Men have earlier first-time event of CHD and higher postprandial TAG response compared with women. The aim of this exploratory sub-study was to investigate if intake of meals with the same amount of fat from different dairy products affects postprandial lipoprotein subclasses differently in healthy women and men. A total of thirty-three women and fourteen men were recruited to a randomised controlled cross-over study with four dairy meals consisting of butter, cheese, whipped cream or sour cream, corresponding to 45 g of fat (approximately 60 energy percent). Blood samples were taken at 0, 2, 4 and 6 h postprandially. Lipoprotein subclasses were measured using NMR and analysed using a linear mixed model. Sex had a significant impact on the response in M-VLDL (P=0·04), S-LDL (P=0·05), XL-HDL (P=0·009) and L-HDL (P=0·001) particle concentration (P), with women having an overall smaller increase in M-VLDL-P, a larger decrease in S-LDL-P and a larger increase in XL- and L-HDL-P compared with men, independent of meal. Men showed a decrease in XS-VLDL-P compared with women after intake of sour cream (P<0·01). In men only, XS-VLDL-P decreased after intake of sour cream compared with all other meals (v. butter: P=0·001; v. cheese: P=0·04; v. whipped cream: P=0·006). Meals with the same amount of fat from different dairy products induce different postprandial effects on lipoprotein subclass concentrations in men and women.

The aim of the present study was to identify molecular mechanisms involved in liver fat and cholesterol accumulation in ovariectomised (Ovx) rats fed with high-cholesterol diets. VLDL assembly and bile acid metabolism were specifically targeted. After being either Ovx or sham-operated, the rats were fed a standard diet or a high-fat diet containing 0, 0·25 or 0·5 % cholesterol for 6 weeks. Although Ovx rats exposed to dietary cholesterol intake accumulated the greatest amount of hepatic fat and cholesterol, plasma cholesterol levels were lower (P< 0·05) in these animals than in the corresponding control rats. Accompanying this observation, ovariectomy and dietary cholesterol intake resulted in a down-regulation (P< 0·05) of the expression of genes associated with VLDL assembly, including microsomal TAG transfer protein, diacylglycerol acyltransferase 2, acyl-CoA:cholesterol acyltransferase 2 and apoB-100 as well as genes associated with bile acid metabolism including farnesoid X receptor and bile salt export pump (P< 0·01). These results indicate that high-fat/high-cholesterol diets and ovariectomy concomitantly disrupt hepatic lipid output through defects in VLDL assembly and, most probably, secretion. The results also point to a defect in hepatic bile acid secretion. The present study offers novel insights into intrahepatic lipid metabolism, which may be relevant to metabolic complications found in postmenopausal women.

Minor components from dietary oils can modulate the atherogenic response of the TAG-rich lipoproteins (TRL) in which they are transported. In the present study we investigated the influence of TRL isolated from man after the intake of oleic acid-rich oils with different minor component compositions on VLDL secretion by rat primary hepatocytes. TRL were isolated from nine men after the intake of meals enriched with high-oleic sunflower oil (HOSO) or virgin olive oil (VOO) or VOO enriched with minor components (EVO). TRL were incubated with rat primary hepatocytes and the lipid accumulation was analysed in the cells and the secreted VLDL. The expression of genes for proteins related to hepatic lipid metabolism and VLDL production was also measured. Incubation of hepatocytes with TRL derived from HOSO as compared to VOO led to lower intracellular lipid accumulation and VLDL production despite higher mRNA expression for diacylglycerol-acyltransferase, microsomal TAG transfer protein, apoB and PPARα. When TRL derived from EVO were used there were no changes in VLDL secretion. These results suggest that incorporation of minor components from dietary high-oleic oils into TRL modulates the effect of these atherogenic particles on VLDL secretion.

During the past four decades, research efforts directed toward reducing shell egg cholesterol content have centred on genetic selection or alteration of the laying hens' diet with various nutrients, natural products, non-nutritive factors, or pharmacological agents. However, the vast majority of these experimental approaches elicited only minimal changes (<10%) at best or, as in the case of dietary azasterols and triparanol, resulted in the unacceptable replacement of yolk cholesterol by desmosterol. In contrast, when 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors (‘statins’), garlic paste, or pharmacological amounts of copper were orally administered to chickens, yolk cholesterol levels were reduced by up to 46%, 32%, or 34%, respectively. The previous paper in this two-part series provided a justification for low-cholesterol egg production and reviewed cholesterol metabolism in the laying hen, avian embryonic cholesterol needs, and genetic and nutritional approaches to chicken egg cholesterol reduction. The present paper provides a comprehensive overview of the use of non-nutritive dietary factors and select pharmacological compounds as egg cholesterol-lowering agents, and discusses emerging strategies for lowering the cholesterol content of shell eggs. With the recent advances in avian genomics and transgenesis, it is anticipated that the greatest advances in the area of yolk cholesterol reduction will be attained through manipulation of key genes whose protein products mediate intestinal sterol absorption, hepatic cholesterol and lipoprotein synthesis, and/or lipoprotein uptake by growing oocytes. However, the future commercial availability of low-cholesterol eggs produced by transgenic hens ultimately will be influenced by the nature of the regulatory environment for bioengineered foods, public acceptance, and economics.

Different classes of fibres differ in their potential to lower lipid levels. In order to examine how chemically diverse fibres differ in their hypolipidaemic activity, mucilages of varying chemical composition isolated from three different sources were administered to experimental animals and the metabolism of lipids and lipoproteins was studied. The mucilages used were a galactomannan isolated from fenugreek (Trigonella foenum-graecum) seeds, a glucomannan from Dioscorea esculenta tubers and an arabinogalactan from Colocasia esculenta tubers. Rats were fed these mucilages at a dose of 4 mg/100 g body weight per d for 8 weeks and the changes in the levels of total cholesterol and triacylglycerols in serum, liver and aorta were analysed. All these mucilages decreased lipid levels both in serum and tissues. Among these mucilages, glucomannan showed the most hypolipidaemic effect followed by galactomannan and arabinogalactan. Further, hepatocytes were isolated from the livers of mucilage-fed rats and the synthesis and secretion of lipoproteins were studied using metabolic labelling. There was a decrease in the synthesis and secretion of apoB-containing lipoproteins, mainly VLDL, by hepatocytes isolated from mucilage-fed rats when compared to control (P < 0·05). This was further confirmed by pulse chase analysis. Among the different mucilages, mannose-rich glucomannan showed the most effect followed by galactomannan, and mannose-free arabinogalactan showed minimal effect. Comparison of relative viscosity and water-holding capacity showed that mannan-rich mucilages like galactomannan and glucomannan, which showed greater hypolipidaemic effect, had greater relative viscosity and water-holding capacity. The present results suggested that the hypolipidaemic effect of dietary fibre involves a decrease in hepatic production of VLDL and further that it varies with the nature of the fibre.

In laying hens, cholesterol is primarily biosynthesized in the liver and incorporated into vitellogenin (VTG) and triglyceride-rich very low density lipoprotein (VLDL) particles, which are secreted into the bloodstream and subsequently taken up by growing oocytes via receptor-mediated endocytosis. VLDL and VTG are then intracellularly transformed into yolk, constituting ∼60% and 24% of yolk dry matter and ∼95% and 5% of yolk cholesterol, respectively. During the past four decades, research efforts directed toward reducing shell egg cholesterol content have centred on genetic selection or alteration of the laying hens’ diet with various nutrients, natural products, non-nutritive factors, or pharmacological agents. The present paper will provide a justification for low-cholesterol egg production, primarily in the context of the heterogeneity of response to dietary cholesterol in humans, and will review cholesterol metabolism in the laying hen, avian embryonic cholesterol needs, and genetic and nutritional approaches to chicken egg cholesterol reduction. A subsequent paper will provide a comprehensive overview of the use of non-nutritive dietary factors and select pharmaceuticals as egg cholesterol-lowering agents, and will discuss emerging strategies for lowering the cholesterol content of shell eggs.

The aim of the present study was to determine the influence of the dietary fatty acid profile on the lipoprotein composition in sea bream fed different vegetable oils. Six experimental diets were formulated combining fish oil with three vegetable oils (soybean, rapeseed, linseed) in order to obtain 60–80 % (w/w) fish-oil replacement. VLDL, LDL and HDL in plasma samples were obtained by sequential centrifugal flotation. The lipid class, protein content and fatty acid composition of each lipoprotein fraction were analysed. HDL was the predominant lipoprotein in sea bream plasma containing the highest proportion of protein (34 %) and phosphatidylcholine. LDL presented a high content of cholesterol, whereas triacylglycerol comprised a larger proportion of VLDL. The lipid class of the lipoprotein fractions was affected by the dietary vegetable oils. Thus, a high dietary inclusion of soyabean and linseed oil (80 %) increased the cholesterol in HDL and LDL in comparison to fish oil. Similarly, the triacylglycerol concentration of VLDL was increased in fish fed 80 % soyabean and linseed oils owing to the low n-3 highly unsaturated fatty acid content of these diets. Lipoprotein fatty acid composition easily responded to dietary fatty acid composition. VLDL was the fraction more affected by dietary fatty acid, followed by LDL and HDL. The n-3 highly unsaturated fatty acid content increased in the order VLDL less than LDL and less than HDL, regardless of dietary vegetable oils.

Incorporation of coconut oil (CO) rich in lauric acid into the milk diet induces a lipid infiltration of the liver (steatosis) in 1-month-old calves. Among possible steps involved in diet-induced liver steatosis, the ability of the calf liver to synthesize apolipoprotein (Apo) B and to secrete it as part of VLDL particles was investigated. Liver samples were taken from calves fed for 17 d on a conventional milk replacer containing CO (n 5) and beef tallow (BT, n 4) as reference. Samples were cut into slices 0·5 mm thick and subsequently incubated for 12 h in a medium containing a [35S]methionine–[35S]cysteine mix and 0·8 mM-sodium laurate or oleate, the major fatty acids of CO and BT diets respectively. Concentrations of total [35S]proteins, [35S]albumin and [35S]ApoB in liver cells were 2-fold lower (P=0·08, 0·0004 and 0·03 respectively) in CO- than in BT-fed calves. Although the total amount of proteins secreted (including albumin) was similar in both groups of calves, the amount of VLDL-[35S]Apo secreted was 2-fold lower (P=0·004) in CO- than in BT-fed calves. These results suggest that a CO-enriched milk diet induces in preruminant calves a lipid infiltration of the liver by decreasing ApoB synthesis, leading to a reduction in secretion of VLDL particles.