Springer Science and Business Media LLC

Cardiovascular disease is the major cause of death in the Western world, but some recent studies indicate that vitamin K may play a role in atherosclerosis protection. The aim of this study was to evaluate the effect of phylloquinone supplementation on blood lipids, inflammatory markers and fibrinolytic activity in postmenopausal women. Thirty-one postmenopausal women completed this placebo-controlled, randomized crossover study and received 500 µg phylloquinone or placebo in addition to their habitual diet during two periods of 6 weeks’ duration. Blood concentration of lipids, inflammatory markers and fibrinolytic parameters were measured after each period. Inflammatory markers, fibrinolytic parameters, total cholesterol and LDL-C were unaffected by the supplementation, whereas a 15% increase was seen in triacylglycerols (P = 0.015) and a 5% decrease in HDL-C (P = 0.06). Six weeks supplementation with a dose of phylloquinone similar to that obtainable from the diet induced a deterioration of the lipid profile with no improvement in any of the other risk markers analysed. Thus, these results do not support a cardioprotective effect of vitamin K as has been suggested by others.

The aim of this study is to investigate the involvement of DNA-dependent protein kinase (DNA-PK) in palmitate and oleate-induced lipid accumulation in hepatocytes. We treated HepG2 with free fatty acids (FFA) (0.33 mM palmitate and 0.66 mM oleate) mixture to induce lipid accumulation. Cellular lipid was determined by Nile Red staining followed by flow cytometry detection as well as phase contrast and fluorescence microscope examination. Cell viability was detected by MTT assay. Apoptosis was detected by DAPI staining. Lipogenic gene expression was examined by real-time PCR at mRNA level and Western blotting at protein level. Promoter transcriptional activity was measured by dual luciferase assay. FFA treatment neither affected HepG2 cells viability nor induced DNA fragmentation, while induced cellular lipid accumulation was associated by the upregulation of sterol regulatory element-binding protein-1 (SREBP1) and fatty acid synthase (FAS) at both mRNA and protein levels. Interestingly, we also found that both the protein phosphatase 2A (PP2A) protein expression and DNA-PK activity were increased in these cells. Inhibition of PP2A by okadaic acid, knockdown of DNA-PK by siRNA or inhibition of DNA-PK by specific DNA-PK inhibitors curtailed the FFA-induced upregulations of the SREBP1 mRNA expression and the nuclear active SREBP1 protein expression, and reduced FFA-induced upregulation of FAS promoter transcriptional activity and lipid accumulation. This is the first time suggesting that inhibition of DNA-PK reduced FFA-induced lipid accumulation in hepatocytes. This finding might help us better understand non-alcoholic steatohepatitis pathogenesis.

To investigate the long-term association between four dietary quality indices and the risk of gastrointestinal (GI) cancer. Baseline details of the dietary intake of participants, assessed by a single food frequency questionnaire from the prospective Lifelines population-based cohort were translated to diet quality scores using several dietary and dietary-lifestyle indices. Incident cases of GI cancer were then assessed by linkage to the Dutch nationwide histo-cytopathology registry. The association between GI cancer risk and diet quality (defined as higher quintiles on dietary indices compared to the first quintile) was assessed by multivariable Cox proportional hazard models. We included 72,695 participants aged 51.20 ± 8.71 years with a median follow-up to cancer diagnosis of 8 years (interquartile range 2 years). During follow-up, 434 colorectal cancers and 139 upper GI cancers were diagnosed. There was a significant reduction in colorectal cancer risk for high categories in the American Cancer Society (ACS) Index (hazard ratio 0.62; 95% CI 0.46–0.84). However, high dietary index scores were not associated with strong beneficial effects on upper GI cancer risk. High quintiles on the ACS Index were associated with a significantly reduced risk of colorectal cancer. This index may be of use in a colorectal cancer prevention program.

We aimed to quantify and compare dietary non-enzymatic antioxidant capacity (NEAC), estimated using two dietary assessment methods, and to explore its relationship with plasma NEAC. Fifty healthy subjects volunteer to participate in this study. Two dietary assessment methods [a food frequency questionnaire (FFQ) and a 24-hour recall (24-HR)] were used to collect dietary information. Dietary NEAC, including oxygen radical absorbance capacity (ORAC), total polyphenols, ferric-reducing antioxidant power (FRAP) and trolox equivalent antioxidant capacity, was estimated using several data sources of NEAC content in food. NEAC status was measured in fasting blood samples using the same assays. We performed nonparametric Spearman’s correlation analysis between pairs of dietary NEAC (FFQ and 24-HR) and diet-plasma NEAC, with and without the contribution of coffee’s NEAC. Partial correlation analysis was used to estimate correlations regardless of variables potentially influencing these relationships. FFQ-based NEAC and 24-HR-based NEAC were moderately correlated, with correlation coefficients ranging from 0.54 to 0.71, after controlling for energy intake, age and sex. Statistically significant positive correlations were found for dietary FRAP, either derived from the FFQ or the 24-HR, with plasma FRAP (r ~ 0.30). This weak, albeit statistically significant, correlation for FRAP was mostly present in the fruits and vegetables food groups. Plasma ORAC without proteins and 24-HR-based total ORAC were also positively correlated (r = 0.35). The relationship between dietary NEAC and plasma FRAP and ORAC suggests the dietary NEAC may reflect antioxidant status despite its weak in vivo potential, supporting further its use in oxidative stress-related disease epidemiology.

High-fat and low-fibre discretionary food intake and FTO genotype are each associated independently with higher risk of obesity. However, few studies have investigated links between obesity and dietary patterns based on discretionary food intake, and the interaction effect of FTO genotype are unknown. Thus, this study aimed to derive dietary patterns based on intake of discretionary foods, saturated fatty acids (SFA) and fibre, and examine cross-sectional associations with BMI and waist circumference (WC), and interaction effects of FTO genotype. Baseline data on 1280 adults from seven European countries were included (the Food4Me study). Dietary intake was estimated from a Food Frequency Questionnaire. Reduced rank regression was used to derive three dietary patterns using response variables of discretionary foods, SFA and fibre density. DNA was extracted from buccal swabs. Anthropometrics were self-measured. Linear regression analyses were used to examine associations between dietary patterns and BMI and WC, with an interaction for FTO genotype. Dietary pattern 1 (positively correlated with discretionary foods and SFA, and inversely correlated with fibre) was associated with higher BMI (β:0.64; 95% CI 0.44, 0.84) and WC (β:1.58; 95% CI 1.08, 2.07). There was limited evidence dietary pattern 2 (positively correlated with discretionary foods and SFA) and dietary pattern 3 (positively correlated with SFA and fibre) were associated with anthropometrics. FTO risk genotype was associated with higher BMI and WC, with no evidence of a dietary interaction. Consuming a dietary pattern low in discretionary foods and high-SFA and low-fibre foods is likely to be important for maintaining a healthy weight, regardless of FTO predisposition to obesity. Clinicaltrials.gov NCT01530139. Registered 9 February 2012 https://clinicaltrials.gov/ct2/show/NCT01530139

The present work aimed to delineate (i) a revised protocol according to recent methodological developments in evidence generation, to (ii) describe its interpretation, the assessment of the overall certainty of evidence and to (iii) outline an Evidence to Decision framework for deriving an evidence-based guideline on quantitative and qualitative aspects of dietary protein intake. A methodological protocol to systematically investigate the association between dietary protein intake and several health outcomes and for deriving dietary protein intake recommendations for the primary prevention of various non-communicable diseases in the general adult population was developed. The developed methodological protocol relies on umbrella reviews including systematic reviews with or without meta-analyses. Systematic literature searches in three databases will be performed for each health-related outcome. The methodological quality of all selected systematic reviews will be evaluated using a modified version of AMSTAR 2, and the outcome-specific certainty of evidence for systematic reviews with or without meta-analysis will be assessed with NutriGrade. The general outline of the Evidence to Decision framework foresees that recommendations in the derived guideline will be given based on the overall certainty of evidence as well as on additional criteria such as sustainability. The methodological protocol permits a systematic evaluation of published systematic reviews on dietary protein intake and its association with selected health-related outcomes. An Evidence to Decision framework will be the basis for the overall conclusions and the resulting recommendations for dietary protein intake.