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PubMed2001

Compared with saturated fatty acids, dietary monounsaturated fatty acids and carbohydrates increase atherosclerosis and VLDL cholesterol levels in LDL receptor-deficient, but not apolipoprotein E-deficient, mice.

Heart-healthy dietary recommendations include decreasing the intake of saturated fatty acids (SFA). However, the relative benefit of replacing SFA with monounsaturated fatty acids (MUFA), polyunsaturated fatty acids (PUFA), or carbohydrates (CARB) is still being debated. We have used two mouse models of atherosclerosis, low density lipoprotein receptor-deficient (LDLRKO) and apolipoprotein E-deficient (apoEKO) mice to measure the effects of four isocaloric diets enriched with either SFA, MUFA, PUFA, or CARB on atherosclerotic lesion area and lipoprotein levels. In LDLRKO mice, compared with the SFA diet, the MUFA and CARB diets significantly increased atherosclerosis in both sexes, but the PUFA diet had no effect. The MUFA and CARB diets also increased very low density lipoprotein-cholesterol (VLDL-C) and LDL-cholesterol (LDL-C) in males and VLDL-C levels in females. Analysis of data from LDLRKO mice on all diets showed that atherosclerotic lesion area correlated positively with VLDL-C levels (males: r = 0.47, P < 0.005; females: r = 0.52, P < 0.001). In contrast, in apoEKO mice there were no significant dietary effects on atherosclerosis in either sex. Compared with the SFA diet, the CARB diet significantly decreased VLDL-C in males and the MUFA, PUFA, and CARB diets decreased VLDL-C and the CARB diet decreased LDL-C in females. In summary, in LDLRKO mice the replacement of dietary SFA by either MUFA or CARB causes a proportionate increase in both atherosclerotic lesion area and VLDL-C. There were no significant dietary effects on atherosclerotic lesion area in apoEKO mice. These results are surprising and suggest that, depending on the underlying genotype, dietary MUFA and CARB can actually increase atherosclerosis susceptibility, probably by raising VLDL-C levels through a non-LDL receptor, apoE-dependent pathway.

Adipose Tissue↗
PubMed1995

Comparison of the effects on the diurnal blood pressure, glucose, and lipid levels of a diet rich in monounsaturated fatty acids with a diet rich in polyunsaturated fatty acids in type 2 diabetic subjects.

The influence on blood pressure, glucose metabolism, and lipid levels of an exchange of polyunsaturated fatty acids with monounsaturated fatty acids in the diet was compared in 16 Type 2 diabetic outpatients. In a cross-over study design the patients were randomly assigned to 3 weeks treatments with a diet containing 30% energy as monounsaturated fatty acids, or an isoenergetic diet with 30% energy as polyunsaturated fatty acids. The contents of total fat, saturated fatty acids, cholesterol, and fibre were similar in the two diets. On the last days of the two diet periods, 24-h ambulatory blood pressure was measured and the responses of glucose, hormones, and lipids to a carbohydrate rich test meal were measured. As compared with the polyunsaturated fatty acids diet, the monounsaturated fatty acids diet reduced 24-h systolic (129 +/- 11 vs 124 +/- 8 mmHg (mean +/- SD), p = 0.02) and diastolic blood pressure (76 +/- 11 vs 73 +/- 8 mmHg, p = 0.02). The two diets had similar, beneficial effects on glycaemic control, and cholesterol and lipoprotein concentrations. A diet rich in monounsaturated fatty acids has beneficial effects on the blood pressure, while similar effects on glucose and lipid levels are observed in normotensive Type 2 diabetic subjects.

Blood Glucose↗
PubMed2006

Effect of dietary conjugated linoleic acid and monounsaturated fatty acid content on pig muscle and adipose tissue lipase and esterase activity.

Three levels (0%, 1%, and 2%) of conjugated linoleic acid (CLA) were combined with two levels (low and high) of monounsaturated fatty acids (MUFA) for pig feeding. The activity of neutral lipase (NL), acid lipase (AL), phospholipase (PL), neutral esterase (NE), and acid esterase (AE) was measured in extracts from muscle and subcutaneous adipose tissues. The addition of CLA in the diet only affected the lipolytic activity in muscle, whereas differences in MUFA content of pig diets were mainly responsible for the lipolytic enzyme modifications observed in adipose tissue. Nevertheless, a significant effect of the interaction CLA x MUFA on the activity of several lipolytic enzymes was observed in both tissues. The effect of either linoleic acid (LA) or CLA on the activity of muscle and adipose lipolytic enzymes was determined by in vitro assays. Remarkable inhibitory or activation effects were detected depending on the enzyme and kind of tissue.

Adipose Tissue↗
PubMed1995

Plasma cholesterol-predictive equations demonstrate that stearic acid is neutral and monounsaturated fatty acids are hypocholesterolemic.

In the present study we used regression analyses to evaluate the effects of stearic acid (18:0) on total cholesterol (TC), low-density-lipoprotein-cholesterol (LDL-C), and high-density-lipoprotein-cholesterol (HDL-C) concentrations (mmol/L). Using data from 18 articles, we developed the following predictive equations (monounsaturated fatty acids, MUFAs; polyunsaturated fatty acids, PUFAs): delta TC = 0.0522 delta 12:0-16:0 - 0.0008 delta 18:0 - 0.0124 delta MUFA - 0.0248 delta PUFA; delta LDL-C = 0.0378 delta 12:0-16:0 + 0.0018 delta 18:0 - 0.0178 delta MUFA - 0.0248 delta PUFA; delta HDL-C = 0.0160 delta 12:0-16:0 - 0.0016 delta 18:0 + 0.0101 delta MUFA + 0.0062 delta PUFA. Our analyses revealed that unlike the other long-chain saturated fatty acids (SFAs), stearic acid had no effect on TC and lipoprotein cholesterol concentrations in men and women. MUFAs elicited an independent hypocholesterolemic effect that we believe is due to the small amount of 12:0-16:0 in the experimental diets evaluated. The observation that stearic acid has unique effects on TC, LDL-C, and HDL-C provides additional compelling evidence that it be distinguished from the other major SFAs in blood cholesterol predictive equations.

Adult↗
PubMed1999

Comparative effects of polyunsaturated- to saturated fatty acid ratio versus polyunsaturated- and monounsaturated fatty acids to saturated fatty acid ratio on lipid metabolism in rats.

This study examined the effects of various polyunsaturated fatty acid (PUFA, P)/saturated fatty acid (SFA, S) ratio versus PUFA + monounsaturated fatty acid (MUFA, M)/SFA ratio on lipid metabolism. The P/S ratio of dietary fat was fixed at a certain level (0.5, 1, 2, or 4, respectively) for each of four pairs of rat groups respectively, and then the P + M/S ratio was changed for the four pairs of rat groups. When the P/S ratio was fixed at 0.5, 1, 2, or 4, the plasma total cholesterol, LDL-cholesterol (C), and HDL-C levels did not show any significant difference in each pair of groups with different P + M/S ratios. However, when the P/S ratio was fixed at 1.0, the higher P + M/S ratio of 5.7 (M/S=4.7, P/M=0.2) resulted in significantly higher plasma total triacylglycerol (TAG), VLDL-TAG, VLDL-C, and VLDL-phospholipid (PL) than the lower P + M/S ratio of 1.4 (M/S=0.4, P/M=2.4). Whereas when SFA was fixed at a similar level, it therefore had approximately the same P + M/S ratio(5.3, 5.6, 5.7), and by increasing the P/S ratio from 1, 2 to 4 (70.4, 52.7 and 23.2% of the total fatty acids as MUFA respectively), the plasma VLDL-C, VLDL-TAG, and VLDL-PL concentrations decreased progressively. When PUFA or MUFA was kept on a similar level (14.9 or 53% respectively), the higher P + M/S ratio (5.7 or 5.3, respectively) resulted in significantly greater accumulation of liver cholesterol than the lower P + M/S ratio of 2.2. When the P/S ratio was fixed at 1 or 4, the diet of higher P + M/S ratio in a pair of the groups also resulted in greater accumulation of liver cholesterol. The results of the study suggests that if the P + M/S ratio was below 3, the change in the P/S ratios (0.5, 1 or 2) did not affect the levels of plasma total and lipoprotein cholesterol and TAG. Increases in the plasma VLDL-C and VLDL-TAG were related to increased MUFA content in the diet. And high MUFA content resulted in greater accumulation of liver cholesterol. It seems that the prerequisites for keeping low plasma and liver cholesterol are (a) low M/S ratio and (b) high P/M ratio and (c) P + M/S ratio not to exceed 3.

Animals↗
PubMed1986

Adrenoleukodystrophy: oleic acid lowers fibroblast saturated C22-26 fatty acids.

Monounsaturated fatty acids, especially oleic acid (C18:1), decreased the content of saturated very-long-chain fatty acids (VLFA) in cultured skin fibroblasts from patients with adrenoleukodystrophy (ALD) and controls. When confluent ALD fibroblasts were incubated with oleic acid for 5 days in lipid-free medium, which eliminates uptake of exogenous VLFA, the mean cell content of C26:0 was decreased by 33.7 +/- 10.1%. Oleic acid inhibited C26:0 synthesis in ALD fibroblasts by 58% and total fatty acid synthesis by 68 to 78%. Therefore, the elevated C26:0 levels in ALD cells may be lowered by inhibiting fatty acid biosynthesis, and inhibition of saturated VLFA synthesis by oleate may be useful in treating ALD.

Adrenoleukodystrophy↗
PubMed1992

Effects of diets rich in monounsaturated fatty acids on plasma lipoproteins--the Jerusalem Nutrition Study. II. Monounsaturated fatty acids vs carbohydrates.

Seventeen male Yeshiva students were randomly allocated to a crossover study with two 12-wk dietary periods of monounsaturated fatty acids (MUFAs) vs a carbohydrate (CHO)-rich diet while concentrations of saturated (SFAs) and polyunsaturated (PUFAs) fatty acids were kept similar. Total plasma cholesterol (TC) decreased significantly by approximately 7.7% and low-density-lipoprotein cholesterol (LDL-C) by 14.4% on the MUFA diet, whereas on the CHO diet no significant change in cholesterol concentrations occurred, in contrast to that predicted by the equations of Keys and Hegsted. Concentrations of high-density-lipoprotein cholesterol (HDL-C) did not change significantly on either diet. On the MUFA diet there was a significantly lower proneness to peroxidation of plasma and LDL lipids and less extensive metabolism of conditioned LDL by peritoneal macrophages. We conclude that dietary MUFAs lower TC and LDL-C concentrations, independently of other dietary fatty acids and in addition may reduce the susceptibility of LDL to oxidative stress.

Adult↗
PubMed2005

Oleic acid, the main monounsaturated fatty acid of olive oil, suppresses Her-2/neu (erbB-2) expression and synergistically enhances the growth inhibitory effects of trastuzumab (Herceptin) in breast cancer cells with Her-2/neu oncogene amplification.

BACKGROUND: The relationship between the intake of olive oil, the richest dietary source of the monounsaturated fatty acid oleic acid (OA; 18:1n-9), and breast cancer risk and progression has become a controversial issue. Moreover, it has been suggested that the protective effects of olive oil against breast cancer may be due to some other components of the oil rather than to a direct effect of OA. METHODS: Using flow cytometry, western blotting, immunofluorescence microscopy, metabolic status (MTT), soft-agar colony formation, enzymatic in situ labeling of apoptosis-induced DNA double-strand breaks (TUNEL assay analyses), and caspase-3-dependent poly-ADP ribose polymerase (PARP) cleavage assays, we characterized the effects of exogenous supplementation with OA on the expression of Her-2/neu oncogene, which plays an active role in breast cancer etiology and progression. In addition, we investigated the effects of OA on the efficacy of trastuzumab (Herceptin), a humanized monoclonal antibody binding with high affinity to the ectodomain of the Her-2/neu-coded p185(Her-2/neu) oncoprotein. To study these issues we used BT-474 and SKBr-3 breast cancer cells, which naturally exhibit amplification of the Her-2/neu oncogene. RESULTS: Flow cytometric analyses demonstrated a dramatic (up to 46%) reduction of cell surface-associated p185(Her-2/neu) following treatment of the Her-2/neu-overexpressors BT-474 and SK-Br3 with OA. Indeed, this effect was comparable to that found following exposure to optimal concentrations of trastuzumab (up to 48% reduction with 20 microg/ml trastuzumab). Remarkably, the concurrent exposure to OA and suboptimal concentrations of trastuzumab (5 microg/ml) synergistically down-regulated Her-2/neu expression, as determined by flow cytometry (up to 70% reduction), immunoblotting, and immunofluorescence microscopy studies. The nature of the cytotoxic interaction between OA and trastuzumab revealed a strong synergism, as assessed by MTT-based cell viability and anchorage-independent soft-agar colony formation assays. Moreover, OA co-exposure synergistically enhanced trastuzumab efficacy towards Her-2/neu overexpressors by promoting DNA fragmentation associated with apoptotic cell death, as confirmed by TUNEL and caspase-3-dependent PARP cleavage. In addition, treatment with OA and trastuzumab dramatically increased both the expression and the nuclear accumulation of p27(Kip1), a cyclin-dependent kinase inhibitor playing a key role in the onset and progression of Her-2/neu-related breast cancer. Finally, OA co-exposure significantly enhanced the ability of trastuzumab to inhibit signaling pathways downstream of Her-2/neu, including phosphoproteins such as AKT and MAPK. CONCLUSIONS: These findings demonstrate that OA, the main monounsaturated fatty acid of olive oil, suppresses Her-2/neu overexpression, which, in turn, interacts synergistically with anti-Her-2/neu immunotherapy by promoting apoptotic cell death of breast cancer cells with Her-2/neu oncogene amplification. This previously unrecognized property of OA offers a novel molecular mechanism by which individual fatty acids may regulate the malignant behavior of breast cancer cells and therefore be helpful in the design of future epidemiological studies and, eventually, dietary counseling.

Antibodies, Monoclonal↗
PubMed1988

Analysis of fatty acids by negative ion gas chromatography/tandem mass spectrometry: structural correlations between alpha-mycolic acid chains and delta-5-monounsaturated fatty acids from Mycobacterium phlei.

The analysis of a complex mixture of monounsaturated fatty acids from mycobacterium phlei is achieved by capillary gas chromatographic separation of their pentafluorobenzyl esters, formation of gas-phase carboxylate anions by electron capture ionization and decomposition of these anions by collision activation. This method allows the structural determination of fatty acid isomers by examination of their collisionally activated dissociation mass-analysed ion kinetic energy spectra. A good correlation is observed between the structure of the unsaturated fatty acids ranging from C24 to C27 and the methyl terminal part of the main chain of diunsaturated mycolic acids.

Fatty Acids↗
PubMed2001

Distinct effects of saturated and monounsaturated fatty acids on beta-cell turnover and function.

Glucotoxicity and lipotoxicity contribute to the impaired beta-cell function observed in type 2 diabetes. Here we examine the effect of saturated and unsaturated fatty acids at different glucose concentrations on beta-cell proliferation and apoptosis. Adult rat pancreatic islets were cultured onto plates coated with extracellular matrix derived from bovine corneal endothelial cells. Exposure of islets to saturated fatty acid (0.5 mmol/l palmitic acid) in medium containing 5.5, 11.1, or 33.3 mmol/l glucose for 4 days resulted in a five- to ninefold increase of beta-cell DNA fragmentation. In contrast, monounsaturated palmitoleic acid alone (0.5 mmol/l) or in combination with palmitic acid (0.25 or 0.5 mmol/l each) did not affect DNA fragmentation. Increasing concentrations of glucose promoted beta-cell proliferation that was dramatically reduced by palmitic acid. Palmitoleic acid enhanced the proliferation activity in medium containing 5.5 mmol/l glucose but had no additional effect at higher glucose concentrations (11.1 and 33.3 mmol/l). The cell-permeable ceramide analog C2-ceramide mimicked both the palmitic acid-induced beta-cell apoptosis and decrease in proliferation. Moreover, the ceramide synthetase inhibitor fumonisin B1 blocked the deleterious effects of palmitic acid on beta-cell viability. Additionally, palmitic acid but not palmitoleic acid decreased the expression of the mitochondrial adenine nucleotide translocator and induced release of cytochrome c from the mitochondria into the cytosol. Finally, palmitoleic acid improved beta-cell-secretory function that was reduced by palmitic acid. Taken together, these results suggest that the lipotoxic effect of the saturated palmitic acid involves an increased apoptosis rate coupled with reduced proliferation capacity of beta-cells and impaired insulin secretion. The deleterious effect of palmitate on beta-cell turnover is mediated via formation of ceramide and activation of the apoptotic mitochondrial pathway. In contrast, the monounsaturated palmitoleic acid does not affect beta-cell apoptosis, yet it promotes beta-cell proliferation at low glucose concentrations, counteracting the negative effects of palmitic acid as well as improving beta-cell function.

Animals↗
PubMed1997

What is the desirable ratio of saturated, polyunsaturated, and monounsaturated fatty acids in the diet?

By reducing intakes of animal fats and gradually reducing intakes of trans fatty acids, a one-third reduction in cholesterol-raising fatty acids seems practical, from 12% to 7-8% of total energy intake. The intake of polyunsaturated fatty acids should not exceed current intakes, approximately 7% of total energy. Although further research is needed to determine a recommended ratio of oleic acid to carbohydrates, on the basis of the relatively low rates of coronary artery disease and cancer in both the Mediterranean region (where oleic acid intake is high at the expense of carbohydrates) and in populations consuming low-fat, high-carbohydrate diets, a reasonable compromise is a diet in which total fat is approximately 30% of energy, allowing for an intake of oleic acid of 15-16% of total energy.

Dietary Fats↗
PubMed2006

A genomic explanation connecting "Mediterranean diet", olive oil and cancer: oleic acid, the main monounsaturated fatty acid of olive oil, induces formation of inhibitory "PEA3 transcription factor-PEA3 DNA binding site" complexes at the Her-2/neu (erbB-2) oncogene promoter in breast, ovarian and stomach cancer cells.

Olive oil is an integral ingredient of the "Mediterranean diet" and accumulating evidence suggests that it may have a potential role in lowering risk of several cancers. We recently hypothesized that the anti-cancer actions of olive oil may relate to its monounsaturated fatty acid (MUFA) oleic acid (OA; 18:1n-9) content to specifically regulate oncogenes. In this study, transient transfection experiments with human Her-2/neu promoter-driven luciferase gene established the ability of OA to specifically repress the transcriptional activity of Her-2/neu gene. Gene repression was seen in tumour-derived cell lines with Her-2/neu gene amplification and overexpression, including SK-Br3 (56% reduction), SK-OV3 (75% reduction) and NCI-N87 (55% reduction) breast, ovarian and stomach cancer cell lines, respectively. Also marginal decreases in promoter activity were observed in cancer cells expressing physiological levels of Her-2/neu (20% reduction in MCF-7 breast cancer cells). Remarkably, OA treatment in Her-2/neu-overexpressing cancer cells was found to induce up-regulation of the Ets protein polyomavirus enhancer activator 3 (PEA3), a transcriptional repressor of Her-2/neu promoter. Also, an intact PEA3 DNA-binding-site at endogenous Her-2/neu gene promoter was essential for OA-induced repression of this gene. Moreover, OA treatment failed to decrease Her-2/neu protein levels in MCF-7/Her2-18 transfectants, which stably express full-length human Her-2/neu cDNA controlled by a SV40 viral promoter. OA-induced transcriptional repression of Her-2/neu through the action of PEA3 protein at the promoter level may represent a novel mechanism linking "Mediterranean diet" and cancer.

Breast Neoplasms↗
PubMed2006

[Protective effect of dietary monounsaturated fatty acid on cardiovascular system].

Monounsaturated fatty acid(MUFA) is a sort of fatty acids, including a double bond in its carbon chain. Substantial evidence exists to suggest that MUFA can positively regulate the metabolism of serum lipids, decrease the susceptibility of LDL to oxidative modification, protect the artery endothelium, and decrease prothrombotic environment. The protective effect of MUFA to the cardiovascular system was introduced in the paper.

Blood Coagulation↗
PubMed1992

Effect of dietary monounsaturated fatty acids on plasma lipoproteins and apolipoproteins in women.

To determine the effects of dietary fat saturation on plasma lipoproteins, we studied 21 free-living normolipidemic women (13 pre- and 8 postmenopausal) on three consecutive diet periods. During the first 4 wk they consumed a saturated diet rich in palm oil and butter [19% saturated fatty acids (S), 14% monounsaturated fatty acids (M), and 3.5% polyunsaturated fatty acids (P)], followed by 6 wk of a monounsaturated diet rich in olive oil (11% S, 22% M, and 3.6% P), and 6 wk of a polyunsaturated diet rich in sunflower oil (10.7% S, 12.5% M, and 12.8% P). Compared with the diet rich in saturated fatty acids, both diets rich in unsaturated fatty acids had similar lowering effects on total and low-density-lipoprotein cholesterol. High-density lipoprotein cholesterol and apolipoprotein A-I were higher in the monounsaturated-rich period than in the polyunsaturated-rich (10.5% and 12.7% respectively, P less than 0.001) and the saturated-rich period (5.3%, and 7.9%, respectively, P less than 0.05). These effects were independent of menopause status. Our data show that at this level of fat intake (36% as calories), a monounsaturated-rich diet results in a less atherogenic lipid profile than either polyunsaturated- or saturated-rich diets.

Adult↗
PubMed1997

Intake of a diet high in trans monounsaturated fatty acids or saturated fatty acids. Effects on postprandial insulinemia and glycemia in obese patients with NIDDM.

OBJECTIVE: High intake of trans fatty acids and saturated fatty acids (SFAs) is known to increase the risk of coronary heart disease. We studied the effects of diets enriched in various fatty acids on postprandial insulinemia and fasting serum levels of lipids and lipoproteins in obese patients with NIDDM. RESEARCH DESIGN AND METHODS: Sixteen obese NIDDM patients were studied in a free-living outpatient regimen. After a run-in period, the patients received three different isocaloric diets for 6 weeks using a randomized crossover design. The patients were instructed to keep the energy intake from carbohydrate and protein constant at 50 and 20 E% (percent of energy intake), respectively, on all three diets. The fat composition of the diets differed: saturated fat (SAT) diet (20 E% SFAs, 5 E% polyunsaturated fatty acids [PUFAs], and 5 E% monounsaturated fatty acids [MUFAs]) versus cis monounsaturated fatty acid (CMUFA) diet (20 E% cis-MUFAs, 5 E% PUFAs, and 5 E% SFAs) versus trans monounsaturated fatty acid (TMUFA) diet (20 E% trans-MUFAs, 5 E% PUFAs, and 5 E% SFAs). Fasting serum levels of lipids and lipoproteins were measured at baseline and in the fasting state before meal tolerance tests at the end of each study period. Insulin secretion was assessed from incremental serum insulin and C-peptide responses during the meal tests. RESULTS: BMI, waist-to-hip ratio, and glycemic control remained stable throughout the study. After meal stimulation, postprandial glycemic responses were similar on all diets; however, serum insulin and C-peptide responses were greater following the TMUFA and SAT diets than following the baseline or CMUFA diets (P < 0.05). No statistical difference was found in fasting levels of serum lipids (total cholesterol, triglyceride, phospholipid, and nonesterified fatty acids) or lipoproteins of HDL cholesterol, VLDL cholesterol, LDL cholesterol, and apolipoprotein B between diets. CONCLUSIONS: In the presence of unchanged glycemia, both dietary trans fatty acids and SFAs induce an increase in postprandial insulinemia in obese patients with NIDDM.

Blood Glucose↗
PubMed2003

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.

Apolipoproteins↗
PubMed1977

Fatty acid synthetase from Brevibacterium ammoniagenes: formation of monounsaturated fatty acids by a multienzyme complex.

A multienzyme fatty acid synthetase complex isolated from Brevibacterium ammoniagenes has been purified to a specific activity of 1440 nmol of malonyl-CoA incorporated per min/mg. The enzyme is homogeneous, as judged by gel electrophoresis on agarose gels, and has a molecular weight of 1.2 X 10(6). Both NADPH and NADH are required for activity. In contrast to other fatty acid synthetase complexes, the enzyme catalyzes the synthesis of both long-chain saturated and monounsaturated fatty acids from malonyl-CoA and acetyl-CoA. The formation of unsaturated fatty acids is oxygen-independent and sharply reduced by 3-decynoyl-N-acetylcysteamine, a known inhibitor of Escherchia coli beta-hydroxydecanoyl thioester dehydrase (EC 4.2.1.60).

Aerobiosis↗
PubMed1990

Dietary influences on serum lipids and lipoproteins.

Substantial data are available to indicate that the diet influences serum levels of cholesterol and lipoproteins. These data are derived from studies in laboratory animals, from epidemiologic studies, and from human investigations. Most research has focused on effects of diet on serum total cholesterol concentrations. In recent years, however, attention has shifted to individual lipoproteins, i.e., low density lipoproteins (LDL), high density lipoproteins (HDL), and very low density lipoproteins (VLDL). Three nutritional factors have been identified that raise serum LDL levels; these are saturated fatty acids, cholesterol itself, and excess caloric intake leading to obesity. The major cholesterol-raising saturated fatty acid in the diet is palmitic acid. Several nutrients can be substituted for saturated fatty acids to produce a reduction in LDL-cholesterol levels. These are polyunsaturated fatty acids, monounsaturated fatty acids, carbohydrates, and even one saturated fatty acid, stearic acid. The latter appears to be converted rapidly into a monounsaturated fatty acid in the body. Any of these nutrients can be used for replacement of cholesterol-raising saturated fatty acids in the diet. However, their relative effects on other metabolic processes remain to be determined fully. At present it appears that carbohydrates and monounsaturated fatty acids represent the preferred replacements for saturated fatty acids, although modest increases in polyunsaturated fatty acids and stearic acid, at the expense of cholesterol-raising saturates, probably are safe and may provide for greater variety in the diet.

Animals↗