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Background: Obesity is a state of excess energy storage resulting in body fat accumulation, and postmenopausal obesity is a rising issue. In this study using ovariectomized (OVX) rats, we mimicked low estrogen levels in a postmenopausal state in order to investigate the effects of different amounts and types of dietary fatty acids on body fat accumulation and body lipid metabolism., Methods: At 9 weeks of age, rats ( n = 40) were given an ovariectomy, eight of which were sham-operated to serve as a control group (S). We then divided OVX rats into four different intervention groups: diet with 5% soybean oil (C), and diet with 5% (L), 15% (M), and 20% (H) ( w / w ) experimental oil, containing 60% monounsaturated fatty acids (MUFAs) and with a polyunsaturated/saturated fatty acid (P/S) ratio of 5., Results: After OVX, compared to the S group, the C group showed significantly higher body weight, and insulin and leptin levels. Compared to the C group, the H group had lower hepatic triglyceride level and FAS enzyme activity, and higher hepatic ACO and CPT-1 gene expressions and enzyme activities., Conclusions: An OVX leads to severe weight gain and lipid metabolism abnormalities, while according to previous studies, high fat diet may worsen the situation. However, during our experiment, we discovered that the experimental oil mixture with 60% MUFAs and P/S = 5 may ameliorate these imbalances.

Replacing intake of SFA with PUFA reduces serum cholesterol levels and CVD risk. The effect on glycaemic regulation is, however, less clear. The main objective of the present study was to investigate the short-term effect of replacing dietary SFA with PUFA on glycaemic regulation. Seventeen healthy, normal-weight participants completed a 25-d double-blind, randomised and controlled two-period crossover study. Participants were allocated to either interventions with PUFA products or SFA products (control) in a random order for three consecutive days, separated by a 1·5-week washout period between the intervention periods. Glucose, insulin and TAG were measured before and after an oral glucose tolerance test. In addition, fasting total cholesterol, NEFA and plasma total fatty acid profile were measured before and after the 3-d interventions. Fasting and postprandial glucose, insulin, and TAG levels and fasting levels of NEFA and plasma fatty acid profile did not differ between the groups. However, replacing dietary SFA with PUFA significantly reduced total cholesterol levels by 8 % after 3 d (P = 0·002). Replacing dietary SFA with PUFA for only 3 d has beneficial cardio-metabolic effects by reducing cholesterol levels in healthy individuals.

Metabolic fates of fatty acids in tissue may be influenced by extracellular concentration and profile of fatty acids. Previous work has demonstrated the ability of C18:3n-3 cis to ameliorate the effects of C16:0- or C18:0-induced depression of pyruvate carboxylase (PC) mRNA expression. Pyruvate carboxylase catalyzes oxaloacetate synthesis and connects gluconeogenesis from lactate and fatty acid metabolism. Our objective was to determine the effects of co-presence of saturated and unsaturated fatty acids on cellular partitioning of [1- 14 C]C16:0 metabolism to CO 2 or acid-soluble products (ASP) in Madin-Darby bovine kidney cells and the role of PC in this relationship. We hypothesized that the ratio of saturated to unsaturated fatty acid pretreatments regulates [1- 14 C]C16:0 partitioning to CO 2 or ASP. Cells were exposed for 21 h to either individual fatty acids, C16:0, C18:0, C18:1n-9 cis, or C18:3n-3 cis, or to fatty acid combinations in 10:90, 25:75, 50:50, 75:25, or 90:10 ratios for 3 combinations: C16:0/C18:3n-3 cis, C18:0/C18:3n-3 cis, or C18:1n-9 cis/C18:3n-3 cis. Total fatty acid concentration was 1.0 mM during the 21-h pretreatment phase. Following the 21-h incubation phase with fatty acid combinations, cells were incubated in the presence of 1.0 mM [1- 14 C]C16:0 for 3 h to determine the rate of metabolism to CO 2 and ASP collection (per µg DNA -1 ·h -1 ). Pretreatment with either C16:0 or C18:0 alone significantly depressed subsequent oxidation of [1- 14 C]C16:0 to ASP by 62.7 and 41.2%, respectively, compared with C18:3n-3 cis pretreatment. Similar patterns were observed for [1- 14 C]C16:0 oxidation to CO 2 . Expression of PC mRNA was significantly decreased with exposure to either C16:0 or C18:0 compared with expression after exposure to either C18:3n-3 cis or control 1% BSA in Dulbecco's modified Eagle's medium. Expression of cytosolic phosphoenolpyruvate carboxykinase (PCK1) mRNA followed a similar pattern. Fatty acid treatments containing C18:1n-9 cis did not alter PC or PCK1 expression from control or C18:3n-3 cis results. Pearson coefficient correlations were determined for PC mRNA expression and rate of [1- 14 C]C16:0 metabolism to CO 2 or ASP, including ketones, and for PCK1 mRNA expression and rate of [1- 14 C]C16:0 metabolism to CO 2 or ASP. Production of CO 2 from [1- 14 C]C16:0 was positively correlated (r = 0.63) with PC expression, whereas ASP production from [1- 14 C]C16:0 only tended to positively correlate (r = 0.51) with PC mRNA expression. Production of CO 2 or ASP from [1- 14 C]C16:0 were both positively correlated (r = 0.80 and r = 0.69, respectively) with PCK1 expression. Results show a regulation of ketone production by Madin-Darby bovine kidney cells in response to saturated and unsaturated fatty acid pretreatments., (Copyright © 2020 American Dairy Science Association. Published by Elsevier Inc. All rights reserved.)

In order to evaluate fatty acid (FA) sensing systems based on binding to FAT/CD36 in hypothalamus of Chinese perch (Siniperca chuatsi) and its sensitivity to FAs with the same chain length and different unsaturation levels. The effects of Stearate (SA; C18:0), oleate (OA; C18:1 n-9), linoleic acid (LA; C18:2 n-6), and α-linolenic acid (ALA; C18:3 n-3) on hypothalamic FA sensing were evaluated by intracerebroventricular (ICV) administration. Food intake was assessed after 2, 4, 6, 8 and 12 h. Gene expression associated with FA sensing mechanism such as cd36, pparα and srebp1c, and neuropeptides controlling appetite such as pomca, cart, agrp2 and npy were assessed after 6 h. The ICV treatment of OA, LA and ALA activated FAT/CD36 and PPARα, rather than SA, and modulated gene expression levels of hypothalamic neuropeptides associated with appetite. And then, OA, LA and ALA inhibited food intake, which was consistent with the activation of hypothalamus FA sensing. Our data indicated some mechanisms of the hypothalamic FA sensing systems also existed in Chinese perch. It's worth noting that polyunsaturated fatty acids (PUFA) could also activate hypothalamic FA sensing mechanisms in Chinese perch. The unsaturation of FA appears to be extremely important for FA sensing mechanisms, since no major influences in Chinese perch after SA treatment. Our findings will contribute to the study of long-chain FAs sensing mechanisms in fish hypothalamus and highlight the importance of PUFAs in fish species., Competing Interests: Declaration of Competing Interest All of the authors declare that there are no conflicts of interest., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Background: SFA intake increases LDL cholesterol whereas PUFA intake lowers it. Whether the lipid response to dietary fat differs between normal-weight and obese persons is of relevance to dietary recommendations for obese populations., Objectives: We compared the effect of substituting unsaturated fat for saturated fat on LDL cholesterol and apoB concentrations in normal-weight (BMI ≤ 25 kg/m2) and obese (BMI: 30-45) subjects with elevated LDL cholesterol., Methods: We randomly assigned 83 men and women (aged 21-70 y) stratified by BMI (normal: n = 44; obese: n = 39) and elevated LDL cholesterol (mean ± SD, normal weight 4.6 ± 0.9 mmol/L; obese 4.4 ± 0.8 mmol/L) to either a PUFA diet enriched with oil-based margarine ( n = 42) or an SFA diet enriched with butter (n = 41) for 6 wk., Results: Seven-day dietary records showed differences of ∼9 energy percent (E%) in SFA and ∼4 E% in PUFA between the SFA and PUFA groups. In the total study population, the PUFA diet compared with the SFA diet lowered LDL cholesterol (-0.31 mmol/L; 95% CI: -0.47, -0.15 mmol/L, compared with 0.32 mmol/L; 95% CI: 0.18, 0.47 mmol/L; P < 0.001) and apoB (-0.08 g/L; 95% CI: -0.11, -0.05 g/L, compared with 0.07 g/L; 95% CI: 0.03, 0.10 g/L; P < 0.001). Tests of the BMI × diet interaction were significant for total cholesterol, LDL cholesterol, and apoB ( P values ≤ 0.009). In normal-weight compared with obese participants post-hoc comparisons found that the respective changes in LDL cholesterol were 9.7% (95% CI: 5.3%, 14.2%) compared with 5.3% (95% CI: -0.7%, 11.2%), P = 0.206, in the SFA group, and -10.4% (95% CI: -15.2%, -5.7%) compared with -2.3% (95% CI: -7.4%, 2.8%), P = 0.020, in the PUFA group. ApoB changes were 7.5% (95% CI: 3.5%, 11.4%) compared with 3.0% (95% CI: -1.7%, 7.7%), P = 0.140, in the SFA group, and -8.9% (95% CI: -12.6%, -5.2%) compared with -3.8% (95% CI: -6.3%, -1.2%), P = 0.021, in the PUFA group. Responses to dietary fat were not associated with changes in polyprotein convertase subtisilin/kexin type 9 concentrations., Conclusions: BMI modifies the effect of PUFAs compared with SFAs, with smaller improvements in atherogenic lipid concentrations in obese than in normal-weight individuals, possibly supporting adjustment of dietary recommendations according to BMI. This trial was registered with www.clinicaltrials.gov as NCT02589769., (Copyright © American Society for Nutrition 2019.)

Background: Replacing dietary saturated fatty acids (SFAs) with polyunsaturated fatty acids (PUFA) reduces the plasma low-density lipoprotein (LDL) cholesterol and subsequently the risk of cardiovascular disease. However, beyond changes in LDL cholesterol, we lack a complete understanding of the physiologic alterations that occur when improving dietary fat quality., Objectives: The aim of this study was to gain knowledge of metabolic alterations paralleling improvements in the fat quality of the diet., Methods: We recently conducted an 8-wk, double-blind, randomized controlled trial replacing SFAs with PUFAs in healthy subjects with moderate hypercholesterolemia (n = 99). In the present substudy, we performed comprehensive metabolic profiling with multiple platforms (both nuclear magnetic resonance- and mass spectrometry-based technology) (n = 99), and analyzed peripheral blood mononuclear cell gene expression (n = 95) by quantitative real-time polymerase chain reaction., Results: A large number of lipoprotein subclasses, myristoylcarnitine and palmitoylcarnitine, and kynurenine were reduced when SFAs were replaced with PUFAs. In contrast, bile acids, proprotein convertase subtilisin/kexin type 9, acetate, and acetoacetate were increased by the intervention. Some amino acids were also altered by the intervention. The mRNA levels of LXRA and LDLR were increased, in addition to several liver X receptor α target genes and genes involved in inflammation, whereas the mRNA levels of UCP2 and PPARD were decreased in peripheral blood mononuclear cells after replacing SFAs with PUFAs. Partial least squares-discriminant analysis showed that the 30 most important variables that contributed to class separation spanned all classes of biomarkers, and was in accordance with the univariate analysis., Conclusions: Applying metabolomics in randomized controlled dietary intervention trials has the potential to extend our knowledge of the biological and molecular effects of dietary fat quality. This study was registered at clinicaltrials.gov as NCT01679496., (Copyright © American Society for Nutrition 2019.)

Introduction: Inflammation plays a key role in the development of insulin resistance and atherosclerosis. Fatty acids and fiber intake can selectively alter gene expression by modifying inflammation., Purpose: We compared the postprandial expression of inflammatory genes after 2 distinct high-fat breakfast meals, before and after 1-month dietary interventions., Methods: This crossover clinical trial included 18 individuals at low-to-moderate cardiometabolic risk participating in evaluations before and after two 4-week breakfast interventions-one rich in saturated fatty acids (SFA) and the other in unsaturated fatty acids (unSFA) and fiber. Participants underwent meal tests with similar compositions to the breakfasts. Variables were compared by Student t test. The expression of inflammatory genes in leukocytes was analyzed using RT-PCR., Results: Before and after the intervention with the SFA-enriched breakfast, this meal test induced a higher relative postprandial IL-1β expression compared to the responses to the unSFA and fiber-enriched meal (p = 0.02). On the other hand, following the intervention with the unSFA-fiber-enriched breakfast, postprandial IL-6 expression showed a reduction tendency comparing to the pre-intervention value (p = 0.08). Although fasting IL-1β, IL-6, MCP-1 and IFN-γ expressions had not changed after interventions, their circulating levels increased after the SFA-enriched meal test but not after the unSFA meal (p value between changes < 0.05)., Conclusions: Our findings indicated that a single SFA-enriched meal is able to acutely induce the IL-1β expression and regularly consumed could trigger systemic inflammation, while increased unSFA consumption could attenuate the inflammatory status. Further investigations are needed to deepen understanding how dietary fatty acids and fiber influence cardiometabolic risk profile by modulating inflammatory gene expression and circulating biomarkers., Clinical Trial Information: This study is registered at the Brazilian Registry of Clinical Trials (ReBEC ID: RBR-98x6b5). Available at: http://www.ensaiosclinicos.gov.br .

Background: High-oleic (HO) seed oils are being introduced as replacements for trans fatty acid (TFA)-containing fats and oils. Negative health effects associated with TFAs led to their removal from the US Generally Recognized As Safe list. HO oils formulated for use in food production may result in changes in fatty acid intake at population levels., Objectives: The purposes of this study were to 1) identify major food sources of soybean oil (SO) and canola oil (CO), 2) estimate effects of replacing SO and CO with HO varieties on fatty acid intake overall and by age and sex strata, and 3) compare predicted intakes with the Dietary Reference Intakes and Adequate Intakes (AIs) for the essential fatty acids (EFAs) α-linolenic acid (ALA) and linoleic acid (LA)., Design: Food and nutrient intakes from NHANES waves 2007-2008, 2009-2010, 2011-2012, and 2013-2014 in 21,029 individuals aged ≥20 y were used to model dietary changes. We estimated the intake of fatty acid with the replacement of HO-SO and HO-CO for commodity SO and CO at 10%, 25%, and 50% and evaluated the potential for meeting the AI at these levels., Results: Each modeling scenario decreased saturated fatty acids (SFAs), although intakes remained greater than recommended for all age and sex groups. Models of all levels increased the intake of total monounsaturated fatty acids (MUFAs), especially oleic acid, and decreased the intake of total polyunsaturated fatty acids (PUFAs), particularly LA and ALA. Replacement of traditional with HO oils at 25-50% places specific adult age and sex groups at risk of not meeting the AI for LA and ALA., Conclusions: The replacement of traditional oils with HO varieties will increase MUFA intake and reduce both SFA and PUFA intakes, including EFAs, and may place specific age and sex groups at risk of inadequate LA and ALA intake.

Epidemiologists have been studying the effect of n-6 polyunsaturated fatty acids (PUFAs) intake on the risk of cardiovascular disease (CVD) for many decades. Abundant evidence from prospective studies on the clinical endpoints of CVD, including cohort studies measuring n-6 PUFA intake by food frequency questionnaires and nested case-control studies using biomarkers of intake level, strongly support that higher intakes of n-6 PUFAs are associated with a lower risk of CVD. Furthermore, a significant reduction in CVD risk can be achieved when saturated fatty acids (SFAs) is replaced by n-6 PUFAs. Evidence from appropriately designed and vigorously executed randomized controlled trials support that high-PUFA (predominantly linoleic acid) and low-SFA diets, compared to high-SFA diets, reduced the risk of coronary heart disease. Overall, epidemiologic studies provide a solid evidence base of the current dietary guidelines that recommend replacing SFA by PUFA, both n-6 and n-3 PUFA, for CVD prevention., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

Postprandial hypertriacylglycerolaemia is associated with an increased risk of developing CVD. How fat quality influences postprandial lipid response is scarcely explored in subjects with familial hypercholesterolaemia (FH). The aim of this study was to investigate the postprandial response of TAG and lipid sub-classes after consumption of high-fat meals with different fat quality in subjects with FH compared with normolipidaemic controls. A randomised controlled double-blind cross-over study with two meals and two groups was performed. A total of thirteen hypercholesterolaemic subjects with FH who discontinued lipid-lowering treatment 4 weeks before and during the study, and fourteen normolipidaemic controls, were included. Subjects were aged 18-30 years and had a BMI of 18·5-30·0 kg/m2. Each meal consisted of a muffin containing 60 g (70 E%) of fat, either mainly SFA (40 E%) or PUFA (40 E%), eaten in a random order with a wash-out period of 3-5 weeks between the meals. Blood samples were collected at baseline (fasting) and 2, 4 and 6 h after intake of the meals. In both FH and control subjects, the level of TAG and the largest VLDL sub-classes peaked at 2 h after intake of PUFA and at 4 h after intake of SFA. No significant differences were found in TAG levels between meals or between groups (0·25≤P≤0·72). The distinct TAG peaks may reflect differences in the postprandial lipid metabolism after intake of fatty acids with different chain lengths and degrees of saturation. The clinical impact of these findings remains to be determined.

Aims: Over the last 7 years there has been intense debate about the advice to reduce saturated fat and increase polyunsaturated fat to reduce CVD risk. The aim of this review was to examine systematic reviews and meta-analyses since 2010 on this topic plus additional cohort studies and interventions not included in these reviews., Data Synthesis: High saturated and trans fat intake (which elevates LDL like saturated fat) in the Nurses and Health Professional Follow-Up Studies combined is associated with an 8-13% higher mortality and replacement of saturated fat with any carbohydrate, PUFA and MUFA is associated with lower mortality with PUFA being more effective than MUFA (19% reduction versus 11%). With CVD mortality only PUFA and fish oil replacement of saturated fat lowers risk with a 28% reduction in CVD mortality per 5% of energy. Replacing saturated fat with PUFA or MUFA is equally effective at reducing CHD events and replacement with whole grains will lower events while replacement with sugar and starch increases events. Replacement of saturated fat with carbohydrate has no effect on CHD events or death. Only PUFA replacement of saturated fat lowers CHD events and CVD and total mortality. Replacing saturated fat with linoleic acid appears to be beneficial based on the Hooper Cochrane meta-analysis of interventions although other analyses with fewer studies have shown no effect., Conclusions: Reducing saturated fat and replacing it with carbohydrate will not lower CHD events or CVD mortality although it will reduce total mortality. Replacing saturated fat with PUFA, MUFA or high-quality carbohydrate will lower CHD events., (Copyright © 2017 The Italian Society of Diabetology, the Italian Society for the Study of Atherosclerosis, the Italian Society of Human Nutrition, and the Department of Clinical Medicine and Surgery, Federico II University. Published by Elsevier B.V. All rights reserved.)

Obesity and its associated disorders, such as insulin resistance, dyslipidemia, metabolic inflammation, dysbiosis, and non-alcoholic hepatic steatosis, are involved in several molecular and inflammatory mechanisms that alter the metabolism. Food habit changes, such as the quality of fatty acids in the diet, are proposed to treat and prevent these disorders. Some studies demonstrated that saturated fatty acids (SFA) are considered detrimental for treating these disorders. A high fat diet rich in palmitic acid, a SFA, is associated with lower insulin sensitivity and it may also increase atherosclerosis parameters. On the other hand, a high intake of eicosapentaenoic (EPA) and docosahexaenoic (DHA) fatty acids may promote positive effects, especially on triglyceride levels and increased high-density lipoprotein (HDL) levels. Moreover, polyunsaturated fatty acids (PUFAs) and monounsaturated fatty acids (MUFAs) are effective at limiting the hepatic steatosis process through a series of biochemical events, such as reducing the markers of non-alcoholic hepatic steatosis, increasing the gene expression of lipid metabolism, decreasing lipogenic activity, and releasing adiponectin. This current review shows that the consumption of unsaturated fatty acids, MUFA, and PUFA, and especially EPA and DHA, which can be applied as food supplements, may promote effects on glucose and lipid metabolism, as well as on metabolic inflammation, gut microbiota, and hepatic metabolism., Competing Interests: The authors report no conflict of interest.

Purpose: To determine substrate oxidation responses to saturated fatty acid (SFA)-rich meals before and after a 7-day polyunsaturated fatty acid (PUFA)-rich diet versus control diet., Methods: Twenty-six, normal-weight, adults were randomly assigned to either PUFA or control diet. Following a 3-day lead-in diet, participants completed the pre-diet visit where anthropometrics and resting metabolic rate (RMR) were measured, and two SFA-rich HF meals (breakfast and lunch) were consumed. Indirect calorimetry was used to determine fat oxidation (Fox) and energy expenditure (EE) for 4 h after each meal. Participants then consumed a PUFA-rich diet (50 % carbohydrate, 15 % protein, 35 % fat, of which 21 % of total energy was PUFA) or control diet (50 % carbohydrate, 15 % protein, 35 % fat, of which 7 % of total energy was PUFA) for the next 7 days. Following the 7-day diet, participants completed the post-diet visit., Results: From pre- to post-PUFA-rich diet, there was no change in RMR (16.3 ± 0.8 vs. 16.4 ± 0.8 kcal/20 min) or in incremental area under the curve for EE (118.9 ± 20.6-126.9 ± 14.1 kcal/8h, ns). Fasting respiratory exchange ratio increased from pre- to post-PUFA-rich diet only (0.83 ± 0.1-0.86 ± 0.1, p < 0.05). The postprandial change in Fox increased from pre- to post-visit in PUFA-rich diet (0.03 ± 0.1-0.23 ± 0.1 g/15 min for cumulative Fox; p < 0.05), whereas controls showed no change., Conclusions: Adopting a PUFA-rich diet initiates greater fat oxidation after eating occasional high SFA meals compared to a control diet, an effect achieved in 7 days.

Emerging evidence indicates that the fatty acid composition of obesogenic diets influences physiologic outcomes. There are scant data regarding how the content of non-essential fatty acids like monounsaturated fatty acids (MUFA) and saturated fatty acids (SFAs) impact the metabolism of polyunsaturated fatty acids (PUFAs). In this work, we tested the hypothesis that obesogenic diets enriched in oleic acid (OA; 18:1n-9) reduce polyunsaturated fatty acid (PUFA) levels vs an obesogenic diet enriched in SFAs. Adult male mice were fed for eight weeks either (1) a control 16% fat energy (en) diet with 5.7% en OA and 4.4% en SFA, (2) a 50% fat en diet with 33% en OA and 9.9% en SFA, or (3) a 50% en diet with a high SFA diet with 33% en SFA and 9.1% en OA. Dietary levels and intake of linoleic acid (LA; 18:2n-6) and α-linolenic acid (ALA; 18:3n-3) were constant between the experimental groups. Several peripheral organs (liver, heart, kidney, and adipose) were analyzed for lipid composition and oxylipin analysis was performed for liver and adipose. Our data demonstrate that a high OA diet reduced tissue content of LA and ALA (≥30%) in phospholipid and neutral lipid fractions, reduced the content of some LA-derived and ALA-derived oxylipins in liver and adipose, and conversely, elevated hepatic content of PGF 2α . In all tissues examined, except for adipose, levels of arachidonic acid (ARA; 20:4n-6) and docosahexaenoic acid (DHA; 22:6n-3) were either elevated or unaffected by the obesogenic diets. Our data indicate that the non-essential fatty content of obesogenic diets impacts PUFA content in peripheral tissues and influences the levels of bioactive oxylipins., (Published by Elsevier Ltd.)

Background: Substitution of carbohydrates with fat in a diet for type 2 diabetes patients is still debated., Objective: This study aimed to investigate the association between dietary carbohydrate intake and isocaloric substitution with (i) total fat, (ii) saturated fatty acids (SFA), (iii) mono-unsaturated fatty acids (MUFA) and (iv) poly-unsaturated fatty acids (PUFA) with all-cause and cardiovascular (CVD) mortality risk and 5-year weight change in patients with type 2 diabetes., Methods: The study included 6192 patients with type 2 diabetes from 15 cohorts of the European Prospective Investigation into Cancer and Nutrition (EPIC). Dietary intake was assessed at recruitment with country-specific food-frequency questionnaires. Cox and linear regression were used to estimate the associations with (CVD) mortality and weight change, adjusting for confounders and using different methods to adjust for energy intake., Results: After a mean follow-up of 9.2 y ± SD 2.3 y, 791 (13%) participants had died, of which 268 (4%) due to CVD. Substituting 10 g or 5 energy% of carbohydrates by total fat was associated with a higher all-cause mortality risk (HR 1.07 [1.02-1.13]), or SFAs (HR 1.25 [1.11-1.40]) and a lower risk when replaced by MUFAs (HR 0.89 [0.77-1.02]). When carbohydrates were substituted with SFAs (HR 1.22 [1.00-1.49]) or PUFAs (HR 1.29 [1.02-1.63]) CVD mortality risk increased. The 5-year weight was lower when carbohydrates were substituted with total fat or MUFAs. These results were consistent over different energy adjustment methods., Conclusions: In diabetes patients, substitution of carbohydrates with SFAs was associated with a higher (CVD) mortality risk and substitution by total fat was associated with a higher all-cause mortality risk. Substitution of carbohydrates with MUFAs may be associated with lower mortality risk and weight reduction. Instead of promoting replacement of carbohydrates by total fat, dietary guideline should continue focusing on replacement by fat-subtypes; especially SFAs by MUFAs., (Copyright © 2015 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.)

Human studies and some animal work have shown more docosahexaenoic acid (DHA) and arachidonic acid (ARA) was accumulated or converted from precursors in females compared to males. This study explored in-depth the effect of gender on fatty acid composition and polyunsaturated fatty acid metabolism in rats fed one of two well-defined diets containing 10% total fat. One diet contained 15% of linoleic acid (LA) and 3% of α-linolenic acid (ALA) of the total fatty acids (LA+ALA diet), while the other diet contained 15% LA and 0.05% ALA (LA diet). At the age of 20 weeks, all animals were orally administered a single dose of a mixture of deuterium-labeled LA and ALA. Caudal venous blood was then drawn at 0, 2, 4, 8, 12, 24, 48, 96 and 168h. The concentrations of the deuterated precursors and their metabolites in plasma total lipids were quantified by GC/MS negative chemical ionization. Endogenous fatty acids were quantified by GC/FID analysis. When expressed as the percentage of oral dosage, female rats accumulated more precursors and more products, deuterated DHA and deuterated n-6 docosapentaenoic acid ( 2 H 5 -DPAn-6), in plasma than did male rats in both the LA+ALA diet and the LA diet. For the endogenous non-labeled PUFA, greater concentrations of DHA and DPAn-6 were similarly observed in female rats compared to males within each diet. A lower concentration of non-labeled ARA was observed only in female rats fed the LA+ALA diet. In summary, greater endogenous and exogenous DHA and DPAn-6 was observed in female rat plasma and this was independent of dietary ALA status., (Published by Elsevier Ltd.)

Breast milk samples and 24-hour food records were obtained from lactating mothers on day 1 (colostrum), day 14 (transitional milk) and day 42 (mature milk) from Hangzhou (n = 202), Lanzhou (n = 133) and Beijing (n = 142), China. Fatty acid methyl esters were prepared by standard methods, separated and quantified by gas chromatography. We aimed to investigate the fatty acid composition (% of total fatty acid) in human milk of three lactating stages from three regions in China and the relationship with maternal dietary intake during lactation. Present results showed that the fatty acid composition of breast milk varied with lactating period and geographical regions in China. In all the milk samples, the total saturated fatty acid (SFA) remained stable. However, C10:0 and C12:0 increased over the lactation period, total monounsaturated fatty acid (MUFA) significantly increased from colostrum (34.50%) to transitional milk (37.06%), and total polyunsaturated fatty acid (PUFA) showed its highest percentage in colostrum (29.58%). In particular, C22:6n-3 and C22:5n-3 were lowest in mature milk (0.38% and 0.41%, respectively), and C18:3n-3 (1.83%) was lowest in colostrum. There were significant differences among the three regions in total MUFA and PUFA in breast milk. The Hangzhou samples had the lowest C18:1n-9 and highest C22:6n-3. Additionally, C22:6n-3, total PUFA and n-3 PUFA were lowest in the Lanzhou samples. Different dietary habits were largely the drivers behind the different fatty acid profiles among the three regions.

Background: Maternal fat intake during pregnancy in relation to offspring metabolic outcomes has been studied primarily in animal models, yet little is known about the association in humans. The aim of this study was to examine the association of total and subtype of fat consumption in pregnancy with anthropometric measures and biomarkers of adiposity and glucose metabolism in the offspring., Methods: A source population was 965 Danish pregnant women recruited in 1988-1989 with offspring follow-up at 20 years. Information on fat intake was collected in the 30(th) week of gestation, and we subdivided fat according to saturated (SFA), monounsaturated (MUFA), and polyunsaturated (PUFA) fat. Offspring body mass index (BMI) and waist circumference (WC) were recorded at follow-up (n = 670-678), and biomarkers were quantified in a subset (n = 443) of participants. Multivariable linear and log-binomial regression were used to calculate effect estimates and 95% CI for a 1:1%energy substitution of carbohydrates for fat., Results: The mean (standard deviation) BMI was 22.1 (3.3) and 22.8 (2.9) kg/m(2) in female and male offspring, respectively. The median (10th to 90th percentile) of maternal fat intake was 31% of energy [23,39]. We found no overall associations for maternal fat intake with female offspring anthropometry. However, for male offspring higher intake of MUFA during pregnancy was associated with higher insulin levels at 20 years (Q4 vs. Q1: %Δ: 37, 95% CI: 1, 86) accompanied by a non-significant 3.6 (95% CI: -1.1, 8.2) cm increase in WC. High maternal total fat intake (>=35% energy) was also associated with higher BMI (0.9, 95% CI: 0.2, 1.6) and WC (4.0, 95% CI: 1.6, 2.3) among male offspring., Conclusions: A high fat diet during pregnancy may increase adiposity in adult male offspring. We surmise that maternal MUFA intake during this time included both MUFA and trans fat misclassified as MUFA, and that the associations observed may be more reflective of the latter exposure., (Copyright © 2015 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.)

Background: High-fat diets induce intestinal barrier alterations and promote intestinal diseases. Little is known about the effects of long-chain fatty acids (LCFAs) on mucin 2 (MUC2) production by goblet cells, which are crucial for intestinal protection., Objective: We investigated the effects of LCFAs on the differentiation of colonic goblet cells, MUC2 expression, and colonic barrier function., Methods: Upon reaching confluence, human colonic mucus-secreting HT29-MTX cells were stimulated (21 d) with a saturated LCFA (palmitic or stearic acid), a monounsaturated LCFA (oleic acid), or a polyunsaturated LCFA (linoleic, γ-linolenic, α-linolenic, or eicosapentaenoic acid). In addition, rat pups underwent oral administration of oil (palm, rapeseed, or sunflower oil) or water (10 μL/g body weight, postnatal days 10-15). Subsequently, colon goblet cells were studied by Western blotting, reverse transcriptase-quantitative polymerase chain reaction, and immunohistochemistry and colonic transmucosal electrical resistance was measured by using Ussing chambers., Results: In vitro, palmitic acid enhanced MUC2 production (140% of control) and hepatocyte nuclear factor 4α expression, whereas oleic, linoleic, γ-linolenic, α-linolenic, and eicosapentaenoic acids reduced MUC2 expression (at least -50% of control). All unsaturated LCFAs decreased the expression of human atonal homolog 1, a transcription factor controlling goblet cell differentiation (at least -31% vs. control). In vivo, rats fed palm oil had higher palmitic acid concentrations (3-fold) in their colonic contents and increased mucus granule surfaces in their goblet cells (>2-fold) than did all other groups. Palm oil also increased colonic transmucosal electrical resistance (245% of control), yet had no effect on occludin and zonula occludens-1 expression. In contrast, sunflower and rapeseed oils decreased goblet cell number when compared with control (at least -10%) and palm oil (at least -14%) groups., Conclusions: Palm oil in rat pups and palmitic acid in HT29-MTX cells increase the production of MUC2 and strengthen the intestinal barrier. In contrast, unsaturated LCFAs decrease MUC2 expression. These data should be taken into account in the context of preventive or therapeutic nutritional programs., (© 2015 American Society for Nutrition.)

Background: Public health strategies to lower cardiovascular disease (CVD) risk involve reducing dietary saturated fatty acid (SFA) intake to ≤10% of total energy (%TE). However, the optimal type of replacement fat is unclear., Objective: We investigated the substitution of 9.5-9.6%TE dietary SFAs with either monounsaturated fatty acids (MUFAs) or n-6 (ω-6) polyunsaturated fatty acids (PUFAs) on vascular function and other CVD risk factors., Design: In a randomized, controlled, single-blind, parallel-group dietary intervention, 195 men and women aged 21-60 y from the United Kingdom with moderate CVD risk (≥50% above the population mean) followed one of three 16-wk isoenergetic diets (%TE target compositions, total fat:SFA:MUFA:n-6 PUFA) that were rich in SFAs (36:17:11:4, n = 65), MUFAs (36:9:19:4, n = 64), or n-6 PUFAs (36:9:13:10, n = 66). The primary outcome measure was flow-mediated dilatation; secondary outcome measures included fasting serum lipids, microvascular reactivity, arterial stiffness, ambulatory blood pressure, and markers of insulin resistance, inflammation, and endothelial activation., Results: Replacing SFAs with MUFAs or n-6 PUFAs did not affect the percentage of flow-mediated dilatation (primary endpoint) or other measures of vascular reactivity. Of the secondary outcome measures, substitution of SFAs with MUFAs attenuated the increase in night systolic blood pressure (-4.9 mm Hg, P = 0.019) and reduced E-selectin (-7.8%, P = 0.012). Replacement with MUFAs or n-6 PUFAs lowered fasting serum total cholesterol (-8.4% and -9.2%, respectively), low-density lipoprotein cholesterol (-11.3% and -13.6%), and total cholesterol to high-density lipoprotein cholesterol ratio (-5.6% and -8.5%) (P ≤ 0.001). These changes in low-density lipoprotein cholesterol equate to an estimated 17-20% reduction in CVD mortality., Conclusions: Substitution of 9.5-9.6%TE dietary SFAs with either MUFAs or n-6 PUFAs did not significantly affect the percentage of flow-mediated dilatation or other measures of vascular function. However, the beneficial effects on serum lipid biomarkers, blood pressure, and E-selectin offer a potential public health strategy for CVD risk reduction. This trial was registered at www.clinicaltrials.gov as NCT01478958., (© 2015 American Society for Nutrition.)

Background: Nonalcoholic fatty liver disease is positively associated with obesity and cardiovascular disease risk. Apo-10'-lycopenoic acid (APO10LA), a potential oxidation product of apo-10'-lycopenal that is generated endogenously by β-carotene-9',10'-oxygenase (BCO2) cleavage of lycopene, inhibited hepatic steatosis in BCO2-expressing mice., Objective: The present study evaluated lycopene and APO10LA effects on hepatic steatosis in mice without BCO2 expression., Methods: Male and female BCO2-knockout (BCO2-KO) mice were fed a high saturated fat diet (HSFD) with or without APO10LA (10 mg/kg diet) or lycopene (100 mg/kg diet) for 12 wk., Results: Lycopene or APO10LA supplementation reduced hepatic steatosis incidence (78% and 72%, respectively) and severity in BCO2-KO male mice. Female mice did not develop steatosis, had greater hepatic total cholesterol (3.06 vs. 2.31 mg/g tissue) and cholesteryl ester (1.58 vs. 0.86 mg/g tissue), but had lower plasma triglyceride (TG) (229 vs. 282 mg/dL) and cholesterol (97.1 vs. 119 mg/dL) than male mice. APO10LA-mitigated steatosis in males was associated with reduced hepatic total cholesterol (18%) and activated sirtuin 1 signaling, which resulted in reduced fatty acids (FAs) and TG synthesis markers [stearoyl-coenzyme A (CoA) desaturase protein, 71%; acetyl-CoA carboxylase phosphorylation, 79%; AMP-activated protein kinase phosphorylation, 67%], and elevated cholesterol efflux genes (cytochrome P450 family 7A1, 65%; ATP-binding cassette transporter G5/8, 11%). These APO10LA-mediated effects were not mimicked by lycopene supplementation. Intriguingly, steatosis inhibition by lycopene induced peroxisome proliferator-activated receptor (PPAR)α- and PPARγ-related genes in mesenteric adipose tissue (MAT) that increases mitochondrial uncoupling [cell death-inducing DNA fragmentation factor, α subunit-like effector a, 55%; PR domain-containing 16, 47%; uncoupling protein 3 (Ucp3), 55%], FA β-oxidation (PPARα, 53%; very long chain acyl-CoA dehydrogenase, 38%), and uptake (FA transport protein 4, 29%; lipoprotein lipase 43%). Expressions of 10 MAT PPAR-related genes were inversely correlated with steatosis score, suggesting that lycopene reduced steatosis by increasing MAT FA utilization., Conclusions: Our data suggest that lycopene and APO10LA inhibit HSFD-induced steatosis in BCO2-KO male mice through differential mechanisms. Sex disparity of BCO2-KO mice was observed in the outcomes of HSFD-induced liver steatosis and plasma lipids., (© 2015 American Society for Nutrition.)

The effects of saturated fatty acids (SFAs) on cardiovascular disease (CVD) risk are modulated by the nutrients that replace them and their food matrices. Replacement of SFAs with polyunsaturated fatty acids has been associated with reduced CVD risk, although there is heterogeneity in both fatty acid categories. In contrast, replacement of SFAs with carbohydrates, particularly sugar, has been associated with no improvement or even a worsening of CVD risk, at least in part through effects on atherogenic dyslipidemia, a cluster of traits including small, dense low-density lipoprotein particles. The effects of dietary SFAs on insulin sensitivity, inflammation, vascular function, and thrombosis are less clear. There is growing evidence that SFAs in the context of dairy foods, particularly fermented dairy products, have neutral or inverse associations with CVD. Overall dietary patterns emphasizing vegetables, fish, nuts, and whole versus processed grains form the basis of heart-healthy eating and should supersede a focus on macronutrient composition.

Background: Muscle mass, intermuscular adipose tissue, and strength are important indicators of physical function. Dietary fatty acids (FAs) have been associated with muscle parameters such as larger size and higher strength, but large, population-based longitudinal data in older adults who are at risk of functional decline are lacking., Objective: The objective of this study was to investigate associations between plasma phospholipid polyunsaturated fatty acids (PUFAs) and measures of muscle size, intermuscular adipose tissue, and muscle strength cross-sectionally and after 5 y of follow-up., Methods: Data are from the Age, Gene/Environment Susceptibility-Reykjavik Study, a prospective cohort aged 66-96 y at baseline. The analytic sample included 836 participants with cross-sectional measures of muscle parameters and 459 participants with data on change in muscle parameters. PUFAs were assessed at study baseline through use of GC. Muscle parameters were assessed at baseline and after a median of 5.2 y. Muscle area and intermuscular adipose tissue were assessed with computed tomography. Maximal grip strength and knee extension strength were assessed with dynometers. Relative changes in muscle parameters (%) were calculated. Multivariate linear regression was performed to calculate unstandardized regression coefficients and P values for trends across tertiles of FAs are reported., Results: Higher concentrations of total PUFAs were cross-sectionally associated with larger muscle size (P-trend: 0.002) and with greater knee extension strength (P-trend: 0.038). Higher concentrations of arachidonic acid were associated with smaller muscle size (P-trend: 0.015). Greater linoleic acid was associated with less intermuscular adipose tissue (P-trend: 0.004), whereas eicosapentaenoic acid (20:5n-3) was positively associated (P-trend: 0.047). Longitudinal analyses showed positive associations for α-linolenic acid with increased knee extension strength (P-trend: 0.014). No other associations were observed., Conclusions: These data illustrate the complex relation between plasma phospholipid PUFAs and muscle parameters; inconsistent cross-sectional relations with muscle size, intermuscular adipose tissue, and strength, and little evidence of a role in changes in muscle parameters., (© 2015 American Society for Nutrition.)

Objective: Dietary strategies in heart failure (HF) are focused on sodium and fluid restriction to minimize the risk for acute volume overload episodes. However, the importance of dietary factors beyond sodium intake in the prognosis of the disease is uncertain. The purpose of this study was to evaluate the association of macro- and micronutrients intake on 1-y mortality in patients with HF., Methods: A secondary analysis of 203 patients with chronic HF enrolled in a randomized trial of sodium reduction was completed. Patients with a complete 3-d food record at baseline were included in this analysis (N = 118); both control and intervention arms were combined. Three-d mean dietary intake was estimated. Cox multivariable regression analysis was used to evaluate the association between dietary factors and 1-y mortality., Results: Among the 118 included patients, 54% were men, median (25th-75th percentiles) age 66 y (52-75 y), median ejection fraction 45% (30%-60%), and ischemic etiology present in 49% of patients. The association with 1-y mortality was significant for both polyunsaturated fatty acids (PUFA; adjusted hazard ratio [HR], 0.67; 95% confidence interval [CI]. 0.51-0.86 for intake as percentage of daily energy) and saturated fatty acids (SFA; adjusted HR, 1.15; 95% CI, 1.03-1.30 for intake as percentage of daily energy). Median of intake as percentage of daily energy was 5.3% for PUFAs and 8.2% for SFAs., Conclusions: Intake of PUFAs and SFAs was independently associated with 1-y all-cause mortality in patients with chronic HF. Limiting dietary SFA and increasing PUFA intake may be advisable in this population., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Excess ectopic fat storage is linked to type 2 diabetes. The importance of dietary fat composition for ectopic fat storage in humans is unknown. We investigated liver fat accumulation and body composition during overfeeding saturated fatty acids (SFAs) or polyunsaturated fatty acids (PUFAs). LIPOGAIN was a double-blind, parallel-group, randomized trial. Thirty-nine young and normal-weight individuals were overfed muffins high in SFAs (palm oil) or n-6 PUFAs (sunflower oil) for 7 weeks. Liver fat, visceral adipose tissue (VAT), abdominal subcutaneous adipose tissue (SAT), total adipose tissue, pancreatic fat, and lean tissue were assessed by magnetic resonance imaging. Transcriptomics were performed in SAT. Both groups gained similar weight. SFAs, however, markedly increased liver fat compared with PUFAs and caused a twofold larger increase in VAT than PUFAs. Conversely, PUFAs caused a nearly threefold larger increase in lean tissue than SFAs. Increase in liver fat directly correlated with changes in plasma SFAs and inversely with PUFAs. Genes involved in regulating energy dissipation, insulin resistance, body composition, and fat-cell differentiation in SAT were differentially regulated between diets, and associated with increased PUFAs in SAT. In conclusion, overeating SFAs promotes hepatic and visceral fat storage, whereas excess energy from PUFAs may instead promote lean tissue in healthy humans., (© 2014 by the American Diabetes Association.)

We aimed to explore whether maternal dietary counseling to increase the intake of unsaturated fatty acids (FA) is reflected in infant FA status. Serum cholesteryl ester (CE) and triacylglycerol (TAG) FA were analyzed from infants of 45 women randomized to receive dietary counseling from the first trimester of pregnancy and 45 control women. Counseling resulted in a higher intake of polyunsaturated FA and a lower intake of saturated FA. The dietary intake was reflected in cord blood TAGs: the n-6 to n-3 FA ratio was lower [mean difference -0.50 (95%CI -0.95 to -0.06)] and the sum of n-3 FA was higher in the intervention than in the control group [1.46 (0.44 to 2.48)% of total FA]. Reasons for the lack of changes in the cord blood CE fraction and FA fractions at 1-month remain unclear, but may indicate that the changes achieved in the maternal diet through counseling were too modest.

Dietary fat intake in childhood may influence the risk for developing chronic diseases. The objective of the present study was to examine secular trends in the parameters of fat intake between 2000 and 2010 in a sample of German children and adolescents (n 808) participating in the Dortmund Nutritional and Anthropometric Longitudinally Designed (DONALD) Study. Dietary data from 4380 3 d weighed dietary records were analysed using repeated-measures regression to determine time trends in fat quantity, i.e. the intake of total fat, and in fat quality, i.e. the ratios of SFA, MUFA and PUFA. In young children (2-3 years) and in adolescents (13-18 years), total fat intake remained stable over time, but decreased by 0·08 % of total energy (%E) per year in 4-12-year-old children. In 2010, median fat intake was at the upper end of the recommendations. SFA intake decreased slightly in 2-3- and 4-12-year-old children by 0·09 and 0·05 %E per year, respectively. MUFA and PUFA intakes remained stable in all the age groups except in adolescents. Here, PUFA intake decreased initially, but increased between 2005 and 2010. In 2010, only between 3 and 18 % of the respective age groups had an intake of SFA or PUFA within the recommendations. In conclusion, fat quantity and quality did not change substantially between 2000 and 2010. Fat quality, in particular, needs to be improved, since a large percentage of our sample did not meet the recommended intakes for SFA and PUFA.

Background: Paraoxonase 1 (PON1) is a cardioprotective, HDL-associated glycoprotein enzyme with broad substrate specificity. Our previous work found associations between dietary cholesterol and vitamin C with PON1 activity. The goal of this study was to determine the effect of specific dietary fatty acid (DFA) intake on PON1 activity., Methods: 1,548 participants with paraoxonase activity measures completed the Harvard Standardized Food Frequency Questionnaire to determine their daily nutrient intake over the past year. Eight saturated, 3 monounsaturated, and 6 polyunsaturated DFAs were measured by the questionnaire. To reduce the number of observations tested, only specific fatty acids that were not highly correlated (r < 0.8) with other DFAs or that were representative of other DFAs through high correlation within each respective group (saturated, monounsaturated, or polyunsaturated) were retained for analysis. Six specific DFA intakes - myristic acid (14 carbon atoms, no double bonds - 14:0), oleic acid (18:1), gadoleic acid (20:1), α-linolenic acid (18:3), arachidonic acid (20:4), and eicosapentaenoic acid (20:5) - were carried forward to stepwise linear regression, which evaluated the effect of each specific DFA on covariate-adjusted PON1 enzyme activity., Results: Four of the 6 tested DFA intakes - myristic acid (p = 0.038), gadoleic acid (p = 6.68 × 10(-7)), arachidonic acid (p = 0.0007), and eicosapentaenoic acid (p = 0.013) - were independently associated with covariate-adjusted PON1 enzyme activity. Myristic acid, a saturated fat, and gadoleic acid, a monounsaturated fat, were both positively associated with PON1 activity. Both of the tested polyunsaturated fats, arachidonic acid and eicosapentaenoic acid, were negatively associated with PON1 activity., Conclusions: This study presents the largest cohort-based analysis of the relationship between dietary lipids and PON1 enzyme activity. Further research is necessary to elucidate and understand the specific biological mechanisms, whether direct or regulatory, through which DFAs affect PON1 activity.

The nutrient composition of diets can vary from batch to batch because of variation in the nutrient composition of ingredients. The concentration of fat in distillers grains can be highly variable and, coupled with a high dietary inclusion rate, can result in substantial variation in the fat concentration of the total diet. Our hypothesis was that variation in dietary fat concentrations over short periods would have negative effects on production measures of dairy cattle. Twenty-four Holstein cows were used in 8 truncated Latin squares (3 cows × 2 periods). Periods were 16 d long, with a 12-d washout period separating the 2 periods. The 3 treatments were 1) control, 2) moderate variation, and 3) high variation. The control treatment was a consistent diet over the 16 d and contained 5.8% (dry basis) total long-chain fatty acids (LCFA), 23.7% distillers grains, and 1.1% of dry matter as corn oil. The average concentration of LCFA over the 16-d period for the moderate variation and high variation treatments was also 5.9%, but concentrations of LCFA varied over time by the addition or removal of corn oil. The moderate variation treatment had a 4-d phase of 5.4% LCFA, followed by a 4-d phase with 6.4% LCFA to complete the cycle, and then the cycle was repeated. The high variation treatment followed the same cycle pattern, but concentration of LCFA was either 4.8 or 7.0%. Over the 16 d, dry matter intake and milk yield were significantly decreased by the high variation treatment (intake = 21.7, 21.8, and 20.7 kg/d; milk = 36.4, 37.6, and 35.4 kg/d for the control, moderate variation, and high variation treatments). The effect of variation appeared to be cumulative; differences were not significant in the first 8-d cycle but were in the second 8-d cycle. Milk fat concentration was low (2.4%) and was not affected by treatment or cycle × treatment. The concentration of trans-10 C18:1 in milk fat was very high (4.2% of total milk fatty acids) but was not affected by treatment. However, cows on the high variation treatment had higher concentrations of trans-10, cis-12 C18:2 in milk fat (0.036, 0.042, and 0.047% of milk fatty acids for the control, moderate variation, and high variation treatments). Overall, an extreme short-term fluctuation in dietary fat concentration was needed before negative effects were observed., (Copyright © 2013 American Dairy Science Association. Published by Elsevier Inc. All rights reserved.)

Aim: To systematically review data from different countries on population intakes of total fat, saturated fatty acids (SFA) and polyunsaturated fatty acids (PUFA), and to compare these to recommendations from the Food and Agriculture Organization of the United Nations/the World Health Organization (FAO/WHO)., Methods: Data from national dietary surveys or population studies published from 1995 were searched via MEDLINE, Web of Science and websites of national public health institutes., Results: Fatty acid intake data from 40 countries were included. Total fat intake ranged from 11.1 to 46.2 percent of energy intake (% E), SFA from 2.9 to 20.9% E and PUFA from 2.8 to 11.3% E. The mean intakes met the recommendation for total fat (20-35% E), SFA (<10% E) and PUFA (6-11% E) in 25, 11 and 20 countries, respectively. SFA intake correlated with total fat intake (r = 0.76, p < 0.01) but not with PUFA intake (r = 0.03, p = 0.84). Twenty-seven countries provided data on the distribution of fatty acids intake. In 18 of 27 countries, more than 50% of the population had SFA intakes >10% E and in 13 of 27 countries, the majority of the population had PUFA intakes <6% E., Conclusions: In many countries, the fatty acids intake of adults does not meet the levels that are recommended to prevent chronic diseases. The relation between SFA and PUFA intakes shows that lower intakes of SFA in the populations are not accompanied by higher intakes of PUFA, as is recommended for preventing coronary heart disease.

With the substantial economic and social burden of CVD, the need to modify diet and lifestyle factors to reduce risk has become increasingly important. Milk and dairy products, being one of the main contributors to SFA intake in the UK, are a potential target for dietary SFA reduction. Supplementation of the dairy cow's diet with a source of MUFA or PUFA may have beneficial effects on consumers' CVD risk by partially replacing milk SFA, thus reducing entry of SFA into the food chain. A total of nine chronic human intervention studies have used dairy products, modified through bovine feeding, to establish their effect on CVD risk markers. Of these studies, the majority utilised modified butter as their primary test product and used changes in blood cholesterol concentrations as their main risk marker. Of the eight studies that measured blood cholesterol, four reported a significant reduction in total and LDL-cholesterol (LDL-C) following chronic consumption of modified milk and dairy products. Data from one study suggested that a significant reduction in LDL-C could be achieved in both the healthy and hypercholesterolaemic population. Thus, evidence from these studies suggests that consumption of milk and dairy products with modified fatty acid composition, compared with milk and dairy products of typical milk fat composition, may be beneficial to CVD risk in healthy and hypercholesterolaemic individuals. However, current evidence is insufficient and further work is needed to investigate the complex role of milk and cheese in CVD risk and explore the use of novel markers of CVD risk.

Plasma cholesterol concentrations increase with consumption of high saturated fatty acid (SFA) and decrease with high polyunsaturated fatty acid (PUFA) diets, leading to shifts in lipid levels consistent with reduction in heart disease risk. Direct measurements of cholesterol absorption, one of the key regulators of plasma cholesterol levels, have not been performed in humans after consumption of high PUFA diets. Thus, cholesterol absorption and fractional synthesis rates (FSRs) were measured in 16 healthy adults (8 males and 9 females) using a randomized cross-over study with a diet containing high (PUFA/SFA) P/S ratio (2:1) and a low P/S ratio (0.5:1). Cholesterol absorption and fractional cholesterol synthetic rates were measured using stable isotopes after 20 days of dietary intervention. Diet did not affect cholesterol absorption or synthesis. There was a significant decrease in plasma cholesterol concentrations (P < 0.02), specifically LDL-cholesterol (P < 0.02), without a change in HDL-cholesterol or triacylglycerol concentrations. Intraluminal cholesterol solubilization and plasma sterol (cholesterol biosynthetic intermediates and plant sterols) levels were not affected by diet. Thus, consumption of diets with a high P/S ratio reduces plasma total and LDL-cholesterol concentrations independent of shifts in cholesterol absorption or synthesis.

Heterothermic rodents increase self-selection of diets rich in polyunsaturated fatty acids (PUFAs) when exposed to cold, short days, or short-day melatonin profiles, and Djungarian hamsters (Phodopus sungorus) do so in long days in response to cold exposure alone. To determine whether Djungarian hamsters are also capable of selecting a thermal environment in response to dietary lipid composition, continuously normothermic hamsters were fed either a PUFA-rich diet or a diet rich in saturated fatty acids (SFAs) for 6-10 wk and given a choice of thermal environments. As predicted, SFA-fed hamsters were more likely than PUFA-fed hamsters to occupy the single heated corner of their cage ([Formula: see text]) and were most likely to show this diet-related difference in behavior when T(a) fell within the thermal neutral zone. Respirometry revealed no effect of diet on whole-animal or mass-specific resting metabolic rate or on lower critical temperature. The results are more consistent with the homeoviscous adaptation hypothesis, which predicts that organisms should make physiological and/or behavioral adjustments that preserve membrane fluidity within a relatively small range, than with the membrane pacemaker hypothesis, which predicts that high PUFA content in membrane phospholipids should increase basal metabolic rate.

The role for the amount of different dietary fatty acids in regulating expression of adiponectin and metabolism of glucose and lipids has been implicated, but the optimal amount has not been established yet. To address this issue, we fed male Wistar rats with either chow diet or various high-fat diets (HFDs) for 12 weeks. The HFDs contained the same percentage of fat (35% energy from fat) but had different proportions of saturated/monounsaturated/polyunsaturated (S/M/P) (1:1.7:1.2, 1:1:1, 2:1.5:1, 1:2:1, or 1:1:2) fat. Glucose and lipid metabolism and adiponectin expression were subsequently examined. In comparison with chow diet, HFD with any proportion of S/M/P increased energy intake but had no obvious effect on body weight gain. The HFD with the S/M/P proportion at 1:1:1 or 1:1:2 significantly decreased the serum triglyceride level and increased the serum level of high-density lipoprotein cholesterol in comparison with the HFD with the S/M/P proportion at 1:1.7:1.2, 2:1.5:1, or 1:2:1. The HFD containing the highest level of saturated fatty acids (S/M/P proportion at 2:1.5:1) increased levels of total cholesterol, low-density lipoprotein cholesterol, and blood glucose. Levels of serum insulin and the homeostasis model assessment of insulin resistance index were significantly increased by HFD with S/M/P proportions at 1:1.7:1.2, 1:1:1, 2:1.5:1, or 1:2:1 but not by the HFD with the S/M/P proportions at 1:1:2 (containing the highest level of polyunsaturated fatty acids). Levels of adiponectin messenger RNA in subcutaneous and visceral adipose tissues were reduced by the HFD with the S/M/P proportion at 1:1.7:1.2 or 1:1:1 but increased by the HFD with the S/M/P proportion at 1:1:2. These changes in expression of adiponectin were inversely associated with those in levels of triglyceride, insulin, and homeostasis model assessment of insulin resistance. Together, the proportion of different fatty acids in diets plays an important role in expression of adiponectin and metabolism of glucose and lipids. Specifically, the proportion of S/M/P at 1:1:2 can promote expression of adiponectin, improve metabolism of glucose and lipids, and increase insulin sensitivity., (Copyright © 2012 Elsevier Inc. All rights reserved.)

Samples of breast milk were collected at postpartum weeks 1, 2, 4, 6, 8, and 12 from 104 Korean mothers who had delivered infants at less than 34 weeks or weighing less than 1.8 kg to investigate changes in fatty acid (FAs). Full-term breast milk (FBM) collected at the end of first week postpartum from 26 Korean women delivering healthy, term infants was used for comparison. Stability in relative FA composition was maintained during the first 3 months of lactation in preterm breast milk (PBM), and the relative composition of polyunsaturated FAs (PUFA), monounsaturated FAs, and saturated FAs remained constant in PBM. However, the ω6/ω3 ratio was significantly higher as lactation progressed owing to lower ω3 PUFA in PBM. The proportions of docosahexaenoic acid (DHA) and arachidonic acid (AA) in PBM gradually decreased over time, but the DHA/AA ratio was kept constant at 1.13, higher than that of Western countries. At the end of the first week, relative proportions of FAs were similar in PBM and FBM, but absolute concentrations of FA were higher in PBM.

Consumption of high fat diet leads to muscle lipid accumulation which is an important factor involved in induction of insulin resistance. Ceramide is likely to partially inhibit insulin signaling cascade. The aim of this study was to examine the effect of different high fat diets on ceramide metabolism in rat skeletal muscles. The experiments were carried out on rats fed for 5 weeks: (1) a standard chow and (2) high fat diet rich in polyunsaturated fatty acids (PUFA) and (3) diet enriched with saturated fatty acids (SAT). Assays were performed on three types of muscles: slow-twitch oxidative (soleus), fast-twitch oxidative-glycolytic, and fast-twitch glycolytic (red and white section of the gastrocnemius, respectively). The activity of serine palmitoyltransferase (SPT), neutral and acid sphingomyelinase (n- and aSMase), and neutral and alkaline ceramidase (n- and alCDase) was examined. The content of ceramide, sphinganine, sphingosine, and sphingosine-1-phosphate was also measured. The ceramide content did not change in any muscle from PUFA diet group but increased in the SAT diet group by 46% and 52% in the soleus and red section of the gastrocnemius, respectively. Elevated ceramide content in the SAT diet group could be a result of increased SPT activity and simultaneously decreased activity of nCDase. Unchanged ceramide content in the PUFA diet group might be a result of increased activity of SPT and alCDase and simultaneously decreased activity of SMases. We conclude that regulation of muscle ceramide level depends on the diet and type of skeletal muscle., (© 2010 Wiley-Liss, Inc.)

Aim: There have been few studies on the relationships of the dietary polyunsaturated to saturated fatty acid ratio (P/S) to cardiovascular risk factors and metabolic syndrome. We hypothesized that there would be favorable relationships., Methods: Metabolic cardiovascular risk factors from dietary nutrient intake were investigated in 1,004 men and women aged 40-59 years from 4 population samples of Japanese. Multiple linear regression analysis was used to examine the relationship of the dietary P/S ratio to the following risk factors: hemoglobin A1c, blood pressure, serum triglycerides, LDL and total cholesterol, and HDL-cholesterol. Adjusted odds ratio of having metabolic syndrome was also calculated., Results: The dietary P/S ratio was significantly and inversely related to serum total and LDL cholesterol with control for possible confounding variables. We did not find any significant relationship between the P/S ratio and single metabolic risk factors or the prevalence of metabolic syndrome., Conclusions: Managing the P/S ratio is important to control serum LDL-cholesterol; however, increasing the P/S ratio may not improve metabolic risk factors. Other countermeasures, such as weight control, greater physical activity, and smoking cessation should be recommended to prevent and control metabolic syndrome.

Background: High fat diets have long been associated with weight gain and obesity, and the weak satiety response elicited in response to dietary lipids is likely to play a role. Suppression of appetite and food intake has consistently been shown to be diminished with high fat relative to either high protein or carbohydrate meals. There is however some evidence that the satiating capacity of lipids may be modulated when physicochemical properties are altered, but studies investigating the effect of lipid saturation on appetite have generated inconsistent findings. This study investigated the effects of changes in fatty acid saturation on post-ingestive satiety and energy intake., Methods: High-fat (HF) test breakfasts (2.0 MJ) containing 26 g lipid were given to 18 healthy, lean men in a 3 treatment randomised cross-over design, each treatment separated by a washout of at least 3 days. The breakfasts were high in saturated (SFA, 65% of total fat), polyunsaturated (PUFA, 76%) or monounsaturated (MUFA, 76%) fatty acids, and comprised 2 savoury muffins. Participants rated appetite sensations using visual analogue scales (VAS) to assess palatability immediately following the meals, and hunger and fullness prior to the HF breakfast and throughout the day. Energy intake was measured by covert weighing of a lunch meal which was served 3.5 h after the breakfast, and from which the participants ate ad libitum., Results: There was no difference in VAS ratings of pleasantness, visual appearance, smell, taste, aftertaste and overall palatability between the 3 high-fat test breakfasts. However, there was also no differential effect of the 3 treatments on ratings of hunger, fullness, satisfaction or prospective food consumption during the 3.5 h following the breakfast meal and over the full 6 h experiment. Energy and macronutrient intake at lunch also did not differ between treatments (mean, sem; SFA: 5275.9 +/- 286.5 kJ; PUFA: 5227.7 +/- 403.9 kJ; MUFA: 5215.6 +/- 329.5 kJ; P > 0.05). The maximum difference in energy intake between treatments was less than 2%., Conclusions: There was no evidence of a difference in post-ingestion satiety between high fat meals which differed in saturation profile in this group of lean, healthy men.

Background: Dietary polyunsaturated fatty acids (PUFAs) have a variety of beneficial effects, and immune cells play an important role in these effects. The mechanisms of action of PUFAs are still not completely understood, but it is known that PUFAs can influence the expression of a broad set of genes., Objective: The objective was to determine the postprandial effects of intake of different fatty acids on the gene expression profiles of peripheral blood mononuclear cells (PBMCs)., Design: In a single-blind crossover study, 21 healthy male volunteers consumed shakes enriched in PUFAs, monounsaturated fatty acids (MUFAs), or saturated fatty acids (SFAs) in random order. Blood samples were collected before and at several time points after intake. Whole-genome gene expression profiles of PBMCs were examined before and 6 h after intake of the PUFA and SFA shakes. In addition, ex vivo incubation of human PBMCs with different fatty acids was performed., Results: Whole-genome expression analysis showed distinct differences between PUFA and SFA consumption. PUFA intake decreased the expression of genes in liver X receptor signaling, whereas SFA intake increased the expression of these genes. PUFA intake also increased the expression of genes related to cellular stress responses. MUFA intake had an intermediate effect on several genes. Ex vivo experiments showed a direct effect of free fatty acids on PBMC gene expression., Conclusion: This study showed that PBMCs can reveal fatty acid-specific gene expression profiles in young healthy men after the consumption of different fatty acids, as evidenced by the opposite effects of PUFA and SFA intakes on the expression of genes involved in liver X receptor signaling. This trial was registered at www.clinicaltrials.gov as NCT01000194.

Dietary oils such as corn oil, olive oil, and canola oil, which primarily contain triacylglycerol and small quantities of fatty acids, are highly palatable to animals. In a previous study, we examined the short-term (60 s) licking behavior of mice and observed that they exhibited a high licking response to a low concentration of fatty acid (linoleic acid), which is comparable to that observed for pure corn oil. This finding suggests that fatty acids contribute to the palatability of dietary oils. In order to supplement our knowledge of the fundamental features of fatty acid palatability in the oral cavity, we assessed the licking behavior of BALB/c mice to investigate the palatability of various types of long-chain fatty acids. The mice showed high licking responses to 1% unsaturated 16- and 18-carbon fatty acids (palmitoleic acid, 16:1; oleic acid, 18:1; linoleic acid, 18:2; and linolenic acid, 18:3), low licking responses to 16- and 20-carbon fatty acids (palmitic acid, 16:0 and arachidonic acid, 20:4), and no significant response to saturated fatty acids (stearic acid, 18:0 and arachidic acid, 20:0) or fatty acid derivatives (methyl linoleate and linole alcohol). Additionally, there were differences in the palatability of 18-carbon unsaturated fatty acids at very low concentrations. At fatty acid concentrations of 0.04% and 0.0625%, the mice showed significant preference for linoleic acid and linolenic acid, but not oleic acid, when compared with mineral oil. These results suggest that mice show high licking responses to 16- and 18-carbon unsaturated long-chain fatty acids at low concentrations. Further, we suggest that sensitivity to fatty acids is affected by the saturated state of the fatty acid, carbon chain length, and terminal carboxyl group.

Weight regain in subjects with anorexia nervosa is associated with an increase in serum leptin concentrations that is hypothesized to impair full weight restoration. As diets rich in n-3 polyunsaturated fatty acids (PUFA) have been described to lower serum leptin concentrations, we tested the hypothesis that consumption of a hypercaloric diet rich in n-3 PUFA is associated with an attenuated increase in serum leptin and a higher efficiency of body weight gain in subjects with anorexia nervosa. Twenty-five female subjects with anorexia nervosa were enrolled into this controlled dietary intervention study. Four subjects discontinued therapy or participation in the study prematurely, and six were excluded. 15 subjects completed the study. Subjects consumed hypercaloric diets rich in either saturated fatty acids (SFA, n = 8) or n-3 PUFA (n = 7) for 5 weeks. Primary endpoints were the change in serum leptin concentrations and body weight gain relative to energy consumed. Serum leptin concentrations increased distinctly throughout the study (P < .001), and to a similar extend in both groups [+2.9 (SD 2.4) vs. +2.8 (SD 3.4) ng/mL in the SFA- and n-3 PUFA group, respectively; P = .487]. The efficiency of body weight gain also did not differ significantly between groups, with a body weight gain of 63.1 (SD 12.4) vs. 79.2 (SD 26.0) g per 4.2 MJ (1000 kcal) consumed in the SFA- and n-3 PUFA group, respectively (P = .132). Hypercaloric diets rich in either SFA or n-3 PUFA do not differ in their effects on serum leptin concentrations and the efficiency of body weight gain in female subjects with anorexia nervosa.

The aim of this study was to investigate whether the toxicity of saturated and polyunsaturated fatty acids (PUFA) on RINm5F cells is related to the phosphorylation state of Akt, ERK and PKC delta. The regulation of these kinases was compared in three experimental designs: (a) 4h-exposure, (b) 4h-exposure and a subsequent withdrawn of the FA for a 20 h period and (c) 24h-exposure. Saturated and PUFA were toxic to RINm5F cells even at low concentrations. Also, evidence is provided for a late (i.e. the effect only appeared hours after the treatment) and a persistent regulation (i.e. maintenance of the effect for several hours) of Akt, ERK and PKC delta phosphorylation by the FA. Late activation of PKC delta seems important for palmitate cytotoxicity. Persistent activation of the survival proteins Akt and ERK by stearate, oleate and arachidonate might play an important role to prevent the toxic effect of posterior PKC delta activation. The results shown may explain why a short-period exposure to FA is not enough to induce cytotoxicity in pancreatic beta-cells, since survival pathways are activated. Besides, when this activation is persistent, it may overcome a posterior induction of death pathways.

Optimal replacement macronutrient/s for dietary saturated fat to reduce cardiovascular disease risk remains controversial. Chickpeas are rich in dietary fiber and polyunsaturated fatty acids. This exploratory study, conducted from September 2004 to May 2005, assessed the effect of incorporating chickpeas in the ad libitum diet of 45 free-living adults. Participants consumed a minimum of 728 g of canned, drained chickpeas per week (the amount in four 300-g cans) as part of their habitual diet for 12 weeks (chickpea phase), followed by 4 weeks of habitual diet without chickpeas (usual phase). In the chickpea phase, mean dietary fiber intake was 6.77 g/day more and mean polyunsaturated fatty acid consumption (as a percentage of total fat) was 2.66% more (both P<0.001), causing the polyunsaturated to saturated fatty acids ratio to change from 0.39 to 0.47 (P=0.045). Serum total cholesterol and low-density lipoprotein cholesterol were 7.7 mg/dL (0.20 mmol/L) and 7.3 mg/dL (0.19 mmol/L) less, respectively, after the chickpea phase (P

Ruminant fat is rich in SFA, partly due to the biohydrogenation of dietary PUFA to SFA in the rumen. This process can be inhibited by the dietary inclusion of fish oil. The only bacteria isolated from the rumen capable of converting PUFA to SFA are closely related to Clostridium proteoclasticum. The aim of this study was to investigate if a correlation could be found in vivo between dietary fish oil inclusions and the composition of the ruminal bacterial community and specifically of C. proteoclasticum. Six Hereford x Friesian steers, prepared with ruminal and duodenal cannulae, received grass silage plus 1 of 3 concentrates resulting in total dietary fish oil contents of 0, 1, or 3% of dry matter. A dual flow marker technique was employed to estimate the relative flow of fatty acids. Steers fed the 3% fish oil diet had 100% increases in trans 18:1 flow, whereas 18:0 flow declined to 39% of steers fed the control diet. 16S ribosomal RNA-based denaturing gradient gel electrophoresis profiles obtained from ruminal digesta showed major changes in the bacterial community within steers fed the 3% fish oil diet. Quantitative PCR indicated only a weak relation between numbers of C. proteoclasticum and 18:0 flow between treatments and in individual steers (P < 0.05, but the percentage variance accounted for only 22.8) and did not provide unambiguous evidence that numbers of C. proteoclasticum in the rumen dictate the ratios of SFA:PUFA available for absorption by the animal. Understanding which microbes biohydrogenate PUFA in the rumen is key to developing novel strategies to improve the quality of ruminant products.

Objective: Little is known about the effects of alterations in fatty acid classes on adiponectin, a hormone secreted by the adipocyte known to be important in the development of diabetes and cardiovascular disease (CVD). Any factor, including diet, that may positively influence adiponectin gene expression or increase circulating levels might be useful for improving such metabolic abnormalities. We investigated the effects of alterations in dietary fatty acid saturation on fasting serum adiponectin and associated peptides., Methods and Procedures: Double-blind, randomized, crossover, 2 x 3-week residential intervention trial where 18 mildly hyperlipidemic adult men were provided with a high saturated:unsaturated fat (SFA:USFA) and lower SFA:USFA treatment separated by an uncontrolled 4-week washout. Only fatty acid profile was altered between treatments. Fasting blood samples were collected on days 0, 1, 7, 14, 21, 22 of each intervention period for the measurement of adiponectin, tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), high-sensitivity C-reactive protein (hsC-RP), leptin, and ghrelin., Results: Body weight was kept constant (+/-1 kg) throughout each treatment. There was no detectable difference in fasting adiponectin at baseline (mean day 0 + day 1) between the treatment groups (mean +/- s.d.; high(SFA:USFA) = 7.0 +/- 1.7 vs. low(SFA:USFA) = 6.7 +/- 1.4 microg/ml, P > 0.05). There were neither significant between-treatment effects of fatty acid saturation (diet x time, P > 0.05) on serum adiponectin nor any significant between-treatment effects on serum TNF-alpha, IL-6, hsC-RP, leptin, or ghrelin (P > 0.05)., Discussion: Fasting serum adiponectin was not detectably affected by alterations in dietary fatty acid profile in mildly hyperlipidemic men. There was no evidence that an increase in SFA content of the diet significantly worsened fasting serum adiponectin over a 3-week intervention period.