Very low-carbohydrate and low-fat diets affect fasting lipids and postprandial lipemia differently in overweight men

Hypoenergetic very low-carbohydrate and low-fat diets are both commonly used for short-term weight loss; however, few studies have directly compared their effect on blood lipids, with no studies to our knowledge comparing postprandial lipemia, an important independently identified cardiovascular risk factor. The primary purpose of this study was to compare the effects of a very low-carbohydrate and a low-fat diet on fasting blood lipids and postprandial lipemia in overweight men. In a balanced, randomized, crossover design, overweight men (n = 15; body fat >25%; BMI, 34 kg/m(2)) consumed 2 experimental diets for 2 consecutive 6-wk periods. One was a very low-carbohydrate (<10% energy as carbohydrate) diet and the other a low-fat (<30% energy as fat) diet. Blood was drawn from fasting subjects on separate days and an oral fat tolerance test was performed at baseline, after the very low-carbohydrate diet period, and after the low-fat diet period. Both diets had the same effect on serum total cholesterol, serum insulin, and homeostasis model analysis-insulin resistance (HOMA-IR). Neither diet affected serum HDL cholesterol (HDL-C) or oxidized LDL (oxLDL) concentrations. Serum LDL cholesterol (LDL-C) was reduced (P < 0.05) only by the low-fat diet (-18%). Fasting serum triacylglycerol (TAG), the TAG/HDL-C ratio, and glucose were significantly reduced only by the very low-carbohydrate diet (-44, -42, and -6%, respectively). Postprandial lipemia was significantly reduced when the men consumed both diets compared with baseline, but the reduction was significantly greater after intake of the very low-carbohydrate diet. Mean and peak LDL particle size increased only after the very low-carbohydrate diet. The short-term hypoenergetic low-fat diet was more effective at lowering serum LDL-C, but the very low-carbohydrate diet was more effective at improving characteristics of the metabolic syndrome as shown by a decrease in fasting serum TAG, the TAG/HDL-C ratio, postprandial lipemia, serum glucose, an increase in LDL particle size, and also greater weight loss (P < 0.05).     

Comparison of a very low-carbohydrate and low-fat diet on fasting lipids, LDL subclasses, insulin resistance, and postprandial lipemic responses in overweight women

OBJECTIVE: Very low-carbohydrate diets are widely used for weight loss yet few controlled studies have determined how these diets impact cardiovascular risk factors compared to more traditional low-fat weight loss diets. The primary purpose of this study was to compare a very low-carbohydrate and a low-fat diet on fasting blood lipids, LDL subclasses, postprandial lipemia, and insulin resistance in overweight and obese women. METHODS: Thirteen normolipidemic, moderately overweight (body fat >30%) women were prescribed two hypocaloric (-500 kcal/day) diets for 4 week periods, a very low-carbohydrate (<10% carbohydrate) and a low-fat (<30% fat) diet. The diets were consumed in a balanced and randomized fashion. Two fasting blood draws were performed on separate days and an oral fat tolerance test was performed at baseline, after the very low-carbohydrate diet, and after the low-fat diet. RESULTS: Compared to corresponding values after the very low-carbohydrate diet, fasting total cholesterol, LDL-C, and HDL-C were significantly (p < or = 0.05) lower, whereas fasting glucose, insulin, and insulin resistance (calculated using the homeostatic model assessment) were significantly higher after the low-fat diet. Both diets significantly decreased postprandial lipemia and resulted in similar nonsignificant changes in the total cholesterol/HDL-C ratio, fasting triacylglycerols, oxidized LDL, and LDL subclass distribution. CONCLUSIONS: Compared to a low-fat weight loss diet, a short-term very low-carbohydrate diet did not lower LDL-C but did prevent the decline in HDL-C and resulted in improved insulin sensitivity in overweight and obese, but otherwise healthy women. Small decreases in body mass improved postprandial lipemia, and therefore cardiovascular risk, independent of diet composition.     

Plasma lipids and lipoproteins during 6 d of maintenance feeding with long-chain, medium-chain, and mixed-chain triglycerides.

This study assessed fasting plasma lipids and lipoproteins and postprandial plasma lipids in healthy male subjects fed liquid-formula diets containing 40% of total energy as long-chain (LCT, primarily C18:1 and C18:2), medium-chain (MCT, C8:0-C10:0), or mixed-chain (structured lipid, STL, mostly C8:0, C10:0, and C22:0) triglycerides for 6 d. None of the diets altered plasma cholesterol concentrations. HDL cholesterol was decreased 14% by the STL diet (P < 0.044) and 15% by the MCT diet (P < 0.004) but was unchanged by the LCT diet. Plasma triglycerides were elevated 42% by the MCT diet (P < 0.006), but were unaltered by either the STL or LCT diets. Neither the STL nor the MCT diets produced changes in fasting lipoprotein lipid composition; however, during the LCT diet, VLDLs became enriched in triglyceride and LDLs became enriched in cholesterol. Postprandial triglyceridemia was significantly greater after subjects consumed the LCT diet than it was after they consumed either the STL or MCT diets, which were similar. Short-term feeding of MCT and STL diets produces significant changes in lipid metabolism. An understanding of the long-term effects of these diets awaits further study.     

老年冠心病患者餐后血脂变化及其对血小板活性的影响

目的　探讨老年冠心病 (CHD)患者餐后血脂代谢特点以及对血小板活性的影响。方法　对 48例老年冠心病 (CHD)患者 (冠心病组 )和 3 0例老年健康自愿者 (对照组 )均禁食 12h后 ,分别接受脂肪餐负荷试验 ,于空腹及餐后 4h测定血清甘油三酯(TG)、总胆固醇 (CH)、高密度脂蛋白 (HDL -C)、低密度脂蛋白 (LDL -C)水平 ,并同时于空腹状态及餐后 4h采用生物活性法测定血小板衍生生长因子 (PDGF)、用酶联免疫标测法 (ELISA)检测血管性假血友病因子 (vWF)浓度。结果　冠心病组餐前及餐后 4hTG(P<0 0 1)、CH(P <0 0 5 )、LDL -C(P <0 0 1)、PDGF(P <0 0 1)、vWF(P <0 0 1)值均显著高于对照组 ,HDL -C(P <0 0 1)显著低于对照组。餐后 4h与餐前比较 ,TG、CH、LDL -C值明显上升 ,而HDL -C下降幅度无明显差异。冠心病组PDGF、vWF值在餐后 4h上升幅度存在显著性差异 (P <0 0 5 )。结论　老年冠心病人存在血脂代谢异常。餐后血脂更能反映老年人的代谢水平。餐后血脂代谢异常对血小板活化起促进作用 ,血小板反复活化可能参与了冠状动脉硬化早期病变     

Chronic effects of a high-fat diet enriched with virgin olive oil and a low-fat diet enriched with alpha-linolenic acid on postprandial endothelial function in healthy men

Traditional cardiovascular risk factors are associated with endothelial dysfunction. The vascular endothelium plays a key role in local vascular tone regulation and can be modulated by dietary fat. We propose to determine the chronic effect of three diets with different fat compositions on postprandial endothelial function and inflammatory biomarkers. Twenty healthy men followed three 4-week diets in a randomised cross-over design: a Western diet, rich in saturated fat (22% SFA, 12% MUFA and 0.4% alpha-linolenic acid (ALA), all fractions are % of energy); a Mediterranean diet, rich in MUFA ( < 10 % SFA, 24 % MUFA and 0.4% ALA); a low-fat diet enriched in ALA ( < 10% SFA, 12% MUFA and 2% ALA). At the end of each dietary period all subjects underwent a postprandial study. Plasma concentrations of lipid parameters, soluble intercellular cell-adhesion molecule-1, soluble vascular cell-adhesion molecule-1 (sVCAM-1), nitrates and nitrites (NOx) and endothelial function studied by laser Doppler were examined at 0, 2, 4, 6 and 8 h. The endothelium-dependent vasodilatory response was greater 4 h after the ingestion of the MUFA-rich diet than after the SFA or ALA low-fat diets (P = 0.031). The 4 h postprandial plasma sVCAM-1 levels were lower after the MUFA meals than after the ALA low-fat diet (P = 0.043). The bioavailability of NOx was higher following the MUFA diet than after the SFA and ALA low-fat diets (P = 0.027). We found no differences in the other parameters measured. Chronic ingestion of a Mediterranean diet avoids the postprandial deterioration of endothelial function associated with Westernised diets in healthy individuals.     

Metabolic effects of dietary fructose in healthy subjects.

To determine if dietary fructose causes adverse metabolic effects, we used a crossover design to compare a diet containing 20% of energy from fructose with an isoenergic high-starch diet that contained less than 3% fructose. Fourteen healthy subjects consumed each diet for 28 d. There were no significant differences between the diets in the mean values of hemoglobin A1C, serum glycosylated albumin, fasting plasma glucose, peak postprandial plasma glucose, integrated plasma glucose, fasting serum lactate, or fasting serum triglycerides. Peak postprandial serum lactate was significantly higher during the fructose diet at days 1, 7, and 14 but not at days 21 or 28. Peak postprandial serum triglycerides were significantly higher only at day 1 of the fructose diet. Day-28 fasting serum total and LDL cholesterol for the fructose diet were 9.0% and 11.0% higher, respectively, than the corresponding values for the starch diet. A high-fructose diet compared with a high-starch diet resulted in significantly higher fasting serum total and LDL cholesterol and also caused transient changes in postprandial serum lactate and triglycerides.     

Contribution of postprandial lipemia to the dietary fat-mediated changes in endogenous lipoprotein-cholesterol concentrations in humans

BACKGROUND: Dietary fats alter LDL and HDL cholesterol while serving as precursors of postprandial triacylglycerol-rich lipoproteins (TRLs). OBJECTIVE: We hypothesized that the saturated fatty acid (SFA)-mediated increase and the polyunsaturated fatty acid (PUFA)-mediated decrease in endogenous lipoprotein cholesterol are promoted by postprandial TRLs. DESIGN: We performed a 16-d crossover diet study to examine the effect of PUFA-rich [ratio of PUFAs to SFAs (P:S) = 2.0] and SFA-rich (P:S = 0.25) diets on fasting and postprandial plasma lipid and lipoprotein-cholesterol concentrations in 16 normolipidemic subjects. RESULTS: Fasting plasma cholesterol decreased significantly after a PUFA-rich diet because of a decrease in LDL (-12.3%; P < 0.05) and HDL (-3.8%; NS), but did not change after an SFA-rich diet. The appearance of postprandial TRLs in plasma at 4 h was linked to a significant lowering of both LDL (-7.4%) and HDL (-4.8%) after a PUFA-rich diet; no such effect was observed after the SFA-rich diet. At 7 h, LDL and HDL cholesterol returned to near fasting concentrations without postprandial TRL accumulation after a PUFA-rich diet but with a significant postprandial TRL accumulation after an SFA-rich diet. Thus, the in vivo postprandial clearance of cholesterol in LDL+HDL was greater after a PUFA-rich diet than after an SFA-rich diet. The appearance of postprandial TRLs in plasma increased the cholesteryl ester transfer protein-mediated transfer of cholesteryl ester from LDL+HDL to TRLs in vitro without a significant influence from dietary fat. CONCLUSION: Dietary fat-mediated alterations in the rate of hepatic removal of postprandial TRLs, which carry cholesterol accepted from LDL+HDL via cholesteryl ester transfer protein in vivo, may contribute to the dietary fat-mediated change in endogenous lipoprotein cholesterol.     

Fasting lipoprotein and postprandial triacylglycerol responses to a low-carbohydrate diet supplemented with n-3 fatty acids

BACKGROUND: The effects of a prolonged low-carbohydrate diet rich in n-3 fatty acids on blood lipid profiles have not been addressed in the scientific literature. OBJECTIVE: This study examined the effects of an eight-week ketogenic diet rich in n-3 fatty acids on fasting serum lipoproteins and postprandial triacylglycerol (TG) responses. DESIGN: Ten men consumed a low-carbohydrate diet rich in monounsaturated fat (MUFA) and supplemented with n-3 fatty acids for eight weeks. Fasting blood samples were collected before and after one week of habitual diet and on two consecutive days after 2, 4, 6 and 8 weeks of the intervention diet. Postprandial TG responses to a fat-rich test meal were measured prior to and after the intervention diet. RESULTS: Compared to the habitual diet, subjects consumed significantly (p < or = 0.05) greater quantities of protein, fat, MUFA and n-3 fatty acids and significantly less total energy, carbohydrate and dietary fiber. Body weight significantly declined over the experimental period (-4.2+/-2.7 kg). Compared to baseline, fasting total cholesterol, LDL cholesterol and HDL cholesterol were not significantly different after the intervention diet (+1.5%, +9.7% and +10.0%, respectively). Fasting TG were significantly reduced after the intervention diet (-55%). There was a significant reduction in peak postprandial TG (-42%) and TG area under the curve (-48%) after the intervention diet. CONCLUSIONS: A hypocaloric low-carbohydrate diet rich in MUFA and supplemented with n-3 fatty acids significantly reduced postabsorptive and postprandial TG in men that were not hypertriglyceridemic as a group before the diet. This may be viewed as a clinically significant positive adaptation in terms of cardiovascular risk status. However, transient increases in total cholesterol and LDL cholesterol were also evident and should be examined further in regard to which particular subfractions are elevated.     

Effect of chronic glucagon administration on the metabolism of triacylglycerol-rich lipoproteins in rats fed a high sucrose diet

Male adult Wistar rats were fed a semipurified diet rich in sucrose (53 g/100 g diet). The effects of chronic glucagon administration (20 micrograms.day-1.rat-1, for 21 d) were studied on plasma lipid levels, triacylglycerol secretion rates and fractional catabolic rates determined by the intravenous fat tolerance test. Triacylglycerol secretion rates of plasma, chylomicron and very low density lipoprotein (VLDL) were measured by using the Triton WR 1339 method. In both fasting and postprandial states, the different rates were not significantly modified by glucagon treatment. However, in the treated animals, significantly decreased triacylglycerol concentrations were observed in plasma and VLDL during fasting (-41 and -46%, respectively) and also in chylomicrons in the postprandial state (-37%) relative to control animals. These data could be accounted for by an increased removal rate of triacylglycerol-rich lipoprotein. The estimated values of fractional rate constants (Triton WR 1339 experiment) were increased for VLDL (+62%) in the fasting state and for chylomicrons (+104%) in the postprandial state. Similarly, the fractional catabolic rate determined with the intravenous fat tolerance test (Intralipid, Kabivitrum, Sweden) was increased 49% by glucagon treatment, suggesting an effect of glucagon on the catabolism of triacylglycerol-rich lipoproteins. Glucagon treatment did not modify the composition of VLDL obtained 60 min after Triton WR 1339 injection, except that in the fasting state apo B100 proportions and concentrations increased, suggesting a specific effect on the hepatic secretion of apo B100 VLDL.     

Effects of dietary fructose on plasma lipids in healthy subjects

BACKGROUND: About 9% of average dietary energy intake in the United States comes from fructose. Such a high consumption raises concern about the metabolic effects of this sugar. OBJECTIVE: The objective of this study was to determine the effect of dietary fructose on plasma lipids. DESIGN: The study was conducted in the General Clinical Research Center at Fairview-University of Minnesota Medical Center. The participants were 24 healthy adult volunteers (12 men and 12 women; 6 of each sex were aged <40 y and 6 of each sex were aged >/=40 y). All subjects received 2 isoenergetic study diets assigned by using a randomized, balanced crossover design. One diet provided 17% of energy as fructose. The other diet was sweetened with glucose and was nearly devoid of fructose. Each diet was fed for 6 wk. Both diets were composed of common foods and contained nearly identical amounts of carbohydrate, protein, fat, fiber, cholesterol, and saturated, monounsaturated, and polyunsaturated fatty acids. All meals were prepared in the metabolic kitchen of the General Clinical Research Center. RESULTS: The responses to the study diets differed by sex. In men, the fructose diet produced significantly higher fasting, postprandial, and daylong plasma triacylglycerol concentrations than did the glucose diet. The daylong plasma triacylglycerol concentration after 6 wk of the fructose diet was 32% greater in men than the corresponding concentration during the glucose diet (P: < 0.001). The fructose diet had no significant effect on fasting or postprandial plasma triacylglycerol concentrations in women. The fructose diet also had no persistent effect on fasting plasma cholesterol, HDL cholesterol, or LDL cholesterol in either men or women. CONCLUSIONS: Dietary fructose was associated with increased fasting and postprandial plasma triacylglycerol concentrations in men. Diets high in added fructose may be undesirable, particularly for men. Glucose may be a suitable replacement sugar.     

Effect of meal fat quality on oxidation resistance of postprandial VLDL and LDL particles and plasma triacylglycerol level

This study was performed to examine the postprandial effects of meals containing dietary fats, with their natural fatty acid composition and tocopherol content, on the plasma triacylglycerols (TG) and tocopherols and on the resistance of VLDL and LDL to oxidation. On six separate days eighteen healthy male subjects were given low-fat meals (LF) or the LF meals enriched with sunflower oil (SO), rapeseed oil (RO), olive oil (OO), palm oil (PO), or butter (B) in a crossover design. The fat-rich meals all resulted in similar postprandial TG responses while the LF test meal did not increase plasma TG level. The postprandial plasma fatty acid profile changed to resemble the fatty acid composition of the ingested test fat. The alpha-tocopherol:gamma-tocopherol ratios in postprandial plasma and VLDL samples were greater than in the test fats. We found that the resistance of VLDL particles to oxidation in the postprandial state as assessed from lag time was increased after the PO-rich meal as compared with the SO-rich meal (p = 0.018), and the propagation rate was greater after the SO- and RO-rich meals compared with the others (p < 0.001). The resistance of LDL particles to oxidation was unaffected by the meals. In postprandial VLDL samples, the content of alpha-tocopherol was greater after the OO- and SO-rich meals compared with the meal rich in PO (P = 0.034 and 0.042 respectively). The gamma-tocopherol content of VLDL was highest after RO-meal as compared with all other test meals (P = 0.0019), and higher after SO as compared with B (P = 0.0148). Large individual differences were noted. In conclusion, meals enriched with different fats lead to the formation of VLDL particles with varying resistance to oxidation.     

Plasma lipid and lipoprotein responsiveness to dietary fat and cholesterol in premenopausal African American and white women

BACKGROUND: Premenopausal African American women have a 2-3 times greater incidence of coronary heart disease (CHD) than do white women. The plasma lipid responsiveness to dietary fat, which may be associated with CHD, has not been adequately studied in premenopausal African American or white women. OBJECTIVE: The objective of our study was to compare the effect of diet on fasting plasma lipids and lipoproteins and postprandial lipemia in premenopausal African American and white women. DESIGN: Thirteen African American and 9 white healthy premenopausal women were fed a low-fat, high-fiber diet and a high-fat, low-fiber diet for 4 wk each in a randomized crossover design. Fasting plasma lipid and lipoprotein concentrations and the 24-h plasma triacylglycerol response to a standard fatty test meal were measured at the end of each dietary period. RESULTS: Plasma total and LDL-cholesterol concentrations were higher after the high-fat, low-fiber diet in both white and African American women (P < 0.0001). The 24-h area under the plasma triacylglycerol curve after the test meal was lower after the low-fat diet than after the high-fat diet (P < 0.04). CONCLUSIONS: African American and white women had lower fasting plasma total and LDL-cholesterol concentrations and less postprandial lipemia after the low-fat than the high-fat diet. Diets low in total and saturated fat and cholesterol and high in fiber may reduce the risk of CHD by lowering fasting plasma total and LDL-cholesterol concentrations and by reducing the lipemic response to fatty meals.     

Dietary cholesterol is secreted in intestinally derived chylomicrons during several subsequent postprandial phases in healthy humans

BACKGROUND: The process of intestinal absorption and chylomicron resecretion of dietary cholesterol in humans is poorly understood. OBJECTIVE: The present study aimed to test the hypothesis that dietary cholesterol ingested during a given meal is resecreted into chylomicrons (and plasma) during several subsequent postprandial periods. DESIGN: Seven healthy subjects ingested 3 comparable mixed test meals (at 0, 8, and 24 h) containing a given amount of fat (49 g) and cholesterol (157 mg); blood samples were taken 3 and 6 h after each test meal and 48 and 72 h after the beginning of the experiment. Heptadeuterated dietary cholesterol was present in the first test meal only, enabling its specific determination with use of gas chromatography-mass spectrometry. Chylomicrons, LDL, and HDL were isolated and lipids were quantified. RESULTS: In apolipoprotein B-48-containing chylomicrons, deuterated cholesterol concentrations were moderate after the first meal (1.3 x 10(-4) mmol/L), reached a maximum after the second meal (2.4 x 10(-4) mmol/L), and were still elevated after the third meal (1.7 x 10(-4) mmol/L). In plasma, LDL and HDL cholesterol enrichment in deuterated cholesterol was lower than in chylomicrons and plateaued after 24--48 h. Estimates of newly secreted exogenous deuterated cholesterol in chylomicrons indicate that 30.7%, 55.2%, and 14.1% of the total was secreted after the first, second, and third meals, respectively. CONCLUSION: Ingested dietary cholesterol is secreted by the small intestine in chylomicrons into the circulation during > or =3 subsequent postprandial periods in healthy humans. This likely results from a complex multistep intestinal processing of cholesterol with dietary fat as a driving force.     

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.     

A ketogenic diet favorably affects serum biomarkers for cardiovascular disease in normal-weight men

Very low-carbohydrate (ketogenic) diets are popular yet little is known regarding the effects on serum biomarkers for cardiovascular disease (CVD). This study examined the effects of a 6-wk ketogenic diet on fasting and postprandial serum biomarkers in 20 normal-weight, normolipidemic men. Twelve men switched from their habitual diet (17% protein, 47% carbohydrate and 32% fat) to a ketogenic diet (30% protein, 8% carbohydrate and 61% fat) and eight control subjects consumed their habitual diet for 6 wk. Fasting blood lipids, insulin, LDL particle size, oxidized LDL and postprandial triacylglycerol (TAG) and insulin responses to a fat-rich meal were determined before and after treatment. There were significant decreases in fasting serum TAG (-33%), postprandial lipemia after a fat-rich meal (-29%), and fasting serum insulin concentrations (-34%) after men consumed the ketogenic diet. Fasting serum total and LDL cholesterol and oxidized LDL were unaffected and HDL cholesterol tended to increase with the ketogenic diet (+11.5%; P = 0.066). In subjects with a predominance of small LDL particles pattern B, there were significant increases in mean and peak LDL particle diameter and the percentage of LDL-1 after the ketogenic diet. There were no significant changes in blood lipids in the control group. To our knowledge this is the first study to document the effects of a ketogenic diet on fasting and postprandial CVD biomarkers independent of weight loss. The results suggest that a short-term ketogenic diet does not have a deleterious effect on CVD risk profile and may improve the lipid disorders characteristic of atherogenic dyslipidemia.     

Fasting Lipoprotein and Postprandial Triacylglycerol Responses to a Low-Carbohydrate Diet Supplemented with n-3 Fatty Acids

Background: The effects of a prolonged low-carbohydrate diet rich in n-3 fatty acids on blood lipid profiles have not been addressed in the scientific literature.

Objective: This study examined the effects of an eight-week ketogenic diet rich in n-3 fatty acids on fasting serum lipoproteins and postprandial triacylglycerol (TG) responses.

Design: Ten men consumed a low-carbohydrate diet rich in monounsaturated fat (MUFA) and supplemented with n-3 fatty acids for eight weeks. Fasting blood samples were collected before and after one week of habitual diet and on two consecutive days after 2, 4, 6 and 8 weeks of the intervention diet. Postprandial TG responses to a fat-rich test meal were measured prior to and after the intervention diet.

Results: Compared to the habitual diet, subjects consumed significantly (p ≤ 0.05) greater quantities of protein, fat, MUFA and n-3 fatty acids and significantly less total energy, carbohydrate and dietary fiber. Body weight significantly declined over the experimental period (?4.2 ± 2.7 kg). Compared to baseline, fasting total cholesterol, LDL cholesterol and HDL cholesterol were not significantly different after the intervention diet (+1.5%, +9.7% and +10.0%, respectively). Fasting TG were significantly reduced after the intervention diet (?55%). There was a significant reduction in peak postprandial TG (?42%) and TG area under the curve (?48%) after the intervention diet.

Conclusions: A hypocaloric low-carbohydrate diet rich in MUFA and supplemented with n-3 fatty acids significantly reduced postabsorptive and postprandial TG in men that were not hypertriglyceridemic as a group before the diet. This may be viewed as a clinically significant positive adaptation in terms of cardiovascular risk status. However, transient increases in total cholesterol and LDL cholesterol were also evident and should be examined further in regard to which particular subfractions are elevated.     

Dietary cholesterol from eggs increases plasma HDL cholesterol in overweight men consuming a carbohydrate-restricted diet

Carbohydrate-restricted diets (CRD) significantly decrease body weight and independently improve plasma triglycerides (TG) and HDL cholesterol (HDL-C). Increasing intake of dietary cholesterol from eggs in the context of a low-fat diet maintains the LDL cholesterol (LDL-C)/HDL-C for both hyper- and hypo-responders to dietary cholesterol. In this study, 28 overweight/obese male subjects (BMI = 25-37 kg/m2) aged 40-70 y were recruited to evaluate the contribution of dietary cholesterol from eggs in a CRD. Subjects were counseled to consume a CRD (10-15% energy from carbohydrate) and they were randomly allocated to the EGG group [intake of 3 eggs per day (640 mg/d additional dietary cholesterol)] or SUB group [equivalent amount of egg substitute (0 dietary cholesterol) per day]. Energy intake decreased in both groups from 10,243 +/- 4040 to 7968 +/- 2401 kJ (P < 0.05) compared with baseline. All subjects irrespective of their assigned group had reduced body weight and waist circumference (P < 0.0001). Similarly, the plasma TG concentration was reduced from 1.34 +/- 0.66 to 0.83 +/- 0.30 mmol/L after 12 wk (P < 0.001) in all subjects. The plasma LDL-C concentration, as well as the LDL-C:HDL-C ratio, did not change during the intervention. In contrast, plasma HDL-C concentration increased in the EGG group from 1.23 +/- 0.39 to 1.47 +/- 0.38 mmol/L (P < 0.01), whereas HDL-C did not change in the SUB group. Plasma glucose concentrations in fasting subjects did not change. Eighteen subjects were classified as having the metabolic syndrome (MetS) at the beginning of the study, whereas 3 subjects had that classification at the end. These results suggest that including eggs in a CRD results in increased HDL-C while decreasing the risk factors associated with MetS.     

Different postprandial metabolic patterns after the consumption of fish oil and lard in healthy Chinese individuals

AimIt is well known that nutritional intervention has positive effects on the secondary prevention of coronary heart disease. Different fat compositions of meals may alter postprandial plasma lipid patterns, which can further influence lipid metabolism in vivo.MethodsIn the present study, we investigated postprandial plasma lipid parameters in twenty healthy volunteers after eating fat meals either with 80 gram lard or 80 gram fish oil. Blood samples were drawn at 0, 0.5, 1, 2, 3, 5 and 7 hours and plasma levels of total triglycerides (TG), total cholesterol (TC), high density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol (LDL-C) were determined.ResultsIt demonstrated that postprandial plasma concentrations of TG, TC and LDL-C were significantly lower whereas HDL-C was higher after eating fish oil compared to the consumption of lard. Moreover, comparing the individuals with or without dyslipidemic family history, the healthy individuals without family history of dyslipidemia after eating fish oil had even lower postprandial plasma TG and LDL-C (P < 0.05) than the subjects with the family history. It is concluded that postprandial response following fish oil could be as a result of reduced TG, TC and LDL-C, and increased HDL-C.ConclusionsPostprandial responses following fish oil consumption may reduce TG, TC and LDL-C plasma levels, and increase HDL-C level. Individuals with dyslipidemic family history may have enhanced postprandial response than the individuals without dyslipidemic family history.     

Effects of dietary fat quantity and composition on fasting and postprandial levels of coagulation factor VII and serum choline-containing phospholipids

Dietary fat influences plasma levels of coagulation factor VII (FVII) and serum phospholipids (PL). It is, however, unknown if the fat-mediated changes in FVII are linked to PL. The present study aimed to investigate the effects of dietary fat on fasting and postprandial levels of activated FVII (FVIIa), FVII coagulant activity (FVIIc), FVII protein (FVIIag) and choline-containing PL (PC). In a randomized single-blinded crossover-designed study a high-fat diet (HSAFA), a low-fat diet (LSAFA), both rich in saturated fatty acids, and a high-fat diet rich in unsaturated fatty acids (HUFA) were consumed for 3 weeks. Twenty-five healthy females, in which postprandial responses were studied in a subset of twelve, were included. The HSAFA diet resulted in higher levels of fasting FVIIa and PC compared with the LSAFA and the HUFA diets (all comparisons P< or =0.01). The fasting PC levels after the LSAFA diet were also higher than after the HUFA diet (P<0.001). Postprandial levels of FVIIa and PC were highest on the HSAFA diet and different from LSAFA and HUFA (all comparisons P< or =0.05). Postprandial FVIIa was higher on the HUFA compared with the LSAFA diet (P<0.03), whereas the HUFA diet resulted in lower postprandial levels of PC than the LSAFA diet (P<0.001). Significant correlations between fasting levels of PC and FVIIc were found on all diets, whereas FVIIag was correlated to PC on the HSAFA and HUFA diet. The present results indicate that dietary fat, both quality and quantity, influences fasting and postprandial levels of FVIIa and PC. Although significant associations between fasting FVII and PC levels were found, our results do not support the assumption that postprandial FVII activation is linked to serum PC.     

Postprandial chylomicrons and VLDLs in severe hypertriacylglycerolemia are lowered more effectively than are chylomicron remnants after treatment with n-3 fatty acids

BACKGROUND: n-3 Fatty acids lower plasma triacylglycerols not only in the fasting state but also in the postprandial state. However, it is not known whether chylomicrons, chylomicron remnants, and VLDLs are all affected equally or whether some lipoprotein species are lowered preferentially. OBJECTIVE: Lipoproteins, including large and small chylomicron remnants, were determined specifically with the aid of a newly developed method involving a combination of size-exclusion chromatography and fluorometric determination of retinyl palmitate, which served as a marker for exogenous fat. DESIGN: Twelve hypertriacylglycerolemic men were treated for 6 wk with 4 capsules containing 85% fish-oil concentrate/d; each capsule contained 850 mg n-3 fatty acid ethyl esters (49.1% eicosapentaenoic acid by wt and 32.2% docosahexaenoic acid by wt). Oral-fat-tolerance tests were performed before and after the treatment. Blood samples were drawn in the fasting state and until 8 h postprandially. RESULTS: Treatment with n-3 fatty acids reduced the fasting VLDL-triacylglycerol concentration by 44% (P < 0.05) and postprandial chylomicrons and VLDLs at 4, 6, and 8 h (P < 0.05) by 49-64% and 36-43%, respectively. Chylomicron remnants were reduced only in the late postprandial phase: large chylomicron remnants by 19% at 6 h and by 43% at 8 h (P < 0.05) and small chylomicron remnants by 31% at 8 h (P < 0.05). CONCLUSION: n-3 Fatty acids effectively lower chylomicrons and VLDLs, but their effect on chylomicron remnants was observed only in the late postprandial phase.