Obesity is an excess of adipose tissue (AT) and is linked with increased inflammation that enhances risk of type-2 diabetes and cardiovascular disease. The BIOCLAIMS study assessed the effect of obesity on AT fatty acid composition and gene expression, and the responses of these to chronic omega-3 FA supplementation.

AT biopsies were collected pre- and post-12 week supplementation with 1.1 g EPA + 0.8 g DHA/day or corn oil. The composition of FA in the total lipid extract of AT from 37 normal-weight and 44 obese subjects was assessed by gas chromatography, whole AT transcriptome from 10 normal-weight and 10 obese subjects was assessed by RNA-Sequencing, and selected gene expression in AT of 27 normal-weight and 38 obese subjects was assessed by qRT-PCR.

789 AT genes were differentially expressed (623 upregulated, 175 downregulated) in obesity compared to normal-weight (FC > 2, P < 0.05). Differentially expressed genes included EGFL6, MMP-7 and -9, 5-LOX, WNT3 and WNT10B, DACT2, CNR1, SLC27A2 and PLA2G7, and were associated with immune and inflammatory response, cell proliferation, activation and movement, Wnt signalling, remodelling and expansion, and lipid incorporation and degradation.

Chronic supplementation with EPA + DHA increased the concentration of AT EPA, DPA and DHA in normal-weight subjects (P < 0.01), and EPA in obese subjects (P = 0.006). EPA + DHA modulated the expression of 26 genes (14 upregulated, 12 downregulated) in normal-weight subjects and 7 genes (3 upregulated, 5 downregulated) in obese subjects (FC > 2, P < 0.05). Of note, EPA + DHA downregulated IGLV1-44, IGLV1-51, PROK2, and TREM1 in normal weight subjects (P < 0.05), and IGLV1-44, IGLV1-47, DACT2 and IDO1 obese subjects (P < 0.05). Genes of note upregulated by EPA + DHA included KCNH2, GCGR, SLC36A2 and FOXC2 in normal-weight subjects, and MAB21L1, LRRTM4, and COX-2, in obese subjects. Differentially expressed genes were associated with a decrease in complement activation and immunoglobulin secretion, negative regulation of cell proliferation, and positive regulation of remodelling, amino acid and glucose transport, and COX pathway metabolite synthesis.

These data indicate an altered AT transcription profile and gene expression in obesity suggesting enhanced immune and inflammatory response, tissue expansion and remodelling, and changes to lipid metabolism, as well as dysregulation in response to supplementary EPA + DHA at a gene expression level. EPA + DHA are able to modulate AT gene expression predominantly associated with reducing immune response, but obesity may involve resistance to the effects on tissue remodelling and nutrient transport.

High sugar consumption promotes endogenous formation of advanced glycation end-products (AGEs), a heterogeneous class of molecules originated from non-enzymatic glycation between reducing sugars and free amino groups of proteins, nucleic acids, or lipids. AGEs accumulation in tissues has been linked to aging and diabetes complications. AGEs might also play an independent role in inflammation and development of cardiovascular disease (CVD). Exogenous dietary AGEs, due to excess intake of modern heat-treated foods, might act synergistically with endogenous AGEs, thus contributing to increase inflammation and CVD. A large amount of ingested AGEs reaches the colon, where they might affect gut microbial metabolism, for example, by acting as substrate for colonic bacterial fermentation, driving alterations of microbiota composition and of intestinal permeability. However in vitro and in vivo studies (animal and human) on the impact of AGEs on the gut microbiota are discordant. This study on mice aims to link the modulation of gut microbiota by AGEs-enriched diet (AGE-D) with metabolic and inflammatory markers.

C57BL/6 mice were randomly allocated into the following dietary regimens: Control (n = 24) and AGE-D (n = 20) for 22 weeks. AGE-D was prepared replacing casein (200 g/kg diet) by an equal amount of modified casein where 10% of arginine was glycated with MG-H1 (methylglyoxal 5-hydro-5-methylimidazolone) for a total of 4 μmol of MG-H1 per g of diet. Faeces were collected using metabolic cages (18 h starving) at week 0, 11 and 22 for fecal DNA extraction and 16SrRNA analysis through Illumina MiSeq using V3-V4 targeted primers. After 22 weeks of dietary manipulation, mice were sacrificed, plasma and organ lipid profiles and serum metabolic and inflammatory profiles were determined.

AGE-D caused a significant reduction in the blood levels of two important components of the incretin system, GIP and GLP-1, when compared to control diet, suggestive of unbalance in the incretin-insulin axis. AGE-D exposure was associated with a significant increase in systemic concentrations of inflammatory cytokines, e.g. IL-1β and IL-17, and PAI-1, which has been suggested as both reliable marker and critical mediator of cellular senescence. We will present how AGEs impact on microbiome community structure and correlate changes in gut microbiota with GIP and GLP-1 levels.

AGEs, characteristic of modern processed foods, appear to impact on the incretin-insulin axis, a key regulator of metabolic disease risk. Diets rich in AGEs may mediate these physiological effects at least in part, by reshaping intestinal microbiota structure.

Nonalcoholic fatty liver disease (NAFLD) is the most common cause of liver disease in Western countries and is strongly associated with obesity and insulin resistance-related comorbidities. Moreover, there is some evidence of a relationship between NAFLD and depression. The aim of this study was to compare the effect of two personalized energy-restricted diets on liver fat and depressive symptoms in overweight or obese subjects with NAFLD after a 6-month follow-up.

Ninety-eight overweight or obese adults with NAFLD were enrolled and randomized to follow one of two different personalized energy-restricted diets (American Heart Association vs. FLiO diet) accompanied by healthy lifestyle advice. Study registered as FLiO: Fatty Liver in Obesity; NCT03183193. Anthropometry, body composition, biochemical features and liver status were assessed at baseline and after a 6-month follow-up. Liver fat was evaluated by Magnetic Resonance Imaging and depressive symptoms using the Beck's Depression Inventory-II (BDI-II).

Participants of both groups showed significant reductions in body weight, total fat mass, glucose, insulin and alanine aminotransferase (p < 0.001 for all these parameters in both groups). A significant decrease in liver fat (p < 0.001 in both groups) and depressive symptoms (p < 0.01 in both groups) was observed after the follow-up. The effects of the intervention in the evaluated variables did not differ when both diets were compared. Consequently, the two groups were considered together as one sample for the further analyses. Correlation analyses evidenced a positive association between the decrease in depressive symptoms and the reduction in body weight (r = 0.241; p = 0.044) and liver fat (r = 0.251; p = 0.046).

Previous studies have reported that the prevalence of depression in patients with chronic liver disease (including NAFLD) is higher than in the general population and that major depressive disorder is associated with more severe hepatic steatosis and with worse outcomes in the treatment of NAFLD subjects. In our study, both healthy personalized energy-restricted diets were able to improve metabolic parameters, liver fat content and depressive symptoms in overweight and obese participants with NAFLD. To our knowledge, this is the first study to report an association between the changes in depressive symptoms and the decrease in liver fat after a dietary randomized controlled trial. Further investigation is needed to clarify the relationship between depression and the development and treatment of NAFLD.

General overnutrition, and a diet rich in fat and sugar are among the key risk factors for the development of metabolic diseases including diabetes type 2 and non-alcoholic fatty liver diseases (NAFLD). While being among the most commonly consumed oils world-wide, the effects of soybean oil on the development of metabolic diseases are yet not understood. Indeed, existing data is in part contradictory. Based on this background, the aim of the present study was to investigate the effects of soybean oil consumption on the development of non-alcoholic steatohepatitis (NASH), the more progressed stage of NAFLD, and insulin resistance.

Female C57BL/6J mice were fed either a liquid standard control diet (C) or a liquid fat-, fructose- and cholesterol-rich diet (FFC, 25E% butterfat, 50% (wt/wt) fructose, 0.155% (wt/wt) cholesterol) or a FFC supplemented with soybean oil (FFC + S, 21E% butterfat + 4E% soy oil), with FFC and FFC + S-fed groups being pair fed for 13 weeks to induce steatohepatitis. After 7 and 12 weeks of feeding, a glucose tolerance test was performed. Indicators of liver damage, inflammation, intestinal barrier function and markers of insulin signaling cascade were measured in intestinal, liver and muscle tissue.

As expected FFC-fed mice developed early signs of NASH and insulin resistance. Despite similar caloric intake and body weight gain, development of NASH and insulin resistance were significantly attenuated in FFC + S-fed mice when compared to FFC-fed animals. Indeed, signs of hepatic inflammation e.g. number of inflammatory foci and neutrophils as well as activity of transaminase in plasma were almost at the level of control in FFC + S-fed mice. Prevalence of macrovesicular steatosis being the predominant type of fat accumulation found in FFC-fed animals was also markedly lower in FFC + S-fed mice. Furthermore, while in muscle and liver tissue of FFC-fed mice insulin receptors mRNA expression was significantly different from C-fed animals, insulin receptors expression in FFC + S-fed mice was almost at the level of controls. The protective effects of soybean oil supplementation on the development of metabolic alterations were associated with a protection against the induction of TLR4 mRNA expression and dependent signaling molecules in liver tissue.

Taking together, our results indicate that supplementation with soybean oil may attenuate the development of diet-induced NASH and insulin resistance in mice and that this may be related to alteration of TLR4-dependent signaling cascade in liver tissue. (Funded in parts by UFOP e.V.)

The quality of dietary protein sources became a particularly sensitive issue in the current debates on a rebalancing between animal and vegetable food sources.

The ability of a protein to meet the nutritional requirements of essential amino acid (EAA) is the basis for assessing the quality of protein.

The objective of this study was to characterize the impact of lysine- and threonine-deficient gluten-based diets on the metabolism of growing rats and to identify molecular markers of these diets.

Growing rats were fed for 3 weeks with a threonine-supplemented and 70% lysine-deficient gluten diet; a lysine-supplemented and 47% threonine-deficient gluten diet; a gluten diet supplemented in lysine and threonine to meet all the AA requirements, and a control diet with milk protein to meet all the AA requirements.

Body weight and food intake were measured daily. At the end of the experiment, tissues and biological fluids were removed. The body composition was analyzed, gene expression measurements involved in protein and lipid metabolism were performed and the urinary metabolome was analyzed by LC-MS. Statistical analysis was done by variance analysis and metabolome analysis by discriminant analysis of independent components.

This EAA deficiency does not modify the food intake. Lysine deficiency induces a decrease in body weight gain, and lean body mass, associated with an increased in proteolysis and a decreased in proteosynthesis, a decreased in bone mineral density, and no effect on lipid metabolism.

Threonine deficiency induces a decrease in body weight gain, and liver and skin weight, without changes in protein metabolism, bone mineral density, and lipid metabolism. After approval of the deficiency model, the metabolomic analysis performed on urine samples revealed the presence of specific discriminating molecules of the diets and types of proteins.

EAA deficiency has an impact on the growth, and bone and protein metabolism of growing rats. These deficiency states have resulted in different metabolome profiles that could lead to the identification of specific molecular markers of protein sources and related to EAA deficiencies.

Non-alcoholic fatty liver disease (NAFLD) is a chronic liver condition, whose prevalence increases in parallel with obesity, diabetes and metabolic syndrome (MetS) rates. The aim of the study was to investigate the relationships between the triglyceride glucose-body mass index (TyG-BMI) with lifestyle, dietary variables, and metabolic risk factors linked to NAFLD in subjects diagnosed with MetS.

A baseline cross-sectional study on 331 participants (aged 65.8 ± 5.1 years) recruited in Navarra was conducted. Subjects were stratified by tertiles of the TyG-BMI index. Dietetic, Mediterranean diet adherence (MedDiet-17 points) and physical activity data were assessed through validated questionnaires. Sociodemographic, lifestyle, anthropometric and biochemical parameters were also recoreded. The Cockcroft-Gault equation was performed to estimate clearance of creatinine. For comparisons between TyG-BMI tertiles and several variables, ANCOVA and chi-square test analyses were performed.

Subjects in T3 of TyG-BMI index were more likely to have diabetes (50.9%). Interestingly, physical activity decreases across tertiles (p = 0.030). There were no differences between tertiles in energy intake and MedDiet adherence. However, total meat consumption is highest in T3. ANCOVA test after adjustment for potential confounders revealed that participants in T3 showed more several clinical and metabolic alterations. Moreover, ALT (p = 0.002) and GGT (p = 0.047) levels increased and mean corpuscular volume decreased across tertiles of the TyG-BMI index.

Obesity, MetS and insulin resistance (IR) play a key role in the development of NAFLD promoting lipotoxicity and overproduction of proinflammatory mediators. This state induces hepatic steatosis and liver injury. Some studies suggest TyG-BMI index as a surrogate marker of IR and risk to NAFLD(1). In our study, patients in the highest TyG-BMI tertile showed more adverse cardio-metabolic profile, lower physical activity and higher total meat intake. In summary, the TyG-BMI index could be a simple and reliable marker to characterize the risk of NAFLD among individuals diagnosed with MetS.

Chewing a greater number of chews per bite has been shown to increase fullness, lower hunger levels and lead to a lower energy intake, when compared to chewing each bite fewer times. Increased levels of fullness and decreased levels of hunger have also been observed after consuming harder textured foods which require more chewing activity and have a longer oro-sensory exposure time. The aim of this study was to investigate whether consumption of foods differing in texture, classified as ‘fast’ or ‘slow’ foods, combined with differences in oral processing behaviours (chewing normally or more slowly), has an impact on self-reported hunger, fullness and satiety outcomes.

This is an interim analysis of a randomised crossover experiment designed to test the impact of both oral processing behaviours and food texture on self-reported hunger, fullness and satiety. Participants consumed two breakfasts of different texture (a ‘fast’ yoghurt and fruit compote option, and a ‘slow’ granola option) twice; once at their normal rate of eating and once after being instructed to eat slowly. Measures of self-reported appetite (hunger, fullness, satiety, desire to eat and prospective food consumption) were assessed using a visual analogue scale at three time points; baseline (minimum 20 minutes before consumption), immediately pre-consumption and post-consumption. Statistical analysis was conducted in SPSS; paired sample t tests and one-way analysis of variance was conducted to measure whether change in appetite ratings between the time points differed between the four breakfast options.

Data were collected from 16 healthy volunteers (study aiming to recruit n = 21; mean age 32.1 y, female n = 13, 81.3%). For all four breakfast options, levels of hunger, desire to eat and prospective food consumption significantly decreased, and levels of fullness and satiety significantly increased between both baseline and post-consumption, (p < 0.05) and between pre-consumption and post-consumption (p < 0.05). However, amongst the four breakfast options, no significant differences were observed in change in these appetite measures between baseline and post-consumption and pre- and post-consumption (p > 0.05).

This interim analysis demonstrates no differences in mean change in appetite measures for breakfast options of different texture chewed normally or more slowly. Analysis of the full study will determine the effect of oral processing behaviours and food texture on self-reported hunger, fullness and satiety outcomes.

Childhood obesity is considered one of the most serious public health problems of the 21st century. Obesity-associated inflammation could be one of the mechanisms that triggers insulin resistance that could drive systemic alterations such as metabolic disorder. Recently, circulating levels of S100A4 has been associated with insulin resistance and subcutaneuous white adipose tissue inflammation independently of body mass index (BMI) in a cohort of obese adults. Nonetheless, the link between S100A4 and insulin resistance in children is still not known yet. Thus, the aim of the study was to determine if S100A4 plasma levels were associated with insulin resistance status in a cohort of prepuberal children.

In this case-control multicentre study, 250 prepuberal children took part and were stratified in six groups according to sex, obesity stage and insulin resistance status. Blood samples were withdrawn in resting conditions after an overnight fasting. Anthropometric measurements and a routine biochemical analyses were performed. Homeostasis model assessment for insulin resistance index (HOMA-IR) was calculated using fasting plasma glucose and insulin values. S100A4 plasma levels were determined by ELISA CSBEL02032HU (Cusabio Biotech, Wuhan, China).

A lineal multiple regresión (α = 0.05) identified a significative association between S100A4 plasma levels and HOMA-IR in the cohort; each HOMA-IR increasing unit correlated with an increase of 0.008mg/dL in S100A4 plasma levels. (SE = 0.003 and p = 0.02). Moreover, we also observed a positive significative association between S100A4 plasma levels and glucose blood levels (p = 0.005) and BMI (p = 0.008). Inter-group comparations analyses revealed significative differences between normal-weight and insulino-resistant obese boys (p = 0.024). The same result was obtained between normal-weight and insulino-resistant obese girls (p = 0.04), finding a higher S100A4 concentration in insulino- resistant children. As expected, plasma S100A4 levels were also higher in obese children versus normal-weight children (p = 0.02).

These data could be clinical relevant due to the possible potential of S100A4 protein as a new circulating biomarker of resistance insulin in a cohort of prepuberal children. These results are supported by other studies in obese adults and adolescents. In conclusion, these results suggest that S100A4 is associated with obesity and insulin resistance in prepuberal children. However, more studies are needed to study the implication and mechanism of this protein in the development of insulin resistance.

Being the predominant osmotically active element inside cells, potassium is a central regulator of the osmotic balance and the electrochemical membrane potential. As such, it has an effect on blood pressure and therefore counteracts the effects of excess dietary sodium intake. Furthermore, potassium affects glucose homeostasis by influencing insulin secretion from the pancreatic β-cells. Due to the health-promoting effects of potassium, the German-speaking countries have recently updated the reference values for potassium. The revised estimates of adequate potassium intake are 4000 mg/d instead of previously recommended 2000 mg/d. However, a typical Western diet on average contains less potassium and more sodium.

The presented data were collected within the Austrian Study on Nutrition 2014/2016, a regularly conducted representative cross-sectional survey to monitor food consumption in Austria. Altogether, data from 2129 adults aged between 18 and 64 years were included in the analysis. In the course of two years, and thus with the consideration of seasonal variations, the survey was conducted on the basis of two non-consecutive 24 hour recalls in accordance with the guidelines of the European Food Safety Authority (EFSA). The survey was approved by the Ethical Committee of the University of Vienna (reference number: 00284).

After exclusion of misreporters the final sample consisted of 2018 individuals, of which 1282 (63.5%) were women. The mean age was 38.8 ± 11.9 years.

Median dietary potassium intake was 2783 mg/d (IQR: 1245). Men had a higher median intake than women (3018 mg/d (IQR: 1303) vs. 2546 mg/d (IQR: 1112), p < 0.001). Significant differences between sexes existed in all age groups (p < 0.001). However, there was no significant correlation between age and dietary potassium intake.

The estimates of adequate potassium intake of 4000 mg/d (DGE et al., 2017) were met by only 13.3% of the participants, 7.4% of women and 19.2% of men. Moreover, only 479 participants (23.8%, 16.7% of women and 30.9% of men) had intakes equal to or above 3500 mg/d, the adequate intake established by EFSA (2016).

Our data show that potassium intake has to be improved in all gender and age groups by increasing the consumption of potassium-rich foods. However, since the estimates of adequate potassium intake have doubled recently, it seems even more difficult to achieve these recommendations in daily food routine.

In previous studies iron deficiency was present in preschool children in the developed world1. The objective of this randomized controlled trial was to investigate whether iron deficiency was present in pre-school children and to what extend laboratory values could be improved with a nutrient rich diet.

A diet consisting of green vegetables, beef, full-fat milk and butter was developed. This diet comes close to the traditional Dutch diet from a century ago. All food products were in age appropriate portions, according to the national guidelines. Children aged one to four years, who were referred to the paediatrician due to recurrent URTI (without immunologic disorders) were allocated to the intervention or the control group. Both groups were given standard care. The intervention group was also given the dietary advise. All parents were asked to note of daily food intake.

No iron deficiency was present in our group of 1–4 years old. Mean Hb was 7.3 mmol/l in both groups. After following the dietary advice for 6 months,the hemoglobulin (Hb) concentration increased in both groups, but a little more in the intervention group :(0,280 mmol/l; p < 0,001 in the dietary intervention group and 0,214 mmol/l in the control group; p = 0,003). MCV values increased in the interventiongroup from 77.9 to 78.8 fl (p = 0.007) whereas a smaller increase was visible in the control group ;78.5 to 78.9 fl (p = 0.18). Ferritin, a marker for iron status but also a marker for inflammation, decreased non-significantly in both groups. There was a significantly correlation with decreasing CRP levels, therefore indicating a decrease in inflammation and not merely representing iron status. Growth parameters (weight, height or BMI) did not change significantly in both groups.

NoHb deficiency was present in our research population. However, a diet consisting of green vegetables, beef, full-fat milk and butter did improve the iron status in pre-school children. Hb and MCV values increased, suggesting some evidence of subclinical iron deficiency in this group.