Effect of altered dietary n-3 fatty acid intake upon plasma lipid fatty acid composition, conversion of [C-13]alpha-linolenic acid to longer-chain fatty acids and partitioning towards beta-oxidation in older men

The effect of increased dietary intakes of alpha-linolenic acid (ALNA) or eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) for 2 months upon plasma lipid composition and capacity for conversion of ALNA to longer-chain metabolites was investigated in healthy men (52 (SD 12) years). After a 4-week baseline period when the subjects substituted a control spread, a test meal containing [U-C-13]ALNA (700 mg) was consumed to measure conversion to EPA, docosapentaenoic acid (DPA) and DHA over 48 h. Subjects were then randomised to one of three groups for 8 weeks before repeating the tracer study: (1) continued on same intake (control, n 5); (2) increased ALNA intake (10 g/d, n 4); (3) increased EPA+DHA intake (1.5 g/d, n 5). At baseline, apparent fractional conversion of labelled ALNA was: EPA 2.80, DPA 1.20 and DRA 0.04%. After 8 weeks on the control diet, plasma lipid composition and [C-13]ALNA conversion remained unchanged compared with baseline. The high-ALNA diet resulted in raised plasma triacylglycerol-EPA and -DPA concentrations and phosphatidylcholine-EPA concentration, whilst [C-13]ALNA conversion was similar to baseline. The high-(EPA+DHA) diet raised plasma phosphatidylcholine-EPA and -DHA concentrations, decreased [C-13]ALNA conversion to EPA (2-fold) and DPA (4-fold), whilst [C-13]ALNA conversion to DHA was unchanged. The dietary interventions did not alter partitioning of ALNA towards beta-oxidation. The present results indicate ALNA conversion was down-regulated by increased product (EPA+DHA) availability, but was not up-regulated by increased substrate (ALNA) consumption. This suggests regulation of ALNA conversion may limit the influence of variations in dietary n-3 fatty acid intake on plasma lipid compositions.

Increased n-6 polyunsaturated fatty acids do not attenuate the effects of long-chain n-3 polyunsaturated fatty acids on insulin sensitivity or triacylglycerol reduction in Indian Asians

Background: Indian Asians in Western countries have a higher rate of coronary artery disease than do the indigenous white populations, and this higher rate may be influenced by a dietary imbalance of n-6 and n-3 polyunsaturated fatty acids (PUFAs). Objective: The objective of the study was to test the hypothesis that a high background dietary intake of n-6 PUFA attenuates the effects of fish-oil supplementation on insulin sensitivity and associated blood lipids of the metabolic syndrome. Design: Twenty-nine Indian Asian men were recruited to participate in a 12-wk dietary intervention trial. Volunteers were randomly assigned to receive either a moderate or a high n-6 PUFA diet featuring modified oils and spreads over a 6-wk period. After this 6-wk period, both groups were supplemented with 4.0 g fish oil/d (2.5 g eicosapentaenoic acid + docosahexaenoic acid) for an additional 6 wk in combination with the dietary treatment. Volunteers participated in a postprandial study and an insulin sensitivity test after the 6-wk dietary intervention and again after the fish-oil supplementation period. Results: There was no significant time X treatment interaction for blood lipids or insulin action after dietary intervention with the moderate or high n-6 PUFA diets in combination with fish oil. After the 6-wk period of fish oil supplementation, fasting and postprandial plasma triacylglycerol concentrations decreased significantly. Conclusion: The background dietary n-6 PUFA concentration did not modulate the effect of fish-oil supplementation on blood lipids or measures of insulin sensitivity in this ethnic group.

Kinetic modeling of the generation of 2-and 3-methylbutanal in a heated extract of beef liver

Quantitative control of aroma generation during the Maillard reaction presents great scientific and industrial interest. Although there have been many studies conducted in simplified model systems, the results are difficult to apply to complex food systems, where the presence of other components can have a significant impact. In this work, an aqueous extract of defatted beef liver was chosen as a simplified food matrix for studying the kinetics of the Mallard reaction. Aliquots of the extract were heated under different time and temperature conditions and analyzed for sugars, amino acids, and methylbutanals, which are important Maillard-derived aroma compounds formed in cooked meat. Multiresponse kinetic modeling, based on a simplified mechanistic pathway, gave a good fit with the experimental data, but only when additional steps were introduced to take into account the interactions of glucose and glucose-derived intermediates with protein and other amino compounds. This emphasizes the significant role of the food matrix in controlling the Maillard reaction.

Interpolymer complexes of hydroxy-propylmethylcellulose with polycarboxylic acids in aqueous solutions

The interactions between hydroxypropylmethylcellulose (HPMC) and poly(acrylic acid) (PAA) as well as poly(methacrylic acid) (PMMA) resulting in formation of hydrophobic interpolymer complexes (IPC) via hydrogen bonding have been studied in aqueous solutions in acidic medium. The formation of IPC of two different compositions (2:1 and 4:1) has been detected for complexes of PAA and HPMC. The critical pH values for complexation of HPMC with PAA and PMAA were determined by the turbidimetric method. It was found that PAA shows the lower complexation ability compared to PMAA due to the more hydrophobic nature of the latter polyacid. The temperature-induced phase separation in HPMC-PAA solution mixtures depends greatly on the components ratio and PAA molecular weight. The complexation ability of hydroxypropylmethylcellulose with respect to poly(acrylic acid) was found to be similar to the complexation ability of methylcellulose, lower than that of hydroxypropylcellulose and higher than that of hydroxyethylcellulose. (c) 2006 Society of Chemical Industry.

Dual role of the beta(2)-adrenergic receptor C terminus for the binding of beta-arrestin and receptor internalization

Homologous desensitization of beta(2)-adrenergic and other G-protein-coupled receptors is a two-step process. After phosphorylation of agonist-occupied receptors by G-protein-coupled receptor kinases, they bind beta-arrestins, which triggers desensitization and internalization of the receptors. Because it is not known which regions of the receptor are recognized by beta-arrestins, we have investigated beta-arrestin interaction and internalization of a set of mutants of the human beta(2)-adrenergic receptor. Mutation of the four serine/threonine residues between residues 355 and 364 led to the loss of agonist-induced receptor-beta-arrestin2 interaction as revealed by fluorescence resonance energy transfer (FRET), translocation of beta-arrestin2 to the plasma membrane, and receptor internalization. Mutation of all seven serine/threonine residues distal to residue 381 did not affect agonist-induced receptor internalization and beta-arrestin2 translocation. A beta(2)-adrenergic receptor truncated distal to residue 381 interacted normally with beta-arrestin2, whereas its ability to internalize in an agonist-dependent manner was compromised. A similar impairment of internalization was observed when only the last eight residues of the C terminus were deleted. Our experiments show that the C terminus distal to residue 381 does not affect the initial interaction between receptor and beta-arrestin, but its last eight amino acids facilitate receptor internalization in concert with beta-arrestin2.

Buffering of recovery from acidification by organic acids

In the United Kingdom, as in other regions of Europe and North America, recent decreases in surface water sulphate concentrations, due to reduced sulphur emissions, have coincided with marked increases in dissolved organic carbon (DOC) concentrations. Since many of the compounds comprising DOC are acidic, the resulting increases in organic acidity may have the potential to offset the benefits of a decrease in mineral (sulphate) acidity. To test this, we used a triprotic model of organic acid dissociation to estimate the proportional organic acid buffering of reduced mineral acidity as measured in the 22 lakes and streams monitored by the UK Acid Waters Monitoring Network. For an average non-marine sulphate decrease of 30 μeq l− 1 over 15 years from 1988–2003, we estimate that around 28% was counterbalanced by rising strong organic acids, 20% by rising alkalinity (partly attributable to an increase in weak organic acids), 11% by falling inorganic aluminium and 41% by falling non-marine base cations. The situation is complicated by a concurrent decrease in marine ion concentrations, and the impact this may have had on both DOC and acidity, but results clearly demonstrate that organic acid increases have substantially limited the amount of recovery from acidification (in terms of rising alkalinity and falling aluminium) that have resulted from reducing sulphur emissions. The consistency and magnitude of sulphate and organic acid changes are consistent with a causal link between the two, possibly due to the effects of changing acidity, ionic strength and aluminium concentrations on organic matter solubility. If this is the case, then organic acids can be considered effective but partial buffers to acidity change in organic soils, and this mechanism needs to be considered in assessing and modelling recovery from acidification, and in defining realistic reference conditions. However, large spatial variations in the relative magnitude of organic acid and sulphate changes, notably for low-deposition sites in northwestern areas where organic acid increases apparently exceed non-marine sulphate decreases, suggest that additional factors, such as changes in sea-salt deposition and climatic factors, may be required to explain the full magnitude of DOC increases in UK surface waters.

Leptin receptor polymorphisms interact with polyunsaturated fatty acids to augment risk of insulin resistance and metabolic syndrome in adults.

The leptin receptor (LEPR) is associated with insulin resistance, a key feature of metabolic syndrome (MetS). Gene-fatty acid interactions may affect MetS risk. The objective was to investigate the relationship among LEPR polymorphisms, insulin resistance, and MetS risk and whether plasma fatty acids, a biomarker of dietary fatty acids, modulate this. LEPR polymorphisms (rs10493380, rs1137100, rs1137101, rs12067936, rs1805096, rs2025805, rs3790419, rs3790433, rs6673324, and rs8179183), biochemical measurements, and plasma fatty acid profiles were determined in the LIPGENE-SU.VI.MAX study of MetS cases and matched controls (n = 1754). LEPR rs3790433 GG homozygotes had increased MetS risk compared with the minor A allele carriers [odds ratio (OR) = 1.65; 95% CI: 1.05–2.57; P = 0.028], which may be accounted for by their increased risk of elevated insulin concentrations (OR 2.40; 95% CI: 1.28–4.50; P = 0.006) and insulin resistance (OR = 2.15; 95% CI: 1.18–3.90; P = 0.012). Low (less than median) plasma (n-3) and high (n-6) PUFA status exacerbated the genetic risk conferred by GG homozygosity to hyperinsulinemia (OR 2.92–2.94) and insulin resistance (OR 3.40–3.47). Interestingly, these associations were abolished against a high (n-3) or low (n-6) PUFA background. Importantly, we replicated some of these findings in an independent cohort. Homozygosity for the LEPR rs3790433 G allele was associated with insulin resistance, which may predispose to increased MetS risk. Novel gene-nutrient interactions between LEPR rs3790433 and PUFA suggest that these genetic influences were more evident in individuals with low plasma (n-3) or high plasma (n-6) PUFA.

NOS3 gene polymorphisms are associated with risk markers of cardiovascular disease, and interact with omega-3 polyunsaturated fatty acids

Objective Omega-3 polyunsaturated fatty acids (n-3 PUFA) may protect against the development of cardiovascular disease (CVD). Genotype at key genes such as nitric oxide synthase (NOS3) may determine responsiveness to fatty acids. Gene–nutrient interactions may be important in modulating the development of CVD, particularly in high-risk individuals with the metabolic syndrome (MetS). Methods Biomarkers of CVD risk, plasma fatty acid composition, and NOS3 single nucleotide polymorphism (SNP) genotype (rs11771443, rs1800783, rs1800779, rs1799983, rs3918227, and rs743507) were determined in 450 individuals with the MetS from the LIPGENE dietary intervention cohort. The effect of dietary fat modification for 12 weeks on metabolic indices of the MetS was determined to understand potential NOS3 gene–nutrient interactions. Results Several markers of inflammation and dyslipidaemia were significantly different between the genotype groups. A significant gene–nutrient interaction was observed between the NOS3 rs1799983 SNP and plasma n-3 PUFA status on plasma triacylglycerol (TAG) concentrations. Minor allele carriers (AC + AA) showed an inverse association with significantly higher plasma TAG concentrations in those with low plasma n-3 PUFA status and vice versa but the major allele homozygotes (CC) did not. Following n-3 PUFA supplementation, plasma TAG concentrations of minor allele carriers of rs1799983 were considerably more responsive to changes in plasma n-3 PUFA, than major allele homozygotes. Conclusions Carriers of the minor allele at rs1799983 in NOS3 have plasma TAG concentrations which are more responsive to n-3 PUFA. This suggests that these individuals might show greater beneficial effects of n-3 PUFA consumption to reduce plasma TAG concentrations.

The role of monounsaturated fatty acids in the mitigation of insulin resistance

With the rising rate of obesity, there is considerable interest in dietary strategies to reduce insulin resistance, a major characteristic of the metabolic syndrome and type 2 diabetes. Diets rich in monounsaturated fatty acids (MUFA) have been suggested as an alternative to low-fat, high-carbohydrate diets to improve glycemic control. However, inconsistent effects have been observed with MUFA-rich diets in both healthy and insulin-resistant individuals. In studies that have reported favorable effects on insulin sensitivity, Mediterranean-style diets have been used that are rich not only in MUFA but also whole-grain foods, fiber, and carbohydrates with a low glycemic index. There is a need for intervention studies to examine the true impact of MUFA-rich oils on glycemic control in both Mediterranean and non-Mediterranean populations. In addition, the metabolic and genotypic status of the participants may also play a role in the inter-individual variability in insulin sensitivity in response to MUFA-rich diets.

Comparison of algal and fish sources on the oxidative stability of poultry meat and its enrichment with omega-3 polyunsaturated fatty acids

Human consumption of long-chain n-3 polyunsaturated fatty acids (LC n-3 PUFA) is below recommendations, and enriching chicken meat (by incorporating LC n-3 PUFA into broiler diets) is a viable means of increasing consumption. Fish oil is the most common LC n-3 PUFA supplement used but is unsustainable and reduces the oxidative stability of the meat. The objective of this experiment was to compare fresh fish oil (FFO) with fish oil encapsulated (EFO) in a gelatin matrix (to maintain its oxidative stability) and algal biomass at a low (LAG, 11), medium (MAG, 22), or high (HAG, 33 g/kg of diet) level of inclusion. The C22:6n-3 contents of the FFO, EFO, and MAG diets were equal. A control (CON) diet using blended vegetable oil was also made. As-hatched 1-d-old Ross 308 broilers (144) were reared (21 d) on a common starter diet then allocated to treatment pens (4 pens per treatment, 6 birds per pen) and fed treatment diets for 21 d before being slaughtered. Breast and leg meat was analyzed (per pen) for fatty acids, and cooked samples (2 pens per treatment) were analyzed for volatile aldehydes. Concentrations (mg/100 g of meat) of C20:5n-3, C22:5n-3, and C22:6n-3 were (respectively) CON: 4, 15, 24; FFO: 31, 46, 129; EFO: 18, 27, 122; LAG: 9, 19, 111; MAG: 6, 16, 147; and HAG: 9, 14, 187 (SEM: 2.4, 3.6, 13.1) in breast meat and CON: 4, 12, 9; FFO: 58, 56, 132; EFO: 63, 49, 153; LAG: 13, 14, 101; MAG: 11, 15, 102; HAG: 37, 37, 203 (SEM: 7.8, 6.7, 14.4) in leg meat. Cooked EFO and HAG leg meat was more oxidized (5.2 mg of hexanal/kg of meat) than the other meats (mean 2.2 mg/kg, SEM 0.63). It is concluded that algal biomass is as effective as fish oil at enriching broiler diets with C22:6 LC n-3 PUFA, and at equal C22:6n-3 contents, there is no significant difference between these 2 supplements on the oxidative stability of the meat that is produced.

Substitution of dietary monounsaturated fatty acids for saturated fatty acids in a free-living population: a feasibility study

The fatty acid composition of the diet of seven free-living subjects (five men and two women) aged 41–56 years was altered for 1 month. The aim was to increase the intake of monounsaturated fatty acids (MUFAs) from subjects current habitual levels of 12% dietary energy to a target intake of 18% dietary energy, and to decrease saturated fatty acid (SFA) from habitual levels of 16% dietary energy to target levels of 10% dietary energy. The change in fatty acid intake was achieved by supplying volunteers with foods prepared using MUFA-containing spreads or olive oil (ready meals, sweet biscuits and cakes) and also by supplying spreads, cooking oil and MUFA-enriched milk for domestic use. Body weight and plasma total cholesterol measurements were made at baseline and at 2 and 4 weeks on the diet as an aid to maintaining subject compliance. MUFA consumption was significantly increased from 12% dietary energy to 16% dietary energy (P<0.01), and SFA intake was reduced from 16% dietary energy to 6% dietary energy (P<0.01) during the 4-week intervention. The diet failed to achieve the target increase in MUFA but exceeded the target reduction in SFA. This was due to the fact that subjects reduced their total fat intake from a mean habitual level of 38% dietary energy to a mean level of 30% dietary energy. During the dietary period, mean plasma cholesterol levels were lower at 2 weeks (P<0.01) and at 4 weeks (P<0.01) than the baseline, with a mean reduction of 20% over the dietary period. This study demonstrates the difficulty of achieving increased MUFA intakes (by SFA substitution) in free-living populations when only a limited range of fatty-acid modified food products are provided to volunteers.

Pretranslational regulation of the expression of the lipoprotein lipase (EC 3.1, l.34) gene by dietary fatty acids in the rat

Although there have been a number of studies of effects of diet and hormones on lipoprotein lipase (EC 3.1.1.34; LPL) activity and levels of LPL mRNA (Raynolds et al. 1990), there have been no studies which have investigated effects of different dietary fatty acids on LPL gene expression. In the present study male Wistar Albino rats were pair-fed diets containing 50 g fat/kg of different fatty acid composition for 2 weeks. The diets fed were (1) a mixed oil (450 g saturated fatty acids, 420 g monounsaturated fatty acids, 130 g polyunsaturated fatty acids/kg; n 8), (2) maize oil (n 8), or (3) fish oil (n 8). Animals were killed, RNA was extracted from liver and perirenal and epididymal fat pads, and analysed by ‘Northern methodology’. Samples were hybridized to a human cDNA probe for LPL (Gotoda et al. 1989). Two transcripts were identified in epididymai and perirenal adipose tissue which were approximately 3·7 and 1·7 kb in size. The results suggested that (1) fish oil-fed animals had significantly greater production of LPL mRNA in epididymai adipose tissue compared with maize oil-fed animals (P < 0·05), (2) maize oil-fed animals had significantly greater production of LPL mRNA in perirenal fat compared with the other dietary groups (P < 0·05), (3) expression in the liver was not significant. Rats fed on a fish oil diet had significantly reduced plasma triacylglycerol concentrations compared with the mixed-oil group (P < 0·05), but there were no significant differences in plasma cholesterol. The differences in LPL could not be explained directly by the changes in plasma immunoreactive-insulin and glucose-dependent insulinotrophic polypeptide levels in the three groups.

Effects of n-3 fatty acids on postprandial triacylglycerol and hormone concentrations in normal subjects

The present study reports results from two investigations to determine effects of a 6-week period of moderate n-3 fatty acid supplementation (2.7 g/d) on fasting and on postprandial triacylglycerol and metabolic hormone concentrations in response to standard test meals. In the first study postprandial responses were followed for 210 min after an early morning test meal challenge; in the second study responses to an evening test meal were followed during the evening and overnight for a total period of 12 h. In both studies postprandial triacylglycerol responses to the test meals were significantly reduced after compared with before fish-oil supplementation. In the second study the triacylglycerol peak response seen between 200 and 400 min in subjects studied before supplementation with fish oils was almost completely absent in the same subjects after 6 weeks of n-3 fatty acid supplementation. Analysis of fasting concentrations of metabolites and hormones was carried out on the combined data from the two studies. There were no significant differences in total, low-density-lipoprotein- or high-density-lipoprotein-cholesterol concentrations during fish-oil supplementation, although there was considerable individual variation in cholesterol responses to the supplement. Concentrations of Apo-B and Apo-A1 were unchanged during supplementation with fish oils. Fasting and early morning postprandial GIP concentrations were lower in subjects taking fish oils, possibly due to acute effects of fish-oil capsules taken on the evening before the studies. In both studies fasting insulin and glucose and postprandial insulin concentrations remained unchanged following fish-oil supplementation. The results do not support the view that triacylglycerol-lowering effects of n-3 fatty acids are due to modulation of insulin secretion mediated via the enteroinsular axis. Further studies are required to determine the precise mechanism by which fish oils reduce both fasting and postprandial triacylglycerol concentrations.