Metabolic inflammation is a very topical area of research, wherein aberrations in metabolic and inflammatory pathways probably contribute to atherosclerosis, insulin resistance (IR) and type 2 diabetes. Metabolic insults arising from obesity promote inflammation, which in turn impedes insulin signalling and reverse cholesterol transport (RCT). Key cells in the process are metabolically activated macrophages, which up-regulate both pro- and anti-inflammatory pathways in response to lipid spillover from adipocytes. Peroxisome proliferator-activated receptors and AMP-activated protein kinase (AMPK) are regulators of cellular homeostasis that influence both inflammatory and metabolic pathways. Dietary fats, such as saturated fatty acids (SFAs), can differentially modulate metabolic inflammation. Palmitic acid, in particular, is a well-characterized nutrient that promotes metabolic inflammation via the NLRP3 (the nod-like receptor containing a pyrin domain) inflammasome, which is partly attributable to AMPK inhibition. Conversely, some unsaturated fatty acids are less potent agonists of metabolic inflammation. For example, monounsaturated fatty acid does not reduce AMPK as potently as SFA and n-3 polyunsaturated fatty acids actively resolve inflammation via resolvins and protectins. Nevertheless, the full extent to which nutritional state modulates metabolic inflammation requires greater clarification.

SFA intakes have decreased in recent years, both in Ireland and across other European countries; however a large proportion of the population are still not meeting the SFA recommendation of <10% of total energy (TE). High SFA intakes have been associated with increased CVD and type-2 diabetes (T2D) risk, due to alterations in cholesterol homoeostasis and adipose tissue inflammation. PUFA, in particular EPA and DHA, have been associated with health benefits, including anti-inflammatory effects. It is well established that dietary fat composition plays an important role in biological processes. A recent review of evidence suggests that replacement of SFA with PUFA has potential to reduce risk of CVD and T2D. The public health and molecular impact of EPA and DHA have been well-characterised, while less is known of effects of α-linolenic acid (ALA). The current dietary guideline for ALA is 0·5% TE; however evidence from supplementation trials suggests that benefit is observed at levels greater than 2 g/d (0·6–1% TE). This review highlights the gap in the evidence base relating to effects of the replacement of SFA with ALA, identifying the need for randomised controlled trials to determine the optimal dose of ALA substitution to define the efficacy of dietary fat modification with ALA.

Evidence suggests that processed red meat consumption is a risk factor for CVD and type 2 diabetes (T2D). This analysis investigates the association between dietary patterns, their processed red meat contributions, and association with blood biomarkers of CVD and T2D, in 786 Irish adults (18-90 years) using cross-sectional data from a 2011 national food consumption survey. All meat-containing foods consumed were assigned to four food groups (n 502) on the basis of whether they contained red or white meat and whether they were processed or unprocessed. The remaining foods (n 2050) were assigned to twenty-nine food groups. Two-step and k-means cluster analyses were applied to derive dietary patterns. Nutrient intakes, plasma fatty acids and biomarkers of CVD and T2D were assessed. A total of four dietary patterns were derived. In comparison with the pattern with lower contributions from processed red meat, the dietary pattern with greater processed red meat intakes presented a poorer Alternate Healthy Eating Index (21·2 (sd 7·7)), a greater proportion of smokers (29 %) and lower plasma EPA (1·34 (sd 0·72) %) and DHA (2·21 (sd 0·84) %) levels (P<0·001). There were no differences in classical biomarkers of CVD and T2D, including serum cholesterol and insulin, across dietary patterns. This suggests that the consideration of processed red meat consumption as a risk factor for CVD and T2D may need to be re-assessed.

Scope: High-fat diet (HFD)-induced obesity impairs macrophage-to-feces reverse cholesterol transport (RCT). It is hypothesized that dietary supplementation with the polyunsaturated fatty acids conjugated linoleic acid (CLA) or alpha linolenic acid (ALA) would prevent HFD-impaired RCT by modulating hepatic protein pathways. Methods and results: ApoE3L.CETP mice are fed a HFD supplemented ± CLA or ALA for 12 weeks and in vivo macrophage-to-feces RCT is determined. Hepatic cholesterol transporters and the hepatic proteome are assessed by immunoblotting and mass spectrometry, respectively. Mice fed HFD alone, but not ALA-HFD or CLA-HFD, exhibit increased systemic cholesterol levels, increased 3 H-cholesterol levels in plasma and liver but not feces during RCT, and reduced hepatic ABCG5/8 expression relative to LFD. ALA-HFD significantly reduces liver weight, hepatic cholesterol levels, and expression of the cholesterol synthesis enzyme farnesyl pyrophosphate synthase relative to HFD. ALA further increases the expression of acetyl-coA oxidase-associated proteins and suppress PPAR -induced proteins relative to HFD. CLA does not significantly attenuate hepatic lipid levels but is associated with reduced hepatic expression of fatty acid binding protein (FABP)-1/FABP4 levels relative to HFD, and reduced inflammatory pathway activation relative to ALA-HFD.

Previous studies have shown that the dietary diversity of young Filipino children to be limited and that the prevalence of nutrient inadequacies is high. This study extends the current knowledge to examine the relationship between diet diversity and the probability of adequacy of micronutrients among Filipino schoolchildren (aged 6 to 12 years), by the wealth status and dwelling location. The dietary intake data were collected using a single 24-h recall from 6460 children in the Filipino National Nutrition Survey 2013. The diet diversity score (DDS) and the probability of adequacies (PA) of 11 micronutrients were calculated, and further stratified by socio-economic status (SES) and dwelling location. The diet diversity was generally low (mean DDS = 4 out of 9). Children from the lowest SES, and living in rural areas, tended to have a lower DDS. Children with a DDS of 1 were likely to be inadequate in all 11 micronutrients. The higher DDS (≥6) was associated with higher PAs for the B vitamins but not for calcium, folate, iron, vitamin A and to large extent, vitamin C. This suggests that it was difficult for this population to achieve adequacy in these 5 micronutrients. More rigorous research on the topic is needed. Better access to nutrient-rich or fortified staple foods, in tandem with increased education on the importance of dietary diversity, are potential strategies to support children in achieving adequate micronutrient intakes.

Socio-economic status (SES) has an impact on food consumption in developing countries. However, the impact of SES on dietary patterns in Filipino school-aged children is currently unknown. The aim of this study was to fill this knowledge gap, using data from the 2013 National Nutrition Survey. Dietary intake of 11,691 children (6–18 years) were assessed using a 24-h recall. All food and beverages were assigned to one of 85 food groups. Mean daily intake, percent consuming (prevalence), and contribution to energy intake were determined, and stratified by SES, in 6–9 years old, 10–12 years old, and 13–18 years old. Rice was the most consumed food and the primary source of energy across all three age groups, independent of SES. Children of poor SES presented greater consumption of fish, vegetables, fruit, and table sugar (p < 0.05). In comparison, children of rich and middle SES presented greater consumption of milk, chicken, pork, sausages, and soft-drinks (p < 0.05). In conclusion, SES impacts the type of foods consumed by Filipino children, with children in the poorest households being most at risk of consuming low-variety diets. This analysis could be used to support public health strategies to improve dietary diversity, and potentially nutrient intake, in Filipino children.

Objective: To apply a dietary modelling approach to investigate the impact of substituting beef intakes with three types of alternative fatty acid (FA) composition of beef on population dietary fat intakes. Design: Cross-sectional, national food consumption survey – the National Adult Nutrition Survey (NANS). The fat content of the beef-containing food codes (n 52) and recipes (n 99) were updated with FA composition data from beef from animals receiving one of three ruminant dietary interventions: grass-fed (GRASS), grass finished on grass silage and concentrates (GSC) or concentrate-fed (CONC). Mean daily fat intakes, adherence to dietary guidelines and the impact of altering beef FA composition on dietary fat sources were characterised. Setting: Ireland. Participants: Beef consumers (n 1044) aged 18–90 years. Results: Grass-based feeding practices improved dietary intakes of a number of individual FA, wherein myristic acid (C14 : 0) and palmitic acid (C16 : 0) were decreased, with an increase in conjugated linoleic acid (C18 : 2c9,t11) and trans-vaccenic acid (C18 : 1t11; P < 0·05). Improved adherence with dietary recommendations for total fat (98·5 %), SFA (57·4 %) and PUFA (98·8 %) was observed in the grass-fed beef scenario (P < 0·001). Trans-fat intakes were increased significantly in the grass-fed beef scenario (P < 0·001). Conclusions: To the best of our knowledge, the present study is the first to characterise the impact of grass-fed beef consumption at population level. The study suggests that habitual consumption of grass-fed beef may have potential as a public health strategy to improve dietary fat quality.

Background Cholesterol retention within plasma membranes of macrophages is associated with increased inflammatory signaling. Cholesterol efflux via the transporters ABCA1, ABCG1, and SR‐BI to high‐density lipoprotein (HDL) particles is a critical mechanism to maintain cellular cholesterol homeostasis. Little is known about the impact of the obese microenvironment on cholesterol efflux capacity (CEC) of macrophages. In this study, the CEC of obese‐derived primary adipose‐tissue macrophages (ATM) is evaluated and the in vivo microenvironment is modeled in vitro to determine mechanisms underlying modulated CEC. Materials and Methods F4/80+ ATM are labeled with 3H‐cholesterol ex vivo, and CEC and ABCA1/ABCG1 protein levels are determined. Total, ABCA1‐dependent, and ABCA1‐independent CECs are determined in J774 macrophages polarized to M1 (LPS&IFNγ), M2 (IL‐4&IL‐13), or metabolic phenotypes (glucose, insulin, and palmitic acid). Results Obese ATM exhibit enhanced CEC and ABCA1 and ABCG1 expression compared to lean ATM. In contrast, ABCA1‐CEC is suppressed from M1 polarized macrophages compared to untreated in vitro, by activation of the JAK/STAT pathway. Incubation of macrophages in vitro in high glucose augments cAMP‐induced ABCA1 protein expression and ABCA1‐CEC. Conclusions These novel findings demonstrate remarkable plasticity of macrophages to respond to their environment with specific modulation of ABCA1 depending on whether classical pro‐inflammatory or metabolic cues predominate.