compared with elaidic acid, 38 mg/dl, which in turn was not lower than with oleic acid, 38 mg/dl. Plasma elaidic acid concentration rose seven-fold with the trans fatty acid diet but did not increase the vulnerability of LDL to oxidative change. The elaidic acid-rich diet led to significant elevations in the level of Lp[a] compared to all the other test diets. The Lp[a] level increased to 296 +/- 220 U/l in the elaidic acid-rich period from 235 +/- 182 (mean +/- SD) in the first ("butter") period (P less than 0.001) compared with 249 +/- 204 in the palmitic acid period (P less than 0.001) and 236 +/- 201 in the oleic acid period (NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

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↗