A previous study showed that flesh quality of large yellow croaker (LYC) was improved by feeding dietary hydroxyproline (Hyp, 0·69 %). The aim of the present study was to explore the underlying mechanisms using transcriptomics and metabolomics analysis. The metabolomics analysis showed that muscle metabolite profiles could be clearly separated between the basal diet and Hyp supplementation diet. Metabolites including betaine, Hyp, lactate, glucose-6-phosphate, trimethylamine N-oxide, taurine, creatine, inosine monophosphate, histamine and serine made significant contribution to the separation. Compared with the control diet, the transcriptomics analysis identified a total of 334 different expressed genes, of which 298 genes were up-regulated and thirty-six genes were down-regulated in the Hyp supplementation group. The altered genes of the Hyp supplementation group were involved in collagen metabolism, lipid metabolism and energy metabolism. The integrated results revealed that the increased muscle collagen content in the Hyp supplementation diet was partly because of its enhancement of biosynthesis and the reduction of degradation. The improvement of muscle quality by dietary Hyp supplementation could also be related to a good utilisation of glucose through enhancement of glycolysis. It was concluded that dietary Hyp supplementation could improve flesh quality because of comprehensive metabolism changes including elevated collagen content, glycolysis, lipid metabolism and flesh flavour of LYC. The present study provided a novel strategy to understand the underlying molecular mechanism of flesh quality of LYC fed diet with Hyp supplementation.

The incidence of obesity and its metabolic complications are rapidly increasing and become a major public health issue. This trend is associated with an increase in the prevalence of non-alcoholic fatty liver disease (NAFLD), insulin resistance and diabetes. The sequence of events leading to NAFLD progression and mitochondrial dysfunction and their interrelation remains to be elucidated. This study aimed to explore the installation and progression of NAFLD and its association with the liver mitochondrial structure and activity changes in rats fed an obesogenic diet up to 20 weeks. Male Wistar rats were fed either a standard or high-fat–high-fructose (HFHFR) diet and killed on 4, 8, 12, 16 and 20 weeks of diet intake. Rats fed the HFHFR diet developed mildly overweight, associated with increased adipose tissue weight, hepatic steatosis, hyperglycaemia and hyperinsulinaemia after 8 weeks of HFHFR diet. Hepatic steatosis and many biochemical modifications plateaued at 8–12 weeks of HFHFR diet with slight amelioration afterwards. Interestingly, several biochemical and physiological parameters of mitochondrial function, as well as its phospholipid composition, in particular cardiolipin content, were tightly related to hepatic steatosis installation. These results showed once again the interrelation between hepatic steatosis development and mitochondrial activity alterations without being able to say whether the mitochondrial alterations preceded or followed the installation/progression of hepatic steatosis. Because both hepatic steatosis and mitochondrial alterations occurred as early as 4 weeks of diet, future studies should consider these four 1st weeks to reveal the exact interconnection between these major consequences of obesogenic diet intake.

Strenuous physical exercise and hyperthermia may paradoxically induce oxidative stress and adverse effects on myocardial function. The purpose of this study was to investigate the effect of 14-d coenzyme Q10 (CoQ10) supplementation and pre-cooling on serum creatine kinase-MB (CK-MB), cardiac Troponin I (cTnI), myoglobin (Mb), lactate dehydrogenase (LD), total antioxidant capacity (TAC), lipid peroxidation (LPO) and CoQ10 concentration in elite swimmers. In total, thirty-six healthy males (mean age 17 (sd 1) years) were randomly selected and divided into four groups of supplementation, supplementation with pre-cooling, pre-cooling and control. During an eighteen-session protocol in the morning and evening, subjects attended speed and endurance swimming training sessions for 5 km in each session. Blood sampling was done before (two stages) and after (two stages) administration of CoQ10 and pre-cooling. ANCOVA and repeated measurement tests with Bonferroni post hoc test were used for the statistical analysis of the data. There was no significant statistical difference among groups for the levels of CK-MB, cTnI, Mb, LD, TAC, LPO and CoQ10 at the presampling (stages 1 and 2) (P>0·05). However, pre-cooling and control groups show a significant increase in the levels of CK-MB, cTnI, Mb, LD and LPO compared with the supplementation and supplementation with pre-cooling groups in the post-sampling (stages 1 and 2) (P<0·05), except for the TAC and CoQ10. Consequently, CoQ10 supplementation prevents adverse changes of myocardial damage and oxidative stress during swimming competition phase. Meanwhile, the pre-cooling strategy individually has no desired effect on the levels of CK-MB, cTnI, Mb, LD, LPO, TAC and CoQ10.

Ca homoeostasis is important to human health and tightly controlled by powerful hormonal mechanisms that display ethnic variation. Ethnic variations could occur also in Arctic populations where the traditional Inuit diet is low in Ca and sun exposure is limited. We aimed to assess factors important to parathyroid hormone (PTH) and Ca in serum in Arctic populations. We included Inuit and Caucasians aged 50–69 years living in the capital city in West or in rural East Greenland. Lifestyle factors were assessed by questionnaires. The intake of Inuit diet was assessed from a FFQ. 25-Hydroxyvitamin D (25OHD2 and 25OHD3) levels were measured in serum as was albumin, Ca and PTH. The participation rate was 95 %, with 101 Caucasians and 434 Inuit. Median serum 25OHD (99·7 % was 25OHD3) in Caucasians/Inuit was 42/64 nmol/l (25, 75 percentiles 25, 54/51, 81) (P<0·001). Total Ca in serum was 2·33/2·29 mmol/l (25, 75 percentiles 2·26, 2·38/2·21, 2·36) (P=0·01) and PTH was 2·7/2·2 pmol/l (25, 75 percentiles 2·2, 4·1/1·7, 2·7) (P<0·001). The 69/97 Caucasians/Inuit with serum 25OHD <50 nmol/l differed in PTH (P=0·001) that rose with lower 25OHD levels in Caucasians, whereas this was not the case in Inuit. Ethnic origin influenced PTH (β=0·27, P<0·001) and Ca (β=0·22, P<0·001) in multivariate linear regression models after adjustment for age, sex, BMI, smoking, alcohol and diet. In conclusion, ethnic origin influenced PTH, PTH response to low vitamin D levels and Ca levels in populations in Greenland. Recommendations are to evaluate mechanisms underlying the ethnic influence on Ca homoeostasis and to assess the impact of transition in dietary habits on Ca homoeostasis and skeletal health in Arctic populations.

Polycystic ovary syndrome (PCOS) is one of the most common causes of infertility in women of reproductive age. Insulin resistance is a main pathophysiologic feature in these patients. According to some studies, the intake of probiotic bacteria may improve glucose homoeostasis. The aim of this study was to investigate the effect of synbiotics on metabolic parameters and apelin in PCOS patients. This randomised double-blind placebo-controlled trial was conducted on eighty-eight PCOS women aged 19–37 years old. The participants were randomly assigned to two groups receiving (1) synbiotic supplement (n 44), and (2) placebo (n 44) for 12 weeks. Fasting blood samples were taken at baseline and after 12 weeks. The two groups showed no difference in fasting blood sugar (adjusted mean difference: 0·60; 95 % CI −3·80, 5·00, P=0·727), plasma glucose fasting 2-h (adjusted mean difference 2·09; 95 % CI −9·96, 14·15, P=0·134), HbA1c (adjusted mean difference 0·06; 95 % CI −0·09, 0·22, P=0·959), homoeostatic model assessment-insulin resistance (HOMA-IR) (adjusted mean difference: 0·02; 95 % CI −0·99, 1·03, P=0·837), quantitative insulin sensitivity check index (QUICKI) (adjusted mean difference: −0·02; 95 % CI −0·33, 0·29, P=0·940) and C-reactive protein (CRP) (adjusted mean difference: 0·24; 95 % CI −1·61, 2·08, P=0·141) by the end of the intervention. A significant difference was observed in the mean apelin 36 before and after the intervention between synbiotic and placebo groups (adjusted mean difference: −4·05; 95 % CI −7·15, −0·96, P=0·004). A 12-week synbiotic supplementation has no significant beneficial effects on HOMA-IR and CRP in PCOS patients, whereas the level of apelin 36 significantly decreased.

Environmental enteric dysfunction (EED) and systemic inflammation (SI) are common in developing countries and may cause stunting. In Bangladesh, >40 % of preschool children are stunted, but EED and SI contributions are unknown. We aimed to determine the impact of EED and SI (assessed with multiple indicators) on growth in children (n 539) enrolled in a community-based randomised food supplementation trial in rural Bangladesh. EED was defined with faecal myeloperoxidase, α-1 antitrypsin and neopterin and serum endotoxin core antibody and glucagon-like peptide-2, consolidated into gut inflammation (GI) and permeability (GP) scores, and urinary lactulose:mannitol α-1 acid glycoprotein (AGP) characterised SI. Biomarker associations with anthropometry (15-, 18- and 24-month length-for-age (LAZ), weight-for-length (WLZ) and weight-for-age (WAZ) z scores) were examined in pairwise correlations and adjusted mixed-effects regressions. Stunting, wasting and underweight prevalence at 18 months were 45, 15 and 37 %, respectively, with elevated EED and SI markers common. EED and SI were not associated with 15–24-month length trajectory. Elevated (worse) GI and GP scores predicted reduced 18–24-month WLZ change (β −0·01 (se 0·00) z score/month for both). Elevated GP was also associated with reduced 15–18-month WLZ change (β −0·03 (se 0·01) z score/month) and greater 15-month WLZ (β 0·16 (se 0·05)). Higher AGP was associated with reduced prior and increased subsequent WLZ change (β −0·04 (se 0·01) and β 0·02 (se 0·00) z score/month for 15–18 and 18–24 months). The hypothesised link from EED to stunting was not observed in this sample of Bangladeshi 18-month-olds, but the effects of EED on constrained weight gain may have consequences for later linear growth or for other health and development outcomes.

Elevated circulating cholesterol levels are a risk factor for CVD which is also associated with sub-optimal vascular function. There is emerging evidence that anthocyanins can cause beneficial cardio-protective effects by favourably modulating lipoprotein profiles. We compared the effects of blood orange juice which is rich in anthocyanins and blonde orange juice without anthocyanins on LDL-cholesterol and other biomarkers of CVD risk, vascular function and glycaemia. In all, forty-one participants (aged 25–84 years) with a waist circumference >94 cm (men) and >80 cm (women) completed a randomised, open label, two-arm cross-over trial. For 28 d participants ingested (i) 500 ml blood orange juice providing 50 mg anthocyanins/d and (ii) 500 ml blonde orange juice without anthocyanins. There was a minimum 3-week washout period between treatments. LDL-cholesterol and other biomarkers associated with CVD risk and glycaemia were assessed at the start and end of each treatment period. No significant differences were observed in total, HDL- and LDL-cholesterol, TAG, glucose, fructosamine, nitric oxide, C-reactive protein, aortic systolic blood pressure and diastolic blood pressure or carotid-femoral and brachial-ankle pulse wave velocity after 28 d ingestion of blood orange juice compared with standard orange juice. The lack of effect on LDL-cholesterol may be due to the modest concentration of anthocyanins in the blood orange juice.

We investigated the effects of high-Ca fat-free milk phase (MD) (prescription of approximately 1500 mg of Ca/d) v. low-Ca phase (CD) (prescription of approximately 800 mg of Ca/d) in an energy-restricted diet on the metabolic syndrome (MetS) and cardiometabolic measures in individuals with type 2 diabetes mellitus (T2DM) and low habitual Ca consumption (<600 mg/d). In this randomised cross-over design, fourteen adults with T2DM (49·5 (sd 8·6) years, BMI 29·4 (sd 4·5) kg/m2) consumed either MD or CD for 12 weeks, with a washout of 18 weeks between phases. A breakfast shake containing 700 mg (MD) or 6·4 mg (CD) of Ca was consumed in the laboratory. In addition, energy-restricted diets were prescribed (800 mg of dietary Ca/d). Waist circumference (WC), fasting glucose, fasting TAG, systolic (SBP) and diastolic blood pressure (DBP), fasting total cholesterol, fasting LDL-cholesterol, fasting HDL-cholesterol, HDL:LDL ratio, HDL:TAG ratio and lipid accumulation product (LAP) index were assessed at baseline and after each phase. Ca consumption during the study was equivalent to 1200 mg/d during MD and 525 mg/d during CD. There was a greater reduction in WC, SBP, DBP and LAP index after MD compared with CD. HDL:LDL ratio increased and total cholesterol, LDL-cholesterol, SBP, DBP and LAP index decreased only in MD. The consumption of approximately 1200 mg of Ca/d (700 mg from fat-free milk+500mg from other dietary sources) associated with an energy-restricted diet decreased some of the MetS components and cardiometabolic measures in adults with T2DM.

Insufficient vitamin D status (serum 25-hydroxyvitamin D (S-25(OH)D)<50 nmol/l) is common among immigrants living at the northern latitudes. We investigated ethnic differences in response of S-25(OH)D to vitamin D3 supplementation, through a 5-month randomised controlled trial, in East African and Finnish women in Southern Finland (60°N) from December 2014 to May 2015. Vitamin D intakes (dietary and supplemental) were also examined. Altogether, 191 subjects were screened and 147 women (East Africans n 72, Finns n 75) aged 21–64 years were randomised to receive placebo or 10 or 20 µg of vitamin D3/d. S-25(OH)D concentrations were assessed by liquid chromatography–tandem MS. At screening, 56 % of East Africans and 9 % of Finns had S-25(OH)D<50 nmol/l. Total vitamin D intake was higher in East Africans than in Finns (24·2 (sd 14·3) v. 15·2 (sd 13·4) µg/d, P<0·001). Baseline mean S-25(OH)D concentrations were higher in Finns (60·5 (sd=16·3) nmol/l) than in East Africans (51·5 (sd 15·4) nmol/l) (P=0·001). In repeated-measures ANCOVA (adjusted for baseline S-25(OH)D), mean S-25(OH)D increased by 8·5 and 10·0 nmol/l with a 10-µg dose and by 10·7 and 17·1 nmol/l with a 20-µg dose for Finns and East Africans, respectively (P>0·05 for differences between ethnic groups). In conclusion, high prevalence of vitamin D insufficiency existed among East African women living in Finland, despite higher vitamin D intake than their Finnish peers. Moderate vitamin D3 supplementation was effective in increasing S-25(OH)D in both groups of women, and no ethnic differences existed in the response to supplementation.

Previous studies show associations between dairy product consumption and type 2 diabetes, but only a few studies conducted detailed analyses for a variety of dairy subgroups. Therefore, we examined cross-sectional associations of a broad variety of dairy subgroups with pre-diabetes and newly diagnosed type 2 diabetes (ND-T2DM) among Dutch adults. In total, 112 086 adults without diabetes completed a semi-quantitative FFQ and donated blood. Pre-diabetes was defined as fasting plasma glucose (FPG) between 5·6 and 6·9 mmol/l or HbA1c% of 5·7–6·4 %. ND-T2DM was defined as FPG ≥7·0 mmol/l or HbA1c ≥6·5 %. Logistic regression analyses were conducted by 100 g or serving increase and dairy tertiles (T1ref), while adjusting for demographic, lifestyle and dietary covariates. Median dairy product intake was 324 (interquartile range 227) g/d; 25 549 (23 %) participants had pre-diabetes; and 1305 (1 %) had ND-T2DM. After full adjustment, inverse associations were observed of skimmed dairy (OR100 g 0·98; 95 % CI 0·97, 1·00), fermented dairy (OR100 g 0·98; 95 % CI 0·97, 0·99) and buttermilk (OR150 g 0·97; 95 % CI 0·94, 1·00) with pre-diabetes. Positive associations were observed for full-fat dairy (OR100 g 1·003; 95 % CI 1·01, 1·06), non-fermented dairy products (OR100 g 1·01; 95 % CI 1·00, 1·02) and custard (ORserving/150 g 1·13; 95 % CI 1·03, 1·24) with pre-diabetes. Moreover, full-fat dairy products (ORT3 1·16; 95 % CI 0·99, 1·35), non-fermented dairy products (OR100 g 1·05; 95 % CI 1·01, 1·09) and milk (ORserving/150 g 1·08; 95 % CI 1·02, 1·15) were positively associated with ND-T2DM. In conclusion, our data showed inverse associations of skimmed and fermented dairy products with pre-diabetes. Positive associations were observed for full-fat and non-fermented dairy products with pre-diabetes and ND-T2DM.

Accumulating evidence indicates that saturated fat intake is related to mortality risk increase, whereas unsaturated fat intake is associated with reduced mortality risk. The aim of the present study was to estimate the mortality risk reduction related to a dietary change from saturated fat to mono- or polyunsaturated fat intake. The American National Health and Nutrition Examination Surveys conducted between 1999 and 2010 were linked to the 2011 national US death registry resulting in an observational prospective mortality study. Proportional hazards Cox models were used to evaluate the association between saturated, monounsaturated and polyunsaturated fat with all-cause and cause-specific mortality. Substitution analysis was conducted to estimate an iso-energetic substitution of 10 % of the energy from dietary fat intake applied to the substitution of saturated fat with an equal amount of energy from monounsaturated or polyunsaturated fat. The highest tertile intakes of saturated fat resulted in an increased risk (12 %) of all-cause and specific-cause mortality, whereas the highest tertile intakes of polyunsaturated fat resulted in a reduced risk (7 %) of all-cause and specific-cause mortality when compared with the corresponding lowest tertile. Iso-energetic substitution revealed that a substitution of 10 % of energy (from total fat) from saturated fat to an equal amount of energy from monounsaturated or polyunsaturated fat resulted in a significant reduction of the mortality risk ranging from 4 to 8 %. Iso-energetic substitution of saturated fat with monounsaturated and polyunsaturated fat reduced all-cause and specific-cause mortality in US adults.

Few studies have investigated the effect of maternal factors on child eating practices. Our study aimed to explore mother–child dietary behaviours and their associations with socio-demographic factors. A cross-sectional analysis was conducted using data from control participants (n 243) in the Healthy Beginnings Trial, which involved first-time mothers and their 2-year-old children. Mother–child dietary behaviours were assessed using short dietary questions (short FFQ) and their associations with socio-demographic factors were examined using binary logistic regression. The dietary intake of 2-year-old children was characterised by low vegetable consumption and high discretionary food intake. In multivariate analysis, lower-income mothers (<Australian $40 000 per annum) reported their child was more likely to consume less fruit (<1 serve/d) (adjusted OR (AOR): 5·83; 95 % CI 1·49, 22·80) and ate hot chips more frequently (≥2 times/week) (AOR: 4·80; 95 % CI 1·28, 18·04), compared with higher-income mothers (≥Australian $40 000 per annum). Younger mothers (<25 years) reported their child consumed more sugary drinks and soft drink (>0·5 cups/d) AOR 2·93 (95 % CI 1·03, 8·35), compared with older mothers (≥25 years). Non-Australian-born mothers reported their child consumed more fruit juice (>0·5 cups/d) AOR 2·04 (95 % CI 1·02, 4·05), sweet snacks AOR 1·96 (95 % CI 1·02, 3·76) and fast food (≥2 times/week) AOR 3·67 (95 % CI 1·29, 10·43) compared with Australian-born mothers. Significant positive correlations between maternal and child dietary intake were observed for all dietary variables except milk, with the largest association for fast foods (Pearson’s r 0·52, P<0·001). This study shows that maternal factors are associated with child dietary behaviours. Targeting young mothers (<25 years) of potential disadvantage, before commencement of early feeding practices, has the potential to improve children’s diets.

Recent evidence has raised the possibility of the existence of a sixth taste modality – that is, taste for fat – which is mediated by lingual CD36 and plays a role in obesity. Consequently, the genetic polymorphism of CD36 has been shown to be associated with altered oro-sensory detection of dietary lipids. In the present study, we investigated the relationship between oro-sensory perception of linoleic acid (LA), two CD36 polymorphisms (rs1527483 and rs3212018), obesity parameters and craving habits for dietary lipids in young Czech adults. We also sequenced 5 and 6 exons of CD36 to trace out any new mutation that might be responsible for the difference in taste perception. We observed that craving for dietary lipids was correlated with anthropometric parameters (P<0·05) and LA detection threshold (P=0·033). The participants with the CC genotype of the rs1527483 polymorphism had lower BMI (P=0·011), waist circumference (P=0·005), waist:height ratio (P=0·010) and higher sensitivity for LA (P=0·037) than the participants with the CT and TT genotypes. Interestingly, we did not observe any association between the rs3212018 polymorphism and the studied parameters. Moreover, we did not observe any mutation in exons 5 and 6 of the CD36 gene in these subjects. Finally, we can state that rs1527483, but not rs3212018, is associated with high body weight in young Czech subjects.