MUFA Diet Research Articles

Long-term effect of varying the source or amount of dietary carbohydrate on postprandial plasma glucose, insulin, triacylglycerol, and free fatty acid concentrations in subjects with impaired glucose tolerance

Reducing the glycemic load (GL) is considered beneficial for managing insulin resistance. The GL can be reduced either by reducing carbohydrate intake or by reducing the glycemic index (GI). We studied whether these 2 dietary maneuvers have the same long-term effects on postprandial plasma glucose, insulin, triacylglycerol, and free fatty acid (FFA) concentrations in subjects with impaired glucose tolerance (IGT). Thirty-four subjects with IGT were randomly assigned to high-carbohydrate, high-GI (high-GI); high-carbohydrate, low-GI (low-GI); and low-carbohydrate, high-monounsaturated fatty acid (MUFA) diets for 4 mo. Plasma glucose, insulin, and FFAs were measured from 0800 to 1600 at baseline in response to high-GI meals (60% carbohydrate, GI = 61, GL = 63) and after 4 mo in response to meals representative of the study diet. Carbohydrate intake (% of energy), GI, and GL in the high-GI, low-GI, and MUFA groups (breakfast and lunch meals combined), respectively, were 60%, 61, and 63; 60%, 53, and 55; and 49%, 61, and 52. Compared with the change after 4 mo of the high-GI diet, both the low-GI and MUFA diets reduced 0-8-h mean plasma glucose concentrations by 0.35 mmol/L (P < 0.05). Mean plasma insulin was approximately 20% higher (P < 0.05) and FFAs approximately 12% lower (P < 0.05) after the low-GI diet than after the high-GI diet, with no significant effect of MUFA. Changes in 0-8-h mean plasma triacylglycerols in the 3 treatment groups differed significantly: -0.14, 0.04, and 0.18 mmol/L, respectively, with the high-GI, MUFA, and low-GI diets. In subjects with IGT, reducing the GI of the diet for 4 mo reduced postprandial plasma glucose by the same amount as did reducing carbohydrate intake. The 2 dietary maneuvers had different effects on postprandial plasma insulin, triacylglycerols, and FFAs.

Effects of dietary saturated, monounsaturated and n-3 fatty acids on fasting lipoproteins, LDL size and post-prandial lipid metabolism in healthy subjects

Background: The influence of the quality of dietary fat on some aspects of lipid metabolism—i.e. lipoprotein concentrations, post-prandial lipids and LDL size—is not completely understood, especially in healthy individuals. Objectives: Aim of this study was to evaluate the effects of different types of dietary fat (monounsaturated vs. saturated fatty acids, and n-3 or placebo supplementation) on fasting lipoproteins, LDL size and post-prandial lipids in healthy people. Design: One hundred and sixty-two individuals were randomly assigned to follow two isoenergetic diets, one rich in saturated fatty acids (SFA diet) and the other in monounsaturated fatty acids (MUFA diet). Each group was further randomised to receive supplementation with fish oil (3.6 g/day) or placebo. Results: The type of diet significantly affected LDL cholesterol and triacylglycerol content, which was higher with the SFA diet and lower with the MUFA diet. The changes between the two diets were statistically significant for cholesterol ( P<0.01) and triacylglycerol ( P<0.03). VLDL cholesterol and triacylglycerol were significantly reduced and LDL cholesterol significantly increased by fish oil supplementation. Plasma triacylglycerol was significantly lower in those taking n-3 fatty acids, also 1 and 3 h after a test-meal. Neither type of diet nor n-3 supplementation affected LDL size. Conclusions: A moderate substitution of saturated fatty acids with monounsaturated fatty acids has beneficial effects on lipid metabolism also in healthy individuals. A moderate supplementation of long-chain n-3 fatty acids in healthy individuals reduces both fasting and post-prandial triacylglycerol concentrations but increases LDL cholesterol, irrespective of the type of diet.

The cholesterolaemic effects of dietary fats in cholesteryl ester transfer protein transgenic mice.

In order to investigate the role of cholesteryl ester transfer protein (CETP) in the cholesterolaemic response to dietary fats, we analysed plasma lipid profiles of CETP-transgenic and control C57BL/6 mice fed standard chow (AIN-93G; AIN), a low-fat diet, and diets high in butter (saturated fatty acids; SFA), high-oleic acid safflower oil (monounsaturated fatty acids; MUFA), and safflower oil (polyunsaturated fatty acids; PUFA) for 5 weeks. Each group contained four or five mice. There were significant diet and dietxgenotype effects on plasma total cholesterol (TC; and respectively), liver TC ( and respectively), and esterified cholesterol (EC; and respectively); diet effects on plasma triacylglycerol liver free cholesterol and body weight a genotype effect on body-weight gain and a dietxgenotype effect on energy intake In transgenic mice the SFA diet caused significantly higher plasma TC than the PUFA diet In control mice MUFA and PUFA diets, but not the SFA diet, caused significantly higher plasma TC than the low-fat and AIN diets Transgenic mice fed PUFA had lower plasma TC while transgenic mice fed MUFA had lower LDL+VLDL-cholesterol than controls in the same dietary groups. Transgenic mice fed MUFA and PUFA diets also had significantly higher liver TC and respectively) and EC and respectively) than controls fed the same diets. In the present study we showed that: (1) CETP transgenic mice had a cholesterolaemic response to dietary fats similar to that in human subjects; (2) CETP transgenic mice fed PUFA showed significantly lower plasma TC, while those fed MUFA had lower LDL+VLDL-cholesterol than controls; (3) hepatic accumulation of cholesterol, possibly resulting from the combination of the enhanced cholesteryl ester transfer to apolipoprotein B-containing lipoproteins and increased hepatic uptake of cholesterol, may contribute to the cholesterol-lowering effect of MUFA and PUFA in CETP-transgenic mice; (4) CETP may play a role in appetite and/or energy regulation.

The effect of apolipoprotein B xbaI polymorphism on plasma lipid response to dietary fat.

Lipid response to dietary fat and cholesterol is, to a large extent, genetically controlled. Apolipoprotein B (apo B) plays a dominant role in cholesterol homeostasis. Several polymorphic sites within or adjacent to the gene locus for apo B have been detected. The X+ allele of the XbaI restriction fragment polymorphism of the apo B gene has been found to be associated with higher serum cholesterol and/or triglyceride levels. In order to study the influence of this mutation on the plasma lipid response in diets of varying fat content, 72 healthy male subjects were studied, 21 X- X- (X-) and 51 X+ (X+ X- or X+ X+). These subjects followed three consecutive 28-day diet periods: one rich in saturated fats (SAT diet; 38% fat, 20% saturated); a National Cholesterol Education Program type I diet (NCEP-I diet) (28% fats, < 10% saturated); and a third monounsaturated (MUFA diet) (38% fats, 22% monounsaturated). The different genotypes can be observed to have significant effects on total and LDL cholesterol concentrations (P < 0.017). X+ individuals had higher levels of total and LDL cholesterol after the consumption of a SAT diet (P < 0.012; P < 0.006, respectively), NCEP diet (P < 0.060; P < 0.054, respectively) and MUFA diet (P < 0.022; P < 0.042, respectively) in comparison with X- individuals. A significant interaction between genotypes and dietary effects was observed for diet-induced changes in plasma triglycerides (P < 0.032). Significant decreases in the absolute values of triglyceride concentrations (-0.18 mmol L(-1), P < 0.024) were noted in the X- subjects after the high intake of a MUFA diet, while no significant differences were observed in the X+ individuals (0.006 mmol L(-1), P < 0.858). Our results suggest that the total triglyceride response to diet is influenced by the apo B XbaI polymorphism.

Low-fat and high–monounsaturated fatty acid diets decrease plasma cholesterol ester transfer protein concentrations in young, healthy, normolipemic men

Cholesterol ester transfer protein (CETP) mediates the transfer of cholesteryl esters from HDL to apolipoprotein (apo) B-containing lipoproteins. The possible atherogenic role of this protein is controversial. Diet may influence plasma CETP concentrations. The objective was to determine whether the changes in plasma lipids observed after consumption of 2 lipid-lowering diets are associated with changes in plasma CETP concentrations. : We studied 41 healthy, normolipidemic men over 3 consecutive 4-wk dietary periods: a saturated fatty acid-rich diet (SFA diet: 38% fat, 20% saturated fat), a National Cholesterol Education Program Step I diet (NCEP Step I diet: 28% fat, 10% saturated fat), and a monounsaturated fatty acid-rich diet (MUFA diet: 38% fat, 22% monounsaturated fat). Cholesterol content (27.5 mg/MJ) was kept constant during the 3 periods. Plasma concentrations of total, LDL, and HDL cholesterol; triacylglycerol; apo A-I and B; and CETP were measured at the end of each dietary period. Compared with the SFA diet, both lipid-lowering diets significantly decreased plasma total and LDL cholesterol, apo B, and CETP. Only the NCEP Step I diet lowered plasma HDL cholesterol. Positive, significant correlations were found between plasma CETP and total (r = 0.3868, P < 0.0001) and LDL (r = 0.4454, P < 0.0001) cholesterol and also between changes in CETP concentrations and those of total (r = 0.4543, P < 0.0001) and LDL (r = 0.4554, P < 0.0001) cholesterol. The isoenergetic substitution of a high-saturated fatty acid diet with an NCEP Step I or a high-monounsaturated fatty acid diet decreases plasma CETP concentrations.

Acute ingestion of different dietary fatty acid species modulates postprandial lipid responses in New Zealand white rabbits

Although several investigations have linked the degree of fatty acid saturation to plasma lipid responses in the postprandial state, further evaluation is necessary. In this study, we compared the effect of saturated (SFA), monounsaturated (MUFA), and polyunsaturated (PUFA) fatty acids on postprandial lipid metabolism using complementary in vivo and in vitro approaches. Fat (10 g) cholesterol (0.5 g) test meals that provided either lard (SFA), olive oil (MUFA), or sunflower oil (PUFA) were ingested by chow-fed New Zealand white rabbits ( n = 8). In addition, hepatic uptake of triglyceride-cholesterol-rich lipoproteins (TCRL) isolated from rabbits chronically ingesting SFA, MUFA, or PUFA diets was measured using freshly isolated chow-fed rabbit hepatocytes. Whatever dietary fatty acids ingested, postprandial triglyceridemia and occurrence of radiolabelled dietary lipids in plasma were not markedly different. Conversely, SFA induced higher postprandial cholesterolemia and phospholipemia than MUFA ( P < 0.05) whereas PUFA prevented postprandial cholesterol increase. TCRL disappearance from cultured liver cell media was delayed with SFA-rich TCRL and faster with PUFA whereas MUFA-rich TCRL showed an intermediate figure. From these data, we conclude that SFA, MUFA, and PUFA elicited different postprandial plasma and lipoprotein lipid responses. The fatty acid composition of TCRL had a major impact on their subsequent metabolism, especially uptake by cultured hepatocytes. The SFA-induced hypercholesterolemia could be related to an altered hepatic uptake whereas a faster clearance and hepatic uptake could explain the cholesterol-lowering effect of PUFA in rabbits. MUFA, like PUFA, accelerate uptake by hepatocytes but favor cholesterol ester enrichment of TCRL.

A high- trans fatty acid diet and insulin sensitivity in young healthy women

Epidemiological and experimental studies suggest that a diet rich in saturated fat affects insulin sensitivity. Monoenes and dienes that have an usaturated bond with the trans configuration ( trans fatty acids) resemble saturated fatty acids with respect to structure, but no published data are available on the effect of trans fatty acids on insulin sensitivity. Therefore, the effects of diets high in trans fatty acids (TFA diet) and oleic acid (monounsaturated fat [MUFA] diet) on glucose and lipid metabolism were studied in 14 healthy women. Subjects consumed both experimental diets for 4 weeks according to a randomized crossover study design. Both experimental diet periods were preceded by consumption of a standardized baseline diet for 2 weeks. The diets provided 36.6% to 37.9% of energy (E%) as fat. In the TFA diet, there was 5.1 E% trans fatty acids, and in the MUFA diet, 5.2 E% oleic acid, substituted for saturated fatty acids in the baseline diet. A frequently sampled intravenous glucose tolerance test (FSIGT) was performed at the end of the experimental diet periods. Glucose effectiveness (S G) and the insulin sensitivity index (S I) did not differ after the two experimental diet periods. There was also no difference in the acute insulin response between the diets. The total cholesterol to high-density lipoprotein (HDL) cholesterol ratio and serum total triglyceride, HDL, and low-density lipoprotein (LDL) triglyceride and apolipoprotein B (apoB) concentrations were higher ( P < .05) after the TFA diet. In conclusion, in young healthy women, the TFA diet resulted in a higher total/HDL cholesterol ratio and an elevation in triglyceride and apo B concentrations but had no effect on glucose and insulin metabolism compared with the MUFA diet.

Solid monounsaturated diet lowers LDL unsaturation trait and oxidisability in hypercholesterolemic (Type IIb) patients

Lowering high cholesterol concentration decreases the probability of atherosclerotic-related pathology onset. MUFA and PUFA decrease total plasma and LDL cholesterol but PUFA may increase the susceptibility of LDL to undergo oxidative modifications thus becoming more atherogenetic. Olive oil, the predominant fat source in Mediterranean diet, may combine the advantages of both lowering cholesterol level and decreasing LDL susceptibility to oxidation. We studied the effects of feeding MUFA vs PUFA enriched diet on LDL composition and feature in hypercholesterolemic (IIb) patients Antioxidant values remained constant during the study while LDL fatty acids composition reflected the dietary intake: MUFA concentration increased 11% whereas PUFA decreased 10% after olive oil diet (p < 0.05). PUFA/MUFA ratio and the unsaturation index were lower at the end of MUFA-enriched diet. The challenge, in vitro, of oleate-enriched LDL with Cu2+ yielded to lower lag-phase (p < 0.05) in diene conjugated production; the same LDL gave lower lipid hydroperoxide contents after exposition to AAPH. We conclude that oleate-enriched LDL and with lower PUFA content were more resistant to oxidative modifications, as measured by different peroxidation indexes. This feature acquired with the diet may be an useful tool for lowering LDL oxidation and indirectly their atherogenicity.

Plasma Lipid Response to Hypolipidemic Diets in Young Healthy Non-Obese Men Varies with Body Mass Index

Lipid response to dietary fat is highly variable among individuals of a population. The aim of this study was to establish whether being overweight is one of the factors that determines this response. Forty-one non-obese healthy men were divided into two groups according to body mass index as follows: controls, <25 kg/m2; overweight, >25 kg/m2 but <30 kg/m2. After consuming a saturated fat–rich diet (SAT diet: 38% fat, 20% saturated) for 4 wk, subjects were switched to a low fat diet [National Cholesterol Education Program (NCEP)-I diet: 28% fat, 10% saturated] for 4 wk and then to a monounsaturated fat–rich diet (MUFA diet: 38% fat, 22% monounsaturated) for 4 wk. Data were analyzed by Student’s t test and two-way ANOVA for repeated measures. After consuming the NCEP-I diet, the overweight subjects had a smaller decrease relative to the SAT diet period in plasma total cholesterol [−0.30 vs. −0.67 mmol/L (−7 vs. −16%), P < 0.02] and low density lipoprotein-cholesterol concentrations [−0.24 vs. −0.55 mmol/L (−9 vs. −21%), P < 0.04] than controls. However, in the overweight subjects, the MUFA diet produced a greater decrease in plasma triglycerides than in the controls relative to the SAT diet period [−0.36 vs. −0.03 mmol/L (−26 vs. −4%), P < 0.006] and to the NCEP-I diet period [−0.29 vs. 0.01 mmol/L (−22 vs. 1%), P < 0.01). Plasma cholesterol concentrations changed to a lesser extent, and triglyceride concentration to a greater extent, in overweight but non-obese young men than in those of normal weight in response to changes in dietary fat composition. Our data suggest that in the diet treatment of obese hyperlipemic subjects, it is more important for them to lose weight than to change the fat composition of their diets.

Saturated fat and simple carbohydrates elevate plasma LDL cholesterol concentrations by specific alterations on hepatic cholesterol metabolism

We investigated the independent and interactive effects of saturated fat and simple carbohydrates on plasma and hepatic cholesterol in guinea pigs fed semipurified diets containing 19% fat ( w w ) either high in lauric + myristic (SFA), oleic (MUFA), or linoleic (PUFA) and 33.5% ( w w ) of carbohydrates either sucrose or starch for four weeks. Plasma LDL cholesterol concentrations were 40% higher in the simple carbohydrate groups compared with starch-fed animals (P <0.005). SFA-fed guinea pigs had 75% higher plasma LDL cholesterol than did those fed MUFA or PUFA diets (P< 0.0001). In addition, SFA significantly decreased HDL cholesterol levels by 100–130% compared to MUFA or PUFA diets which had similar effects. Sucrose intake resulted in increased plasma apoB concentrations compared with starch intake (P = 0.001). SFA intake also increased plasma apoB levels by 50% compared with MUFA or PUFA diets (P<0.00001). Guinea pigs fed SFA diets had 60% lower hepatic LDL receptor number than those fed MUFA and PUFA diets while sucrose intake reduced the number of hepatic LDL receptors by 30% (P < 0.01). Hepatic ACAT activity was 1.7 fold higher in animals fed sucrose diets compared with those fed starch (P<0.0001). These studies suggest that SFA and sucrose independently raise plasma LDL cholesterol levels by distinct mechanisms that alter hepatic cholesterol homeostasis and affect the synthesis and catabolism of lipoproteins.

Effect of 360His mutation in apolipoprotein A-IV on plasma HDL-cholesterol response to dietary fat

In order to determine whether genetic variability of apolipoprotein (apo) A-IV is responsible for the improvement in lipid profile when dietary saturated fats are replaced by carbohydrates or monounsaturated fats, 41 healthy male subjects were studied: 33 were homozygous for the 360Gln allele and 8 were heterozygote carriers of the 360His allele. These were administered three consecutive 4-week diets. The first was a diet rich in saturated fat (SAT diet, with 38% fat, 20% saturated. This was followed by a low fat diet (NCEP-I, with < 30% fat, < 10% saturated). The final diet was rich in monounsaturated fat (MUFA diet, with 38% fat, 22% monounsaturated). There was no difference in plasma lipid and apolipoprotein levels of both groups of individuals after consuming the SAT diet. Switching from this diet to the NCEP-I diet, carriers of the 360His allele presented a greater decrease in high density lipoprotein-cholesterol (HDL-C) (-10 vs. -1 mg/dL, P < 0.004) and apoA-I levels (-19 vs. -8 mg/dL, P < 0.037). Similarly, replacement of carbohydrates by monounsaturated fats produced a greater increase in HDL-C (9 vs. 1 mg/dL, P < 0.003) and apoA-I levels (9 vs. 2 mg/dL, P < 0.036) in carriers of the 360His mutation. Lecithin:cholesterol acyltransferase (LCAT) and cholesteryl ester transfer protein (CETP) activities and apoA-IV levels were also measured. However, no genotype-related differences were observed for these parameters. Our results suggest that variability in HDL-C and apoA-I response to diet is, at least partially, determined by the 360His mutation of apoA-IV.

Effect of 347-serine mutation in apoprotein A-IV on plasma LDL cholesterol response to dietary fat.

Lipid response to dietary fat and cholesterol is, to a large extent, genetically controlled. Apoprotein (apo) A-IV has been related to fat absorption and to the activation of some of the enzymes involved in lipid metabolism. One mutation has been described in the apo A-IV gene that causes substitution of Ser for Thr at position 347. To study the influence of this mutation on the plasma LDL cholesterol (LDL-C) response in diets of various fat content and fatty acid saturation, 41 healthy male subjects were studied, 25 of whom were homozygous for the Thr allele (347Thr) and the rest who were either homozygous (n = 2) or heterozygous carriers of the Ser allele (347Ser). They consumed three consecutive diets, each of 4 weeks' duration: one rich in saturated fat (SFA diet: 38% fat, 20% saturated), a National Cholesterol Education Program (NCEP) type 1 diet (28% fat, 10% saturated), and a third rich in monounsaturated fat (MUFA diet; 38% fat, 22% monounsaturated). Carriers of the 347Ser allele presented a greater decrease in total cholesterol (-0.7 vs -0.44 mmol/L, P < .034), LDL-C (-0.62 vs -0.31 mmol/L, P < .012), and apo B (-14 vs -8 mg/dL, P < .01) levels when they were switched from the SFA to the NCEP type 1 diet than homozygous carriers of the 347Thr allele. The change from the NCEP type 1 to the MUFA diet resulted in a greater increase in total cholesterol (0.18 vs -0.05 mmol/L, P < .028) and apo B (5 vs -1 mg/dL, P < .006) levels in the 347Ser than in the 347Thr individuals. In a previous study, we demonstrated that the G-->A polymorphism at position -76 of the gene promoter of apo A-I affects the LDL-C response to dietary fat. We therefore decided to study the effect of the interaction between these mutations on this response. We found that both mutations have an additive effect on total cholesterol, LDL-C, and apo B dietary-induced changes. Our results suggest that total cholesterol and LDL-C response to dietary fat is influenced by the 347Ser mutation of apo A-IV.

Lipid-lowerjng diets enriched with monounsaturated or polyunsaturated fatty acids but low in saturated fatty acids have similar effects on serum lipid concentrations in hyperlipidemic patients

The aim of this study was to compare the effects of a diet enriched with monounsaturated (MUFAs) with one enriched with polyunsaturated (PUFAs) fatty acids on the serum lipoprotein composition in patients with hyperlipidemia. A new model for conducting controlled dietary treatment studies in free-living hyperlipidemic patients was tested. Twenty-six patients with an average age of 51 y participated in a crossover study during two consecutive 3.5-wk treatment periods. The mean serum cholesterol and LDL cholesterol decreased by 17% and 19%, respectively, on the MUFA diet. The corresponding figures on the PUFA diet were 19% and 23%, respectively. The HDL-cholesterol concentration was significantly decreased after both dietary periods. No significant differences in any of the variables studied were found between the diets. It is concluded that MUFAs and PUFAs, within a diet with a restricted content of saturated fat and total fat, are interchangeable with regard to lipid-lowering effects among free-living hyperlipidemic patients.