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Blue whiting (BW) represents an underutilised fish species containing a high-quality protein and amino acid (AA) profile with numerous potentially bioactive peptide sequences, making BW an economic and sustainable alternative source of protein. This study investigated the impact of three different BW protein hydrolysates (BWPH-X, Y and Z) on growth, proliferation and muscle protein synthesis (MPS) in skeletal muscle (C2C12) myotubes. BWPHs were hydrolysed using different enzymatic and heat exposures and underwent simulated gastrointestinal digestion (SGID), each resulting in a high degree of hydrolysis (33.41–37.29%) and high quantities of low molecular mass peptides (86.17–97.12%

IntroductionThe relationship between inflammatory and anti-inflammato�ry markers and telomere length (TL), a biological index of aging, is still poor�ly understood. By applying a 2-sample Mendelian randomization (MR), we investigated the causal associations between adiponectin, bilirubin, C-reac�tive protein (CRP), leptin, and serum uric acid (SUA) with TL.Material and methodsMR was implemented by using summary-level data from the largest ever genome-wide association studies (GWAS) conducted on our interested exposure and TL. Inverse variance weighted method (IVW), weighted median (WM)-based method, MR-Egger, MR-Robust Adjusted Pro�file Score (RAPS), and MR-Pleiotropy RESidual Sum and Outlier (PRESSO) were applied. Sensitivity analysis was conducted using the leave-one-out method.ResultsWith regard to adiponectin, CRP, leptin, and SUA levels, we found no effect on TL for all 4 types of tests (all p > 0.108). Results of the MR-Egger (p = 0.892) and IVW (p = 0.124) showed that bilirubin had no effect on telomere maintenance, whereas the results of the WM (p = 0.030) and RAPS (p = 0.022) were negative, with higher bilirubin concentrations linked to shorter TL. There was a low likelihood of heterogeneity for all the estima�tions, except for bilirubin (IVW p = 0.026, MR Egger p = 0.018). MR-PRESSO highlighted no outlier. For all the estimations, we observed negligible inter�cepts that were indicative of low likelihood of the pleiotropy (all p > 0.161). The results of leave-one-out method demonstrated that the links are not driven because of single nucleotide polymorphisms (SNPs).ConclusionsOur results highlight that neither the anti-inflammatory nor pro-inflammatory markers tested have any significant causal effect on TL. The casual role of bilirubin on TL still needs to be investigated.

Individuals with discordantly high apoB to LDL-cholesterol levels carry a higher risk of atherosclerotic CVD compared with those with average or discordantly low apoB to LDL-cholesterol. We aimed to determine associations between apoB and LDL-cholesterol discordance in relation to nutrient patterns (NP) using National Health and Nutrition Examination Survey data. Participants were grouped by established LDL-cholesterol and apoB cut-offs (Group 1: low apoB/low LDL-cholesterol, Group 2: low apoB/high LDL-cholesterol, Group 3: high apoB/low LDL-cholesterol, Group 4: high apoB/high LDL-cholesterol). Principle component analysis was used to define NP. Machine learning (ML) and structural equation models were applied to assess associations of nutrient intake with apoB/LDL-cholesterol discordance using the combined effects of apoB and LDL-cholesterol. Three NP explained 63·2 % of variance in nutrient consumption. These consisted of NP1 rich in SFA, carbohydrate and vitamins, NP2 high in fibre, minerals, vitamins and PUFA and NP3 rich in dietary cholesterol, protein and Na. The discordantly high apoB to LDL-cholesterol group had the highest consumption of the NP1 and the lowest consumption of the NP2. ML showed nutrients that had the greatest unfavourable dietary contribution to individuals with discordantly high apoB to LDL-cholesterol were total fat, SFA and thiamine and the greatest favourable contributions were MUFA, folate, fibre and Se. Individuals with discordantly high apoB in relation to LDL-cholesterol had greater adherence to NP1, whereas those with lower levels of apoB, irrespective of LDL-cholesterol, were more likely to consume NP3.

Background: Cigarette smoking is associated with changes in blood concentrations of some antioxidant vitamins. This study aimed to determine the association of cigarette smoking with serum concentrations of vitamins A and E in men. Methods: This was a case-control study, in which the participants were 80 male smokers and 84 male nonsmokers (age range: 20-60 years). Data on dietary intake, health status, smoking habits, anthropometric characteristics, and vitamin levels were compared between cases and controls. Results: Smokers had significantly lower concentrations of serum vitamin E (p = 0.001) and vitamin A (p = 0.013) compared with nonsmokers. However, serum vitamin E to cholesterol ratio was not significantly different between smokers and nonsmokers. Moreover, the highest circulating concentrations of vitamin E was observed in smokers who smoked ≤9 cigarettes per day (p

Background Observational studies evaluating the link between sleep duration and kidney function reported controversial results. In the present study, Mendelian Randomization (MR) analysis was applied to obtain unconfounded estimates of the casual association of genetically determined sleep duration with estimated glomerular filtration rate (eGFR) and the risk of chronic kidney disease (CKD). Methods Data from the largest genome-wide association studies (GWAS) on self-reported and accelerometer derived sleep duration, eGFR and CKD were analysed in total, as well as separately in diabetic and non-diabetic individuals. Inverse variance weighted method (IVW), weighted median (WM)-based method, MR-Egger, as well as MR-Pleiotropy RESidual Sum and Outlier (PRESSO) were applied. To rule out the impact of single single-nucleotide polymorphism (SNP), the leave-one-out method was used. Results Overall, individuals with genetically longer self-reported sleep duration had a higher CKD risk (IVW: beta=0.358, p=0.047). Furthermore, in non-diabetics, longer self-reported sleep duration was negatively associated eGFR (IVW: beta=−0.024, p=0.020). Similarly, accelerometer derived sleep duration was negatively related to eGFR in the total population (IVW: beta=−0.019, p=0.047) and the non-diabetic individuals (IVW: beta=−0.025, p=0.014) (Table). No significant association was found between self-reported sleep duration and eGFR in the whole population (IVW: beta=−0.019, p=0.072) and T2DM patients (IVW: beta=0.028, p=0.484). None of the estimated associations was subjected to a significant level of heterogeneity. Furthermore, MR-PRESSO analysis did not show any chance of outliers for all estimates. The pleiotropy test, with very negligible intercept and insignificant p value. The results of the MR-RAPS were identical with the IVW estimates, highlighting again no possibility of pleiotropy. The leave-one-out method demonstrated that the links were not driven by single SNPs. Conclusions For the first time, the present study shed a light on the potential harmful effects of longer sleep duration (measured both objectively and subjectively) on kidney function. This finding was observed in the total population and in non-diabetic individuals, but not in those with diabetes. Further research is needed to elucidate the links between sleep duration, eGFR and CKD. Funding Acknowledgement Type of funding source: None

Background Omega-6 polyunsaturated fatty acids (PUFAs) represent almost 15% of the total energy intake in the Western countries. Their effects on several cardiovascular (CV) risk factors are still controversial. Purpose We performed a systematic review and meta-analysis of randomized control trials (RCTs) as well as a Mendelian randomization (MR) analysis to evaluate the links (or possible causality) between supplementation or serum levels of omega-6 PUFA, CV disease (CVD) and cardiometabolic risk factors. Methods Selected databases were searched until 31 August 2019 to identify prospective studies investigating the effects of omega-6 PUFAs supplementation on CVD events/mortality. Random-effects model meta-analysis was performed for quantitative data synthesis. Trial sequential analysis (TSA) was used to evaluate the optimal sample size to detect a 20% reduction in outcomes after administration of omega-6 PUFAs. Inverse variance weighted method (IVW), weighted median-based method, MR-Egger and MR-Pleiotropy RESidual Sum and Outlier (PRESSO) were applied for MR. Results In the meta-analysis of 9 studies with 4,433 participants we showed that omega-6 PUFAs supplementation was not associated with CVD event risk - RR 0.94 (95% CI: 0.77–1.15, heterogeneity p=0.031; I2=66.2%, n=4 studies). The pooled estimate (RR) of the effect of omega-6 PUFAs supplementation on CVD death was 1.06 (95% C:I 0.73–1.55, heterogeneity p=0.011; I2=66.2%, n=6 studies), on CHD events 0.84 (95% CI: 0.61–1.16, heterogeneity p=0.001; I2=79.4%), on MI 0.87 (95% CI: 0.74–1.01, heterogeneity p=0.381; I2=2.3%) (Figure), and on stroke 1.36 (95% CI: 0.45–4.07, heterogeneity p=0.082; I2=55.3%). In MR analysis we showed that individuals with genetically higher serum adrenic acid (AA; 22:4, n-6) levels had a greater risk of CHD events (IVW=Beta: 0.526, p=0.007), MI (IVW=Beta: 0.606, p=0.017) and stroke (IVW=Beta: 1.694, p=0.009), as well as higher levels of FBG (IVW=Beta: 0.417, p=1.0x10–3), LDL-C (IVW=Beta: 0.806, p=4.9x10–5), HDL-C (IVW=Beta: −0.820, p=4.3x10–17), whereas lower levels of TG (IVW=Beta: −1.064, p=1.2x10–12) and TC (IVW=Beta: −1.064, p=1.2x10–12). Conclusions In the pooled analysis different omega-6 PUFAs supplementation did not affect the risk of MI, stroke and CHD event/mortality or the serum concentration of cardiometabolic parameters (data not presented), however in MR analysis, higher AA levels significantly associated with the risk of CHD, MI and stroke, as well as with elevated levels of FBG, LDL-C and HDL-C and reduced levels of TC and TG. There is probably lack of class effect for omega-6 PUFAs, therefore further studies are needed to assess the effects of omega-6 PUFAs on cardiometabolic outcomes. Funding Acknowledgement Type of funding source: None

Background: The microbiota composition is now considered as one of the main modifiable risk factors for health. No controlled study has been performed on the association between microbiota composition and renal function. We applied Mendelian randomization (MR) to estimate the casual impact of eight microbiota genera on renal function and the risk of chronic kidney disease (CKD). Methods: MR was implemented by using summary-level data from the largest-ever genome-wide association studies (GWAS) conducted on microbiota genera, CKD and renal function parameters. The inverse-variance weighted method (IVW), weighted median (WM)-based method, MR-Egger, MR-Robust Adjusted Profile Score (RAPS), MR-Pleiotropy RESidual Sum and Outlier (PRESSO) were applied. A sensitivity analysis was conducted using the leave-one-out method. Results: The Anaerostipes genus was associated with higher estimated glomerular filtration rate (eGFR) in the overall population (IVW: β = 0.003, p = 0.021) and non-diabetes mellitus (DM) subgroup (IVW: β = 0.003, p = 0.033), while it had a non-significant association with the risk of CKD and eGFR in DM patients. Subjects with higher abundance of Desulfovibrio spp. had a significantly lower level of eGFR (IVW: β = −0.001, p = 0.035); the same results were observed in non-DM (IVW: β = −0.001, p = 0.007) subjects. Acidaminococcus, Bacteroides, Bifidobacterium, Faecalibacterium, Lactobacillus and Megamonas had no significant association with eGFR in the overall population, DM and non-DM subgroups (IVW: p > 0.105 for all groups); they also presented no significant association with the risk of CKD (IVW: p > 0.201 for all groups). Analyses of MR-PRESSO did not highlight any outlier. The pleiotropy test, with very negligible intercept and insignificant p-value, also indicated no chance of pleiotropy for all estimations. The leave-one-out method demonstrated that the observed links were not driven by single single-nucleotide polymorphism. Conclusions: Our results suggest an adverse association of Desulfovibrio spp. and a beneficial association of Anaerostipes spp. with eGFR. Further studies using multiple robust instruments are needed to confirm these results.

The impact of low-density lipoprotein cholesterol (LDL-C) on the risk of stroke is unclear. Therefore, we systematically evaluated the impact of LDL-C levels (cohort studies) and lipid lowering agents (LLAs, randomized controlled trials) on the different types of stroke. Selected databases were