Diets varying in SFA and MUFA content can impact glycaemic control; however, whether underlying differences in genetic make-up can influence blood glucose responses to these dietary fatty acids is unknown. We examined the impact of dietary oils varying in SFA/MUFA content on changes in blood glucose levels (primary outcome) and whether these changes were modified by variants in the stearoyl-CoA desaturase (SCD) gene (secondary outcome). Obese men and women participating in the randomised, crossover, isoenergetic, controlled-feeding Canola Oil Multicenter Intervention Trial II consumed three dietary oils for 6 weeks, with washout periods of ˜6 weeks between each treatment. Diets studied included a high SFA/low MUFA Control oil (36·6 % SFA/28·2 % MUFA), a conventional canola oil (6·2 % SFA/63·1 % MUFA) and a high-oleic acid canola oil (5·8 % SFA/74·7 % MUFA). No differences in fasting blood glucose were observed following the consumption of the dietary oils. However, when stratified by SCD genotypes, significant SNP-by-treatment interactions on blood glucose response were found with additive models for rs1502593 (P = 0·01), rs3071 (P = 0·02) and rs522951 (P = 0·03). The interaction for rs3071 remained significant (P = 0·005) when analysed with a recessive model, where individuals carrying the CC genotype showed an increase (0·14 (sem 0·09) mmol/l) in blood glucose levels with the Control oil diet, but reductions in blood glucose with both MUFA oil diets. Individuals carrying the AA and AC genotypes experienced reductions in blood glucose in response to all three oils. These findings identify a potential new target for personalised nutrition approaches aimed at improving glycaemic control.

The long-term cholesterol-lowering effect of replacing intake of SFA with PUFA is well established, but has not been fully explained mechanistically. We examined the postprandial response of meals with different fat quality on expression of lipid genes in peripheral blood mononuclear cells (PBMC) in subjects with and without familial hypercholesterolaemia (FH). Thirteen subjects with FH (who had discontinued lipid-lowering treatment ≥4 weeks prior to both test days) and fourteen normolipidaemic controls were included in a randomised controlled double-blind crossover study with two meals, each with 60 g of fat either mainly SFA (about 40% energy) or n-6 PUFA (about 40% energy). PBMC were isolated in fasting, and 4 and 6 h postprandial blood samples. Expression of thirty-three lipid genes was analysed by reverse transcription quantitative PCR. A linear mixed model was used to assess postprandial effects between meals and groups. There was a significant interaction between meal and group for MSR1 (P = 0·03), where intake of SFA compared with n-6 PUFA induced a larger reduction in gene expression in controls only (P = 0·01). Intake of SFA compared with n-6 PUFA induced larger reductions in gene expression levels of LDLR and FADS1/2, smaller increases of INSIG1 and FASN, and larger increases of ABCA1 and ABCG1 (P = 0·01 for all, no group interaction). Intake of SFA compared with n-6 PUFA induced changes in gene expression of cholesterol influx and efflux mediators in PBMC including lower LDLR and higher ABCA1/G1, potentially explaining the long-term cholesterol-raising effect of a high SFA intake.

Subcutaneous fat thickness and fatty acid composition (FAC) play an important role on seasoning loss and organoleptic characteristics of seasoned hams. Dry-cured ham industry prefers meats with low contents of polyunsaturated fatty acids (PUFA) because these negatively affect fat firmness and ham quality, whereas consumers require higher contents in those fatty acids (FA) for their positive effect on human health. A population of 950 Italian Large White pigs from the Italian National Sib Test Selection Programme was investigated with the aim to estimate heritabilities, genetic and phenotypic correlations of backfat FAC, Semimembranosus muscle intramuscular fat (IMF) content and other carcass traits. The pigs were reared in controlled environmental condition at the same central testing station and were slaughtered at reaching 150 kg live weight. Backfat samples were collected to analyze FAC by gas chromatography. Carcass traits showed heritability levels from 0.087 for estimated carcass lean percentage to 0.361 for hot carcass weight. Heritability values of FA classes were low-to-moderate, all in the range 0.245 for n-3 PUFA to 0.264 for monounsaturated FA (MUFA). Polyunsaturated fatty acids showed a significant genetic correlation with loin thickness (0.128), backfat thickness (−0.124 for backfat measured by Fat-O-Meat’er and −0.175 for backfat measured by calibre) and IMF (−0.102). Obviously, C18:2(n-6) shows similar genetic correlations with the same traits (0.211 with loin thickness, −0.206 with backfat measured by Fat-O-Meat’er, −0.291 with backfat measured by calibre and −0.171 with IMF). Monounsaturated FA, except with the backfat measured by calibre (0.068; P<0.01), do not show genetic correlations with carcass characteristics, whereas a negative genetic correlation was found between MUFA and saturated FA (SFA; −0.339; P<0.001). These results suggest that MUFA/SFA ratio could be increased without interfering with carcass traits. The level of genetic correlations between FA and carcass traits should be taken into account in dealing with the development of selection schemes addressed to modify carcass composition and/or backfat FAC.

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.

As part of a feasibility study to prevent gestational diabetes mellitus (GDM), we evaluated the effect of an intensive dietary therapy on quality of diet, weight gain and birth weight in women at high risk of GDM. Women with risk factors for GDM (n 54) were randomly assigned from April 2005 to May 2006 to a lifestyle intervention group (n 27) including dietary advice six times during pregnancy or to a close follow-up group (n 27) in a community-based setting in Finland. Dietary intake was recorded three times during pregnancy using 4 d food records. The main outcome was the incidence of GDM. The secondary outcomes were the changes in nutrient intake, weight gain and birth weight. Overall, seventeen (65 %) women in the intervention group and eighteen (69 %) women in the close follow-up group returned all three food records. PUFA intake increased (P = 0·008) during pregnancy in the intervention as compared to the close follow-up group. There were no clear differences in the changes of saturated fat or fibre intake between the groups. Intensive dietary education resulted in a somewhat lower weight gain during pregnancy (P = 0·062) and higher birth weights of the infants (P = 0·047) without an effect on macrosomia as compared to the close follow-up group. Individualised counselling by a clinical nutritionist as part of a lifestyle intervention improved the quality of dietary fat intake in pregnant women at high risk of GDM.

The aim of the present study was to examine the effect of a single high-fat meal with different fat quality on circulating inflammatory markers and gene expression in peripheral blood mononuclear cells (PBMC) to elucidate the role of fat quality on postprandial inflammation. A postprandial study with fourteen healthy females consuming three test meals with different fat quality was performed. Test days were separated by 2 weeks. Fasting and postprandial blood samples at 3 and 6 h after intake were analysed. The test meal consisted of three cakes enriched with coconut fat (43 % energy as saturated fat and 1 % energy as α-linolenic acid (ALA)), linseed oil (14 % energy as ALA and 30 % energy as saturated fat) and cod liver oil (5 % energy as EPA and DHA and 5 % energy as ALA in addition to 31 % energy as saturated fat). In addition, ex vivo PBMC experiments were performed in eight healthy subjects investigating the effects of EPA and ALA on release and gene expression of inflammatory markers. The IL-8 mRNA level was significantly increased after intake of the cod liver oil cake at 6 h compared with fasting level, which was significantly different from the effect observed after the intake of linseed cake. In contrast, no effect was seen on circulating level of IL-8. In addition, ALA and EPA were shown to elicit different effects on the release and mRNA expression levels of inflammatory markers in PBMC cultured ex vivo, with EPA having the most prominent pro-inflammatory potential.

Recent evidence shows that specific fatty acids affect cell metabolism, modifying the balance between fatty acid oxidation and lipogenesis. These effects may have important implications in addressing the present epidemic of nutrition-related chronic disease. Intake of dietary saturated and n-6 PUFA have increased while n-3 fatty acid intake has decreased. Obesity, type 2 diabetes and insulin resistance are highly prevalent, and both are strongly related to disorders of lipid metabolism characterized by an increased plasma and intracellular fatty acid availability. Thus, it has been hypothesized that change in the quality of dietary fat supply is able to modify the degree of insulin sensitivity. Animal studies provide support for this notion. However, there is limited human data either from normal or diabetic subjects. This review aims to analyse human studies that address this question. To this purpose, the experimental design, dietary compliance, insulin-sensitivity method used and confounding variables are discussed in order to identify the role of dietary fat quality as a risk factor for insulin resistance. Most studies (twelve of fifteen) found no effect relating to fat quality on insulin sensitivity. However, multiple study design flaws limit the validity of this conclusion. In contrast, one of the better designed studies found that consumption of a high-saturated-fat diet decreased insulin sensitivity in comparison to a high-monounsaturated-fat diet. We conclude that the role of dietary fat quality on insulin sensitivity in human subjects should be further studied, using experimental designs that address the limitations of existing data sets.