Differential effects of saturated and monounsaturated fatty acids on postprandial lipemia and incretin responses in healthy subjects.

BACKGROUND: Elevations of postprandial triacylglycerol-rich plasma lipoproteins and suppressions of HDL-cholesterol concentrations are considered potentially atherogenic. Long-term studies have shown beneficial effects of monounsaturated fatty acids (eg, oleic acid) on fasting lipid and lipoprotein concentrations in humans. A direct stimulatory effect of oleic acid on the secretion of glucagon-like peptide 1 (GLP-1) was shown in animal studies. OBJECTIVE: We compared the postprandial responses of glucose, insulin, fatty acids, triacylglycerol, gastric inhibitory polypeptide (GIP), and GLP-1 to test meals rich in saturated and monounsaturated fatty acids. DESIGN: Ten young, lean, healthy persons ingested 3 meals: an energy-free soup consumed with 50 g carbohydrate (control meal), the control meal plus 100 g butter, and the control meal plus 80 g olive oil. Triacylglycerol and retinyl palmitate responses were measured in total plasma, in a chylomicron-rich fraction, and in a chylomicron-poor fraction. RESULTS: No significant differences in glucose, insulin, or fatty acid responses to the 2 fat-rich meals were seen. Plasma triacylglycerol responses were highest after the butter meal, with chylomicron triacylglycerol rising 2.5-5-fold. Retinyl palmitate responses were higher and more prolonged after the butter meal than after the control and olive oil meals, whereas both postprandial HDL-cholesterol concentrations and GLP-1 and GIP responses were higher after the olive oil meal than after the butter meal. CONCLUSIONS: Olive oil induced lower triacylglycerol concentrations and higher HDL-cholesterol concentrations than butter, without eliciting differences in concentrations of glucose, insulin, or fatty acids. Furthermore, olive oil induced higher concentrations of GLP-1 and GIP than did butter, which may point to a relation between fatty acid composition, incretin responses, and triacylglycerol metabolism in the postprandial phase.     

Postprandial effects of dietary trans fatty acids on apolipoprotein(a) and cholesteryl ester transfer

BACKGROUND: The consumption of trans fatty acids adversely affects fasting plasma lipoprotein concentrations. OBJECTIVE: This study aimed to investigate whether postprandial lipoprotein metabolism is affected by the consumption of trans fatty acids. DESIGN: In a randomized crossover study, 19 healthy men consumed fatty meals that were identical except that 10% of energy was provided as trans 18:1 acids in the trans meal and as oleic acid in the cis meal. RESULTS: The meals induced similar responses in plasma lipids. Cholesteryl ester transfer (CET) was activated after consumption of both meals (P < 0.0001); however, it was 28% higher after the trans meal than after the cis meal (280 +/- 129 compared with 219 +/- 116 nmol cholesteryl ester/mL plasma * 6 h; time x diet interaction: P < 0.0001). Plasma apolipoprotein(a) [apo(a)] concentrations remained constant; however, triacylglycerol-rich lipoproteins formed 4 h after ingestion of the trans meal contained a higher concentration of apo(a) than did those formed after ingestion of the cis meal (48.9 +/- 6.6 compared with 39.6 +/- 5.4 U/L; P < 0.02). The change in CET and in the proportion of plasma apo(a) in the triacylglycerol-rich lipoprotein fractions correlated with indexes of alimentary lipemia. CONCLUSIONS: Consumption of meals high in trans fatty acids results in higher CET and postprandial lipoprotein concentrations enriched in apo(a) than does consumption of meals free of trans fatty acids. This study highlights the importance of double-bond configuration in determining postprandial lipoprotein composition.     

Intestinal absorption of beta-carotene ingested with a meal rich in sunflower oil or beef tallow: postprandial appearance in triacylglycerol-rich lipoproteins in women

BACKGROUND: Evidence indicates that different types of fat have different effects on the postprandial plasma triacylglycerol response. Therefore, the type of fat may influence the appearance of beta-carotene in postprandial triacylglycerol-rich lipoproteins, which is used as an indicator of intestinal beta-carotene absorption. OBJECTIVE: We compared in female subjects the appearance of beta-carotene in plasma triacylglycerol-rich lipoproteins after beta-carotene was ingested with a meal containing sunflower oil or beef tallow. DESIGN: Women (n = 11) each ingested 2 different vitamin A-free, fat-rich meals that were supplemented with beta-carotene (47 micromol) and contained equivalent amounts (60 g) of sunflower oil or beef tallow. Blood samples were collected hourly from 0 to 10 h; additional samples were collected at selected intervals until 528 h. In a subgroup of the women (n = 7), plasma chylomicrons and 3 subfractions of VLDLs were separated by cumulative rate ultracentrifugation. RESULTS: The appearance of beta-carotene in chylomicrons and in each VLDL subfraction was lower after ingestion with the meal containing sunflower oil than after ingestion with the meal containing beef tallow (P < 0.03). In chylomicrons, the area under the concentration-versus-time curve (AUC) for beta-carotene was 38.1 +/- 13.6% lower (P < 0.03); in contrast, the AUC for triacylglycerol was higher (P < 0.05) after the sunflower-oil-rich meal than after the beef-tallow-rich meal. CONCLUSIONS: Ingestion of beta-carotene with a meal rich in sunflower oil as compared with a meal rich in beef tallow results in lower appearance of beta-carotene and greater appearance of triacylglycerol in triacylglycerol-rich lipoproteins.     

Consumption pattern of dietary fats in Chile: n-6 and n-3 fatty acids

Chile consumes both vegetable and animal fats. Vegetable oils are almost totally imported but animal fats, mainly from marine origin, are locally produced. The country is the second world producer of fish meal and fish oil, and fish oil has been incorporated into the human nutrition through the manufacture of blends of vegetable oil with fractions of deodorized fish oil. Consumption of such oils contributes as a significant source of n-6 and n-3 fatty acids, mainly for the low-income consumers. The use of fish meal and fish oil for animal nutrition is also an additional source of n-3 fatty acids for the Chilean population. Pork, poultry and eggs are important sources of essential fatty acids, especially long-chain n-3 fatty acids. As result of the consumption of these products, milk from low-income Chilean mothers shows significantly higher total n-3 fatty acids relative to mothers from the USA and Germany. Safety concerns about fats consumption in Chile are regulated by a Food Safety Codex recently promulgated which follows FAO/WHO Codex Alimentarius directives.     

Effect of 6 dietary fatty acids on the postprandial lipid profile, plasma fatty acids, lipoprotein lipase, and cholesterol ester transfer activities in healthy young men

BACKGROUND: There is increasing evidence that postprandial triacylglycerol-rich lipoproteins may be related to atherogenic risk. OBJECTIVE: The objective was to investigate the effect of individual fatty acid intakes on postprandial plasma lipoprotein triacylglycerol and cholesterol concentrations, plasma fatty acids, and preheparin lipoprotein lipase and cholesterol ester transfer protein (CETP) activities. DESIGN: Six test fats high (approximately 43% by wt) in stearic acid, palmitic acid, palmitic + myristic acid, oleic acid, elaidic acid (trans 18:1), and linoleic acid were produced by interesterification. After having fasted for 12 h, 16 healthy young men were served the individual test fats incorporated into meals (1 g fat/kg body wt) in random order on different days separated by washout periods. Blood samples were drawn before and 2, 4, 6, and 8 h after the meals. RESULTS: Different responses to the test-fat meals were observed for plasma lipoprotein triacylglycerol and cholesterol concentrations, plasma fatty acid concentrations, and lipoprotein lipase and CETP activities (diet x time interaction: 0.001 < P < 0.05). Intake of the long-chain saturated fatty acids stearic and palmitic acids resulted in a relatively lower lipemic response than did intake of the unsaturated fatty acids, probably because the saturated fatty acids were absorbed less and at a lower rate; therefore, the lipemic response took longer to return to postabsorptive values. CONCLUSIONS: Fatty acid chain length and degree of saturation appear to affect the extent and duration of lipemia and affect hepatic output indirectly. These effects may not be mediated via effects on lipoprotein lipase and CETP activities.     

Butter differs from olive oil and sunflower oil in its effects on postprandial lipemia and triacylglycerol-rich lipoproteins after single mixed meals in healthy young men

Accumulation of postprandial triacylglycerol-rich lipoproteins is generated by assimilation of ingested dietary fat and has been increasingly related to atherogenic risk. Nevertheless, the influence of different kinds of dietary fatty acids on postprandial lipid metabolism is not well established, except for (n-3) polyunsaturated long-chain fatty acids. Our goal was to evaluate the effects of test meals containing a common edible fat source of saturated (butter), monounsaturated (olive oil) or (n-6) polyunsaturated (sunflower oil) fatty acids on postprandial lipid and triacylglycerol-rich lipoprotein responses. After a 12-h fast, 10 healthy young men ingested mixed meals containing 0 g (control) or 40 g fat, provided as butter, olive oil or sunflower oil in a random order. Fasting and postmeal blood samples were collected for 7 h. The no-fat test meal did not elicit any change over baseline except for plasma phospholipids, insulin and nonesterified fatty acids. Conversely, the three fat-containing meals elicited bell-shaped postprandial changes (P < 0.05) in serum triacylglycerols, free and esterified cholesterol, and nonesterified fatty acids. The butter meal induced a lower postprandial rise of triacylglycerols in serum and chylomicrons (incremental AUC, mmol.h/L: 0.72) than the two unsaturated oils (olive oil: 1.6, sunflower oil: 1.8), which did not differ. Circulating chylomicrons were smaller after the butter meal than after the two vegetable oil meals. The in vitro susceptibility of circulating chylomicrons to hydrolysis by postheparin plasma was higher after sunflower oil than after butter or olive oil. We conclude that butter results in lower postprandial lipemia and chylomicron accumulation in the circulation of young men than olive or sunflower oils after consumption of a single mixed meal.     

Differential effects of saturated and monounsaturated fats on postprandial lipemia and glucagon-like peptide 1 responses in patients with type 2 diabetes

BACKGROUND: Postprandial lipemia is important in the development of coronary artery disease because of elevated postprandial triacylglycerol-rich plasma lipoproteins and suppressed HDL-cholesterol concentrations. We showed in healthy subjects a possible association between postprandial lipid metabolism and the responses of the duodenal incretin hormones glucagon-like peptide 1 (GLP-1) and gastric inhibitory polypeptide after meals rich in saturated and monounsaturated fatty acids (oleic acid), respectively. OBJECTIVE: The objective was to compare the postprandial responses (8 h) of glucose, insulin, fatty acids, triacylglycerol, gastric inhibitory polypeptide, and GLP-1 to saturated- and monounsaturated-rich test meals. DESIGN: Twelve overweight patients with type 2 diabetes ingested 3 meals randomly: an energy-free soup with 50 g carbohydrate (control meal), the control meal plus 100 g butter, and the control meal plus 80 g olive oil. Triacylglycerol responses were measured in total plasma and in a chylomicron-rich and a chylomicron-poor fraction. RESULTS: No significant differences in the glucose, insulin, or fatty acid responses to the 2 fat-rich meals were seen. The plasma triacylglycerol and chylomicron triacylglycerol responses were highest after the butter meal. HDL-cholesterol concentrations decreased significantly after the butter meal but did not change significantly after the olive oil meal. GLP-1 responses were highest after the olive oil meal. CONCLUSIONS: Olive oil induced lower triacylglycerol concentrations and higher HDL-cholesterol concentrations than did butter, without eliciting significant changes in glucose, insulin, or fatty acids. Furthermore, olive oil induced higher concentrations of GLP-1, which may indicate a relation between fatty acid composition, incretin responses, and triacylglycerol metabolism postprandially in patients with type 2 diabetes.     

Ethanol with a mixed meal increases postprandial triacylglycerol but decreases postprandial non-esterified fatty acid concentrations

Plasma triacylglycerol concentrations increase after the acute ingestion of alcohol (specifically ethanol). However, the effect of ethanol when consumed with a mixed meal has not been well studied. The objective of the present study was to determine the perturbations of lipid metabolism that occur after ingestion of ethanol in combination with a mixed meal of specific fatty acid composition. Blood samples were taken from seven healthy male subjects before and after a mixed meal, with and without ethanol. The specific fatty acid composition of the test meal allowed the fatty acids to be traced into the plasma non-esterified fatty acid pool during the postprandial period. Statistical analysis by repeated measures ANOVA showed significant effects of ethanol. For example, postprandial lipaemia was enhanced after the ethanol test meal compared with the control (P < 0.05), mainly due to increases in triacylglycerol-rich lipoproteins in the flotation range Sf 60-400 (VLDL1) (P < 0.05); those in the range Sf 20-60 (VLDL2) and also Sf > 400 (chylomicrons) were not significantly affected. The later postprandial increase in plasma non-esterified fatty acid concentrations was reduced after the ingestion of ethanol (P < 0.001), but the proportions of palmitoleic acid (a marker of fatty acid content of the test meal) and of linoleic acid (a marker of endogenous lipolysis) were not affected. The results suggest a primary effect of ethanol on the stimulation of secretion of large VLDL particles, which then compete for clearance with chylomicrons by lipoprotein lipase. The results do not support an effect of ethanol on the release of non-esterified fatty acid into the plasma. The suppression of plasma non-esterified fatty acid concentrations during the postprandial period may contribute towards the beneficial effects of moderate ethanol consumption.     

Test meals rich in marine long-chain n-3 polyunsaturated fatty acids increase postprandial chylomicron response

Postprandial lipid abnormalities are considered an independent cardiovascular risk factor. Hence, it is important to find nutritional strategies that are able to positively influence these abnormalities. Since the effect of n-3 polyunsaturated fatty acids (PUFA) and polyphenols on postprandial lipids in humans is still under debate, we evaluated the acute response of triglyceride-rich lipoproteins to test meals that are naturally rich in polyphenols and/or marine long-chain (LC) n-3 PUFAs. We hypothesized that LC n-3 PUFA would have a different effect on chylomicron and very low density lipoproteins when compared with polyphenols or their combination. We randomly assigned 78 individuals who were at high cardiometabolic risk to 4 isoenergetic diets. These diets only differed in amount of LC n-3 PUFA and/or polyphenols. Prior to starting the intervention, each subject underwent a test meal similar to the type of diet assigned: low in LC n-3 PUFA and polyphenols (control), rich in LC n-3 PUFA and low in polyphenols, rich in polyphenols and low in LC n-3 PUFA, or rich in both. Blood samples were taken before and up to 6 hours after the test meal in order to evaluate cholesterol and triglycerides (plasma and triglyceride-rich lipoprotein), apolipoprotein B-48 (large very low density lipoprotein), glucagon-like peptide-1, and free fatty acid plasma levels. The levels of chylomicron cholesterol and triglyceride in response to the test meal rich in LC n-3 PUFA were significantly higher than after the control meal (P = .037 and P = .018); there was no difference in the other variables. In conclusion, this study indicates that acute administration of marine LC n-3 PUFA increases postprandial chylomicron response in contrast with their lowering chronic effects. These differences underline the importance of understanding the acute and chronic effects of nutritional, as well as of other types of, interventions.     

In vitro transfer of apolipoproteins from plasma lipoproteins to artificial lipid particles

Our earlier studies in vivo revealed that artificial lipid particles (exo TG) in lipid emulsion acquire apolipoprotein C-II (apo C-II) from high density lipoprotein (HDL). Since the transfer of apo C-II to exo TG terminated within a short time after the intravenous injection of exo TG, it is likely that exo TG has a high affinity for apolipoprotein. This hypothesis has been investigated in vitro. Human plasma was incubated at 37 degrees C with or without a 10% emulsion of soybean oil for 5 min and 60 min. After the incubation, the plasma was separated into HDL, low density lipoprotein (LDL) and very low density lipoprotein (VLDL). Levels of apo C-II, C-III and E in each lipoprotein fraction were quantified. When the plasma was incubated without exo TG, the distribution of apo C-II and C-III in the lipoprotein fractions was unchanged after incubations for 5 and 60 min. However, when the plasma was incubated with exo TG, apo C-II and C-III in the HDL fraction decreased after a 5 min incubation, while those in the VLDL fraction increased. Apo E in each lipoprotein fraction did not change after 5- and 60-min incubations regardless of the presence or absence of exo TG.(ABSTRACT TRUNCATED AT 250 WORDS)     

Trans monounsaturated fatty acids and saturated fatty acids have similar effects on postprandial flow-mediated vasodilation

OBJECTIVE: Several studies suggest that a fatty meal impairs flow-mediated vasodilation (FMD), a measure of endothelial function. We tested whether the impairment was greater for trans fats than for saturated fats. We did this because we previously showed that replacement of saturated fats by trans fats in a controlled diet decreased FMD after 4 weeks. DESIGN: We fed 21 healthy men two different test meals with 0.9-1.0 g fat/kg body weight in random order: one rich in saturated fatty acids (Sat), mainly from palm kernel fat, and one rich in trans fatty acids (Trans) from partially hydrogenated soy bean oil. The study was performed in our metabolic ward. We had complete data for both diets of 21 men. RESULTS: FMD increased from a fasting value of 2.3+/-2.0% of the baseline diameter to 3.0+/-1.7% after the Sat test meal (95% CI for change -0.33, 1.70) and from 2.7+/-2.3 to 3.1+/-2.0% after the Trans test meal (95% CI for change -0.57, 1.29). The increase after the Sat meal was 0.22 (-1.18-1.61) FMD% higher than after the Trans meal. Serum triacylglycerols increased by 0.46+/-0.36 mmol/l after the Sat test meal and by 0.68+/-0.59 mmol/l after the Trans test meal; a difference of 0.23 (0.07, 0.39) mmol/l. Serum HDL-cholesterol was hardly affected by the test meals. The activity of serum paraoxonase, an esterase bound to HDL, increased slightly after the two test meals but the difference between meals was not significant. CONCLUSION: FMD was not impaired and not different after test meals with saturated or trans fatty acids. Thus, differences in long-term effects of these fats are not caused by differences in acute effects on the vascular wall.     

Intestinal lymph lipoproteins in rats fed diets enriched in specific fatty acids

Four groups of rats were fed test diets with fats providing 75% of fatty acids as palmitate, stearate, oleate or linoleate. Absorption of radiolabeled cholesterol and the specific triglyceride into intestinal lymph lipoproteins and the lipid and protein content and composition of intestinal lymph were compared. Cholesterol and triglyceride absorptions were correlated significantly and were less with the saturated fatty acid diets. The fatty acid patterns of triglyceride-rich lymph lipoproteins mirrored the diet. Exogenous cholesterol was recovered primarily in chylomicrons, except with linoleate. In contrast, radiolabeled saturated fatty acids were recovered primarily in very low density lipoproteins and unsaturated fatty acids were recovered in chylomicrons. Lymph chylomicron size and lipid content were greater with unsaturated fat diets. Triglyceride-rich intestinal lipoproteins of rats fed saturated fats were polygonal by electron microscopy, related to the cooling of lymph samples below body temperature. A-I apolipoproteins were increased in relation to C apoproteins as lipid absorption was greater. Plasma triglycerides in all groups increased compared to rats fed the stock diet. A diet enriched in one specific fatty acid has its unique effects on lymph lipoprotein formation presumably affecting some intestinal subcellular mechanisms. Diet-induced changes in plasma lipids and lipoproteins are not directly related to these as yet unknown mechanisms.     

Acute ingestion of a meal rich in n-3 polyunsaturated fatty acids results in rapid gastric emptying in humans

BACKGROUND: n-3 Polyunsaturated fatty acids (PUFAs) have proven benefits for both the development of atherosclerosis and inflammatory conditions. The effects on atherosclerosis may be partly mediated by the observed reduction in fasting and postprandial triacylglycerol concentrations after both acute and chronic n-3 PUFA ingestion. OBJECTIVE: The aim of this study was to assess gastric emptying and gastrointestinal hormone release after the consumption of mixed meals rich in n-3 PUFAs or other classes of fatty acids. DESIGN: Ten healthy women (aged 50-62 y) completed 4 separate study visits in a single-blind, randomized design. On each occasion, subjects consumed 40 g oil rich in either saturated fatty acids, monounsaturated fatty acids, n-6 PUFAs, or n-3 PUFAs as part of a mixed meal. [1-(13)C]Octanoic acid (100 mg) was added to each oil. Gastric emptying was assessed by a labeled octanoic acid breath test, and concentrations of gastrointestinal hormones and plasma lipids were measured. RESULTS: Recovery of (13)C in breath was enhanced after n-3 PUFA ingestion (P < 0.005). The cholecystokinin response after the n-3 PUFA meal was significantly delayed (P < 0.001), and the glucagon-like peptide 1 response was significantly reduced (P < 0.05). CONCLUSION: The inclusion of n-3 PUFAs in a meal alters the gastric emptying rate, potentially as the result of changes in the pattern of cholecystokinin and glucagon-like peptide 1 release.     

Plasma lipoprotein fatty acids are altered by the positional distribution of fatty acids in infant formula triacylglycerols and human milk.

BACKGROUND: Triacylglycerol digestion involves hydrolysis of fatty acids esterified at the glycerol 1,3 positions by gastric and pancreatic lipase to produce 2-monoacylglycerols and unesterified fatty acids, which are then absorbed, reesterified to triacylglycerol, and secreted in chylomicrons. Palmitic acid (16:0) is predominantly esterified to the 2 position of human milk triacylglycerol but to the 1,3 positions in the oils used in infant formulas. OBJECTIVE: We aimed to determine whether the position of 16:0 in human milk and infant formula triacylglycerol influences the position of fatty acids in postprandial plasma chylomicron triacylglycerol. DESIGN: Full-term infants were fed formula with 25-27% 16:0 with either 39% of the 16:0(synthesized triacylglycerol) or 6% of the 16:0 (standard formula) esterified at the triacylglycerol 2 position, or were breast-fed (23% 16:0, 81% at the triacylglycerol 2 position) from birth to 120 d of age. Chylomicron fatty acids and plasma lipids were assessed at 30 and 120 d of age. RESULTS: Infants fed the synthesized triacylglycerol formula, standard formula, or breast milk had 15.8%,8.3%, and 28.0% 16:0 in the chylomicron triacylglycerol 2 position (P < 0.05). These results suggest that >/=50% of the dietary triacylglycerol 2-position 16:0 is conserved through digestion, absorption, and chylomicron triacylglycerol synthesis in breast-fed and formula-fed infants. Infants fed the synthesized triacylglycerol formula had significantly lower HDL-cholesterol and apolipoprotein A-I and higher apolipoprotein B concentrations than infants fed the standard formula. CONCLUSION: Dietary triacylglycerol fatty acid distribution may alter lipoprotein metabolism in young infants.     

Different effects of diets rich in olive oil,rapeseed oil and sunflower-seed oil on postprandial lipid and lipoprotein concentrations and on lipoprotein oxidation susceptibility

Elevated concentrations of fasting and non-fasting triacylglycerol-rich lipoproteins (TRL) as well as oxidative changes of lipoproteins may increase the risk of ischaemic heart disease. To compare the effects of different diets rich in unsaturated fatty acids on the concentrations and in vitro oxidation of fasting and postprandial lipoproteins eighteen males consumed diets enriched with rapeseed oil (RO), olive oil (OO), or sunflower-seed oil (SO) in randomised order for periods of 3 weeks followed by a RO test meal. In the postprandial state the concentrations of cholesterol and triacylglycerol (TAG) in TRL were higher after consumption of OO compared with RO and SO (P<0.04), possibly related to differences in the fasting state. The propagation rates for VLDL and LDL oxidation were higher in the postprandial compared with the fasting state irrespective of diet. In the fasting state, the propagation rates were highest after SO (P<0.001), and in the postprandial state, SO gave rise to a shorter VLDL lag time (P=0.03) and a higher propagation rate than OO consumption (P=0.04). Overall, the SO diet resulted in a higher postprandial propagation rate of LDL (P<0.001) compared with RO and OO, while there was no effect of diet on LDL oxidation lag time. Our results suggest that RO and SO diets lower the postprandial cholesterol and TAG concentrations compared with OO, while RO and OO diets result in similar and lower in vitro susceptibility to oxidation of lipoproteins than SO.     

Plasma clearance of chylomicrons from butterfat is not dependent on saturation: studies with butterfat fractions and other fats containing triacylglycerols with low or high melting points.

BACKGROUND: Dietary fats influence plasma lipids, and changes in the clearance and metabolism of postprandial lipoproteins can affect atherosclerosis. Butterfat is considered hypercholesterolemic but contains a multitude of constituent fatty acids. OBJECTIVES: We determined triacylglycerol and cholesteryl ester clearances of lymph chylomicrons derived from butterfat, fractions of butterfat, and other dietary fats. METHODS: Radiolabeled lymph chylomicrons resulting from the intestinal absorption of different fats were reinjected into recipient rats to measure plasma clearance. Plasma clearance of [14C]triacylglycerol was used as an indicator of chylomicron lipolysis whereas clearance of [3H]cholesteryl ester was used as an indicator of chylomicron remnant removal. RESULTS: [3H]Cholesteryl ester clearance was slower from chylomicrons derived from a solid, high-saturated-butterfat fraction than from whole butterfat, but clearance of chylomicrons from other fractions did not correlate with the fractions' saturated fatty acid contents. Clearance of cholesteryl esters in chylomicrons derived from cocoa butter, palm oil, and butterfat was slower than clearance of cholesteryl esters in chylomicrons derived from safflower oil. Hepatic uptakes of cholesteryl esters were generally lower for chylomicrons from all butterfat fractions, cocoa butter, and palm oil. CONCLUSIONS: In contrast with minor effects on the lipolysis of chylomicron triacylglycerols, chylomicron remnant removal was strongly influenced by the type of dietary fat, with slower cholesteryl ester clearances for saturated fats with higher melting points. However, remnant removal and hepatic uptake of chylomicrons from whole butterfat and fractions of butterfat were not correlated with fat saturation. The mechanisms of this apparent paradox remain unknown but may be attributable to acyl arrangements in the lipid classes of chylomicrons that influence the association with apolipoproteins and receptors and hence remnant removal.     

Acute effects of meal fatty acids on postprandial NEFA, glucose and apo E response: implications for insulin sensitivity and lipoprotein regulation?

Our aim was to determine whether meal fatty acids influence insulin and glucose responses to mixed meals and whether these effects can be explained by variations in postprandial NEFA and Apo, which regulate the metabolism of triacylglycerol-rich lipoproteins (Apo C and E). A single-blind crossover study examined the effects of single meals enriched in saturated fatty acids SFA), n-6 PUFA and MUFA on plasma metabolite and insulin responses. The triacylglycerol response following the PUFA meal showed a lower net incremental area under the curve than following the SFA and MUFA meals (P<0.007). Compared with the SFA meal, the PUFA meal showed a lower net incremental area under the curve for the NEFA response from initial suppression to the end of the postprandial period (180-480 min; P<0.02), and both PUFA and MUFA showed a lower net incremental glucose response (P<0.02), although insulin concentrations were similar between meals. The pattern of the Apo E response was also different following the SFA meal (P<0.02). There was a significant association between the net incremental NEFA (180-480 min) and glucose response (rs=0.409, P=0.025), and in multiple regression analysis the NEFA response accounted for 24 % of the variation in glucose response. Meal SFA have adverse effects on the postprandial glucose response that may be due to greater elevations in NEFA arising from differences in the metabolism of SFA- v. PUFA- and MUFA-rich lipoproteins. Elevated Apo E responses to high-SFA meals may have important implications for the hepatic metabolism of triacylglycerol-rich lipoproteins.     

Diets rich in polyunsaturated fatty acids: effect on hepatic metabolism in rats

OBJECTIVE: We investigated the effect of diets rich in omega-6 and omega-3 fatty acids on hepatic metabolism. METHODS: Male Wistar rats, just weaned, were fed ad libitum for 8 wk with one of the following diets: rat chow (C), rat chow containing 15% (w/w) soybean oil (S), rat chow containing 15% (w/w) fish oil (F), and rat chow containing 15% soy bean and fish oil (SF; 5:1, w/w). Casein was added to the fatty diets to achieve the same content of protein (20%) as the control chow. The rats were killed by decapitation, and the hepatic tissue was removed and weighed. Tissue lipid, glycogen, and protein content, in vivo lipogenesis rate, and adenosine triphosphate citrate lyase and malic enzyme activities were evaluated. Plasma total lipids, triacylglycerol, and cholesterol concentrations were assessed. RESULTS: Body weight gain was higher in F and SF than in C and S rats. Liver weight, lipid content, and lipogenesis rate increased in F and SF rats, although adenosine triphosphate citrate lyase activity decreased. Glycogen concentration decreased in S, F, and SF rats compared with C rats. Plasma total lipids and triacylglycerol concentrations were lower in F and SF than in C rats. Total and high-density lipoprotein cholesterol (HDL-C) plasma levels decreased in F rats, with maintenance of the total:HDL-C ratio. In SF rats, an increase in HDL-C led to a lower total:HDL-C ratio. CONCLUSIONS: These results indicated that an enrichment of the diet with omega-3 polyunsaturated fatty acids produces hypolipidemia but may cause changes in liver metabolism that favor lipid deposition. They also suggested that the addition of a small amount of eicosapentaenoic and docosahexaenoic polyunsaturated fatty acids to an omega-6-rich diet further improve the circulating lipid profile, in comparison with an omega-3-rich diet, but it does not prevent excess liver lipid accumulation.     

Postprandial effect of n-3 polyunsaturated fatty acids on apolipoprotein B-containing lipoproteins and vascular reactivity in type 2 diabetes

BACKGROUND: Plasma lipoproteins may be classified by their apolipoprotein composition. The lipoprotein subclass containing apolipoproteins B and C (LpB:C) is considered the most atherogenic. OBJECTIVE: We evaluated the acute effects of individual fatty acids on apolipoprotein B (apo B)-containing lipoproteins in adults with type 2 diabetes (n = 15). DESIGN: We administered 3 meals in a randomized, double-blind, crossover design. Treatments contained skim milk and 50 g fat from high-oleic acid safflower and canola oils (monounsaturated fatty acid; MUFA), MUFA + 3.5 g alpha-linolenic acid (ALA; MUFA + ALA) from high-ALA canola oil, or MUFA + 4.0 g both eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA; MUFA + EPA/DHA) from sardine oil. Apo B, LpB, LpB:C, LpB:E + LpB:C:E, and LpA-II:B:C:D:E were measured at baseline and 2 and 4 h after the meal. Flow-mediated dilation was measured at baseline and 4 h after the meal. RESULTS: The treatments significantly increased apo B and LpB postprandially (P < 0.03 for both), but the magnitude of the changes did not differ significantly between the treatments. The postprandial change in LpB:C was 23% lower after MUFA + EPA/DHA than after MUFA (treatment x time interaction, P < 0.0001). MUFA + ALA attenuated the increase in LpA-II:B:C:D:E in those with high triacylglycerols (>/=1.69 mmol/L) but was the only treatment to significantly increase this particle in those with low triacylglycerols (treatment x group interaction, P < 0.0001). Examination of change scores did not reveal the source of the interaction of treatment and time (P < 0.007) for LpB:E + LpB:C:E. Furthermore, the subjects with the largest increases in LpB:C exhibited the largest impairment in endothelial function. CONCLUSIONS: The results suggest that unsaturated fatty acids differentially affect concentrations of apo B-containing lipoprotein subclasses. A rise in LpB:C adversely affects endothelial function. Meals containing MUFA + EPA/DHA attenuated the postprandial rise in LpB:C and the impairment of endothelial function.     

Effects of dietary monounsaturated fatty acids on lipoprotein concentrations,compositions, and subfraction distributions and on VLDL apolipoprotein B kinetics: dose-dependent effects on LDL

BACKGROUND: Replacing dietary saturated fatty acids (SFAs) with monounsaturated fatty acids (MUFAs) lowers LDL cholesterol, but the underlying mechanisms remain unclear. OBJECTIVE: We assessed the effects of replacing dietary SFAs with MUFAs on concentrations and subclass distributions of VLDL, intermediate-density lipoprotein, LDL, and HDL and on VLDL apolipoprotein B kinetics. DESIGN: Thirty-five moderately hypercholesterolemic, middle-aged volunteers consumed for 6 wk, in random order, diets containing low (L-MUFA; 7.8% of energy from MUFAs), moderate (M-MUFA; 10.3% from MUFAs), or high (H-MUFA; 13.7% from MUFAs) amounts of MUFAs. Fasting blood samples were taken from all subjects after each intervention. VLDL apolipoprotein B kinetic studies were performed in a subgroup after the L-MUFA and H-MUFA diets. RESULTS: Plasma cholesterol concentrations decreased in a dose-dependent manner with increasing intakes of dietary MUFAs. This change was entirely accounted for by reduced LDL cholesterol (-0.20 and -0.49 mmol/L after the M-MUFA and H-MUFA diets, respectively, compared with the concentration after the L-MUFA diet; P for trend < 0.01). Plasma triacylglycerol and HDL cholesterol were not significantly affected by the dietary intervention, nor were the concentrations of VLDL(1) (S(f) 60-400), VLDL(2) (S(f) 20-60), or intermediate-density lipoprotein (S(f) 12-20). Production and catabolic rates for VLDL(1) and VLDL(2) were also unaffected. HDL and LDL subclass distributions were not significantly altered, but as a consequence of the overall LDL lowering, concentrations of atherogenic LDL-III were 25% lower after the H-MUFA diet than after the L-MUFA diet (P = 0.02). CONCLUSION: The effects of replacing dietary SFAs with MUFAs on lipoprotein metabolism appear to be almost exclusively limited to the LDL density class.