Metabolic Effects of n-3 PUFA as Phospholipids Are Superior to Triglycerides in Mice Fed a High-Fat Diet: Possible Role of Endocannabinoids

Background n-3 polyunsaturated fatty acids, namely docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), reduce the risk of cardiovascular disease and can ameliorate many of obesity-associated disorders. We hypothesised that the latter effect will be more pronounced when DHA/EPA is supplemented as phospholipids rather than as triglycerides. Methodology/Principal Findings In a ‘prevention study’, C57BL/6J mice were fed for 9 weeks on either a corn oil-based high-fat obesogenic diet (cHF; lipids ~35% wt/wt), or cHF-based diets in which corn oil was partially replaced by DHA/EPA, admixed either as phospholipids or triglycerides from marine fish. The reversal of obesity was studied in mice subjected to the preceding cHF-feeding for 4 months. DHA/EPA administered as phospholipids prevented glucose intolerance and tended to reduce obesity better than triglycerides. Lipemia and hepatosteatosis were suppressed more in response to dietary phospholipids, in correlation with better bioavailability of DHA and EPA, and a higher DHA accumulation in the liver, white adipose tissue (WAT), and muscle phospholipids. In dietary obese mice, both DHA/EPA concentrates prevented a further weight gain, reduced plasma lipid levels to a similar extent, and tended to improve glucose tolerance. Importantly, only the phospholipid form reduced plasma insulin and adipocyte hypertrophy, while being more effective in reducing hepatic steatosis and low-grade inflammation of WAT. These beneficial effects were correlated with changes of endocannabinoid metabolome in WAT, where phospholipids reduced 2-arachidonoylglycerol, and were more effective in increasing anti-inflammatory lipids such as N-docosahexaenoylethanolamine. Conclusions/Significance Compared with triglycerides, dietary DHA/EPA administered as phospholipids are superior in preserving a healthy metabolic profile under obesogenic conditions, possibly reflecting better bioavalability and improved modulation of the endocannabinoid system activity in WA

Poor understanding of allergen labelling by allergic and non‐allergic consumers

Background: Understanding consumers’ interpretation of allergy information is crucial for effective food safety policies. We evaluated consumer understanding of allergy information on foods in controlled, experimental studies. Method: Using 18 packaged foods, we evaluated consumer understanding of information about allergens in two experiments: First, a comparison of foods with no stated allergen versus allergen as a stated ingredient versus a precautionary allergen label (PAL); second, a comparison of three common variants of PAL. In each experiment, consumers with and without self-reported food allergy were asked to estimate the risk of allergic reaction and to rate the comprehensibility of the allergen information. In the second experiment, consumers were also asked which form of PAL they preferred. Results: Risk of reaction was assessed as high and low for foods with the allergen stated as ingredient, or without any mention of allergen. However, risk assessment for PAL varied and was judged as higher by non-allergic than allergic participants (82% vs. 58%, p <.001). Understanding of risk associated with PAL also varied by health literacy (p <.001). Both allergic and non-allergic consumers judged all forms of allergy information to be unclear, especially products with no allergy information for non-allergic consumers. Products with a ‘Produced in a Factory’ PAL were perceived as less risky than ‘May contain’ or ‘Traces of’ PALs (p <.001), less than 40% of participants judged PAL information to be comprehensible, and participants preferred ‘May contain’ over the other PALs. Conclusion: Both allergic and non-allergic consumers find allergen information difficult to interpret on packaged foods and misunderstand PAL, incorrectly distinguishing different risk levels for different PAL wording. Clearer allergy information guidelines are called for, and the use of only one PAL wording is recommended

Timeline of dietary studies.

<p>All mice were weaned on Chow diet at 4 weeks of age. In the ‘prevention’ and ‘bioavailability’ studies, 3-month-old mice were switched from Chow to cHF, cHF+ω3TG and cHF+ω3PL diets for a period of 2 or 9 weeks, respectively, as indicated. In the ‘reversal study’, mice were fed cHF diet for a period of 4 month, followed by 9-week-feeding using cHF, cHF+ω3TG and cHF+ω3PL diets. In the ‘bioavailability’ study, cHF+ω3TG and cHF+ω3PL diets with several different concentrations of DHA and EPA were used (see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0038834#s4" target="_blank">Methods</a> and <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0038834#pone-0038834-g002" target="_blank">Figure 2A,B</a>), while in the ‘prevention’ and ‘reversal’ studies these diets were matched for their DHA/EPA content (i.e. 30 g DHA/EPA per kg diet), except for the ‘prevention’ study, in which a subgroup of mice was also treated using cHF+ω3PL diet containing 10 g DHA/EPA per kg diet. See <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0038834#s4" target="_blank">Methods</a> for further details. IPGTT, intraperitoneal (<b>i.p.</b>) glucose tolerance tests.</p

Reversal of hepatic lipid accumulation by dietary LC <i>n</i>-3 PUFA.

<p>Following a 4-month period of cHF-feeding, mice were fed for additional 9 weeks with cHF diet or treated using either cHF+ω3TG or cHF+ω3PL diet supplemented with 30 g DHA/EPA per kg; all diets also contained 2 g metformin per kg. Hematoxyline-eosin staining of liver sections from mice fed cHF (<b>A</b>), cHF+ω3TG (<b>B</b>), or cHF+ω3PL (<b>C</b>) diet. Hepatic lipid content (<b>D</b>). Quantification of mRNA levels of fatty acid oxidation (<b>E</b>) and lipogenic (<b>F</b>) genes in mice fed cHF (black bars), cHF+ω3TG (red bars), or cHF+ω3PL (blue bars) diets. <b>A-C</b>, Scale bars = 200 µm. AOX, acyl-CoA oxidase; ACOT2, acyl-CoA thioesterase 2; FAS; fatty acid synthase; SCD-1, stearoyl-CoA desaturase 1. Data are means±SEM (<i>n</i> = 7). *Significantly different from cHF (t-test or ANOVA); ^†significantly different from cHF+ω3TG (ANOVA).</p

Prevention of obese phenotype by dietary LC <i>n</i>-3 PUFA administered as either triglycerides or phospholipids.

<p>Mice (3-months-old) were placed on various diets and killed after nine weeks of the dietary treatment. Body weight gain was calculated as the difference in body weight between the beginning of the experiment and after eight weeks of treatment. Food intake was monitored weekly during weeks 2 to 8 of the dietary treatment. As shown before <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0038834#pone.0038834-Kuda1" target="_blank">[8]</a>, <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0038834#pone.0038834-Kus1" target="_blank">[58]</a>, there was no difference in food intake between the Chow- and cHF-fed mice. Glucose homeostasis was assessed by glucose tolerance test in mice fasted overnight after eight weeks of treatment (see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0038834#pone.0038834.s001" target="_blank">Fig. S1</a>). Data are means±SEM (<i>n</i> = 7).</p>a,b,c<p>Significant differences (ANOVA) compared with cHF, cHF+ω3TG, and cHF+ω3PL (10 g per kg diet), respectively;</p>d<p><i>p</i>≤0.05 vs. cHF (t-test).</p><p>AU, arbitrary units; AUC, area under the glucose curve; FBG, fasting blood glucose; HMW: total, ratio of high molecular weight to total adiponectin; ND, not determined; NEFA, non-esterified fatty acids; WAT, white adipose tissue.</p

Reversal of adipose tissue hypertrophy and low-grade inflammation by dietary LC <i>n</i>-3 PUFA.

<p>Following a 4-month period of cHF-feeding, mice were fed for additional 9 weeks with cHF diet or treated using either cHF+ω3TG or cHF+ω3PL diet supplemented with 30 g DHA/EPA per kg; all diets also contained 2 g metformin per kg. Hematoxyline-eosin staining of epididymal fat sections from mice fed cHF (<b>A</b>), cHF+ω3TG (<b>B</b>), or cHF+ω3PL (<b>C</b>) diet. <b>D</b> Adipocyte size; morphometric analysis was based on more than 1,000 cells taken randomly from 5 different areas per animal (<i>n</i> = 3). <b>E</b> Amount of MAC-2 immunoreactive macrophages in the above tissue sections, expressed as the number of crown-like structures (<b>CLS</b>; indicated by white arrows in <b>A–C</b>). <b>F</b> Adipose tissue gene expression of monocyte chemoattractant protein-1 (<b>MCP-1</b>), a chemokine which is involved in the recruitment of monocytes to sites of injury and infection. cHF diet, black bars; cHF+ω3TG diet, red bars; cHF+ω3PL diet; blue bars. <b>A-C</b>, Scale bars = 200 µm. Data are means±SEM (n = 7−8; <b>D–F</b>). *Significantly different from cHF; ^†significantly different from cHF+ω3TG (all analyses by ANOVA).</p

EAACI Molecular Allergology User's Guide 2.0

Since the discovery of immunoglobulin E (IgE) as a mediator of allergic diseases in 1967, our knowledge about the immunological mechanisms of IgE-mediated allergies has remarkably increased. In addition to understanding the immune response and clinical symptoms, allergy diagnosis and management depend strongly on the precise identification of the elicitors of the IgE-mediated allergic reaction. In the past four decades, innovations in bioscience and technology have facilitated the identification and production of well-defined, highly pure molecules for component-resolved diagnosis (CRD), allowing a personalized diagnosis and management of the allergic disease for individual patients. The first edition of the "EAACI Molecular Allergology User's Guide" (MAUG) in 2016 rapidly became a key reference for clinicians, scientists, and interested readers with a background in allergology, immunology, biology, and medicine. Nevertheless, the field of molecular allergology is moving fast, and after 6 years, a new EAACI Taskforce was established to provide an updated document. The Molecular Allergology User's Guide 2.0 summarizes state-of-the-art information on allergen molecules, their clinical relevance, and their application in diagnostic algorithms for clinical practice. It is designed for both, clinicians and scientists, guiding health care professionals through the overwhelming list of different allergen molecules available for testing. Further, it provides diagnostic algorithms on the clinical relevance of allergenic molecules and gives an overview of their biology, the basic mechanisms of test formats, and the application of tests to measure allergen exposure.Peer reviewe