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This review intends to act as an overview of fructose malabsorption (FM) and its role in the aetiology of diseases including, but not limited to, irritable bowel syndrome (IBS) and infantile colic and the relationship between fructose absorption and the propagation of some cancers. IBS results in a variety of symptoms including stomach pains, cramps and bloating. Patients can be categorised into two groups, depending on whether the patients’ experiences either constipation (IBS-C) or diarrhoea (IBS-D). FM has been proposed as a potential cause of IBS-D and other diseases, such as infantile colic. However, our knowledge of FM is limited by our understanding of the biochemistry related to the absorption of fructose in the small intestine and FM’s relationship with small intestinal bacterial overgrowth. It is important to consider the dietary effects on FM and most importantly, the quantity of excess free fructose consumed. The diagnosis of FM is difficult and often requires indirect means that may result in false positives. Current treatments of FM include dietary intervention, such as low fermentable oligo-, di-, monosaccharides and polyols diets and enzymatic treatments, such as the use of xylose isomerase. More research is needed to accurately diagnose and effectively treat FM. This review is designed with the goal of providing a detailed outline of the issues regarding the causes, diagnosis and treatment of FM.
The study was conducted to determine the effects of three dietary Se sources, such as sodium-selenite (S-S), seleno-yeast (S-Y) and seleno-methionine (S-M), on Se concentration, glutathione peroxidase (GPX) and TXNRD activities, and mRNA expression of fifteen representative selenoproteins, and protein expression of four endoplasmic reticulum-resided selenoproteins in a wide range of tissues of yellow catfish. Compared with S-S and S-M groups, dietary S-Y significantly decreased growth performance and feed utilisation of yellow catfish. Dietary Se sources significantly influenced Se contents in the spleen, dorsal muscle and the kidney, GPX activities in spleen, kidney, intestine, muscle and mesenteric fat, and TXNRD activities in the heart, intestine and mesenteric fat. Among ten tested tissues, dietary Se sources influenced mRNA expression of GPX4 and SELENOK in three tissues; GPX3, SELENOS and TXNRD2 in four tissues; SELENOF, SELENON and DIO2 in five tissues; SELENOM, GPX1/2 and TXNRD3 in six tissues; SELENOW in seven tissue and SELENOP and SELENOT in eight tissues. Based on these observations above, S-S and S-M seem to be suitable Se sources for improving growth performance and feed utilisation of yellow catfish. Dietary Se sources differentially influence the expression of selenoproteins in various tissues of yellow catfish. For the first time, we determined the expression of selenoproteins in fish in responses to dietary Se sources, which contributes to a better understanding of the functions and regulatory mechanisms of selenoporteins.
Diets varying in SFA and MUFA content can impact glycaemic control; however, whether underlying differences in genetic make-up can influence blood glucose responses to these dietary fatty acids is unknown. We examined the impact of dietary oils varying in SFA/MUFA content on changes in blood glucose levels (primary outcome) and whether these changes were modified by variants in the stearoyl-CoA desaturase (SCD) gene (secondary outcome). Obese men and women participating in the randomised, crossover, isoenergetic, controlled-feeding Canola Oil Multicenter Intervention Trial II consumed three dietary oils for 6 weeks, with washout periods of ˜6 weeks between each treatment. Diets studied included a high SFA/low MUFA Control oil (36·6 % SFA/28·2 % MUFA), a conventional canola oil (6·2 % SFA/63·1 % MUFA) and a high-oleic acid canola oil (5·8 % SFA/74·7 % MUFA). No differences in fasting blood glucose were observed following the consumption of the dietary oils. However, when stratified by SCD genotypes, significant SNP-by-treatment interactions on blood glucose response were found with additive models for rs1502593 (P = 0·01), rs3071 (P = 0·02) and rs522951 (P = 0·03). The interaction for rs3071 remained significant (P = 0·005) when analysed with a recessive model, where individuals carrying the CC genotype showed an increase (0·14 (sem 0·09) mmol/l) in blood glucose levels with the Control oil diet, but reductions in blood glucose with both MUFA oil diets. Individuals carrying the AA and AC genotypes experienced reductions in blood glucose in response to all three oils. These findings identify a potential new target for personalised nutrition approaches aimed at improving glycaemic control.
SCFA increase serotonin (5-hydroxytryptamine, 5-HT) synthesis and content in the colon in vitro and ex vivo, but little is known in vivo. We tested whether dietary indigestible saccharides, utilised as a substrate to produce SCFA by gut microbiota, would increase colonic 5-HT content in mice. Male C57BL/6J mice were fed a purified diet and water supplemented with 4 % (w/v) 1-kestose (KES) for 2 weeks. Colonic 5-HT content and enterochromaffin (EC) cell numbers were lower in mice supplemented with KES than those without supplementation, while monoamine oxidase A activity and mRNA levels of tryptophan hydroxylase 1 (Tph1), chromogranin A (Chga), Slc6a4 and monoamine oxidase A (Maoa) genes in the colonic mucosa, serum 5-HT concentration and total 5-HT content in the colonic contents did not differ between groups. Caecal acetate concentration and Bifidobacterium pseudolongum population were higher in KES-supplemented mice. Similar trends were observed in mice supplemented with other indigestible saccharides, that is, fructo-oligosaccharides, inulin and raffinose. Intragastric administration of live B. pseudolongum (108 colony-forming units/d) for 2 weeks reduced colonic 5-HT content and EC cell numbers. These results suggest that changes in synthesis, reuptake, catabolism and overflow of 5-HT in the colonic mucosa are not involved in the reduction of colonic 5-HT content by dietary indigestible saccharides in mice. We propose that gut microbes including B. pseudolongum could contribute to the reduction of 5-HT content in the colonic mucosa via diminishing EC cells.
This work aimed to evaluate the effects of whey protein concentrate (WPC) admixtured of curcumin on metabolic control, inflammation and oxidative stress in Wistar rats submitted to exhaustive exercise. A total of forty-eight male rats were divided into six experimental groups (n 8): standard diet group (AIN-93M), standard diet submitted to exhaustion test group (AIN-93M ET), WPC admixtured of curcumin group (WPC + CCM), WPC + CCM submitted to exhaustion test group (WPC + CCM ET), CCM group and CCM subjected to exhaustion test group (CCM ET). The swimming exhaustion test was performed after 4 weeks of experiment. The consumption of WPC + CCM as well as isolated CCM did not alter the biometric measurements, the animals’ food consumption and the hepatic and kidney function, as well as the protein balance of the animals (P > 0·05), but reduced the glycaemia and the gene expression of TNF-α and IL-6 and increased the expression of IL-10 (P < 0·05). The animals that were submitted to the exhaustion test (AIN-93M ET) showed higher aspartate aminotransferase values when compared to the animals that did not perform the exercise (AIN-93 M) (P < 0·05). WPC + CCM reduced the concentration of nitric oxide, carbonylated protein and increased the concentration of catalase (P < 0·05). Both (WPC + CCM and CCM) were able to increase the concentrations of superoxide dismutase (P < 0·05). We concluded that the WPC admixtured of CCM represents a strategy capable of decreasing blood glucose and oxidative and inflammatory damage caused by exhaustive physical exercise in swimming.
Linoleic acid (LA), an essential n-6 fatty acid (FA), is critical for fetal development. We investigated the effects of maternal high LA (HLA) diet on offspring cardiac development and its relationship to circulating FA and cardiovascular function in adolescent offspring, and the ability of the postnatal diet to reverse any adverse effects. Female Wistar Kyoto rats were fed low LA (LLA; 1·44 % energy from LA) or high LA (HLA; 6·21 % energy from LA) diets for 10 weeks before pregnancy and during gestation/lactation. Offspring, weaned at postnatal day 25, were fed LLA or HLA diets and euthanised at postnatal day 40 (n 6–8). Maternal HLA diet decreased circulating total cholesterol and HDL-cholesterol in females and decreased total plasma n-3 FA in males, while maternal and postnatal HLA diets decreased total plasma n-3 FA in females. α-Linolenic acid (ALA) and EPA were decreased by postnatal but not maternal HLA diets in both sexes. Maternal and postnatal HLA diets increased total plasma n-6 and LA, and a maternal HLA diet increased circulating leptin, in both male and female offspring. Maternal HLA decreased slopes of systolic and diastolic pressure–volume relationship (PVR), and increased cardiac Col1a1, Col3a1, Atp2a1 and Notch1 in males. Maternal and postnatal HLA diets left-shifted the diastolic PVR in female offspring. Coronary reactivity was altered in females, with differential effects on flow repayment after occlusion. Thus, maternal HLA diets impact lipids, FA and cardiac function in offspring, with postnatal diet modifying FA and cardiac function in the female offspring.
In 2010, British Journal of Nutrition published a consensus review article entitled Prebiotic effects: metabolic and health benefits(1). This was commissioned by International Life Sciences Institute, Europe and had twenty-one co-authors. The current article summarises how this review was planned and written. It deals with three questions regarding the context/background of the paper; what it told us and what happened next.
The objective of this study is to investigate the effects of vitamin A, D and their interaction on the glycaemic control in patients with both diabetes and tuberculosis. Tuberculosis infection and its treatment induce hyperglycaemia and complicate the glycaemic control in patients with diabetes. A randomised controlled trial with a 2 × 2 factorial design was conducted in a tuberculosis-specialised hospital in Qingdao, China. A total of 279 patients who have both diabetes and tuberculosis were included in this analysis. The patients received standard anti-tuberculosis treatment alone (control group), or together with a dose of vitamin A (600 μg RAE/d) or vitamin D (10 μg/d) or a combination of vitamin A (600 μg RAE/d) and vitamin D (10 μg/d) for 2 months. The effects of the intervention on fasting plasma glucose and 2-h postprandial blood glucose were investigated by ANCOVA. The analysis was adjusted for baseline values, age, sex, smoking, drinking and antidiabetic treatment as covariates. No significant effect was observed for vitamin A and D supplementation on fasting plasma glucose, 2-h postprandial blood glucose, BMI and related blood parameters. No interaction was observed between vitamin A and D supplementation for these endpoints. Vitamin A and D supplementation showed a null effect on the glycaemic control for patients with concurrent diabetes and tuberculosis. Future work should evaluate the effect of vitamin A and D supplementation on insulin-related indices for these patients and investigate the effect of vitamin D receptor genotypes.
Recent studies found positive associations between intake of red meat and processed meat and total mortality; however, substitution of red meat with poultry and fish has been poorly investigated. We aimed to investigate associations for substitutions of red meat (unprocessed/processed) and total mortality and deaths due to cancer or CVD. We used data from the Danish Diet, Cancer and Health cohort, including 57 053 participants aged 50–64 years at baseline. Information on diet was collected through a validated 192-item FFQ. Information regarding total mortality, deaths due to cancer and deaths due to CVD was obtained by record linkage. Cox proportional hazards models were used to estimate the hazard ratio (HR) of 150 g/week substitutions of red meat with poultry or fish. During a follow-up (mean 16·1 years), 8840 deaths occurred (4567 were due to cancer; 1816 due to CVD). The adjusted HR for total death when substituting 150 g/week total red meat with poultry was 0·96 (95 % CI 0·95, 1·00) and with fish 0·99 (95 % CI 0·97, 1·01). Corresponding HR for cancer death or CVD death were similar. Substitution of processed red meat with fish or poultry was more consistently associated with a lower mortality than substitution of unprocessed red meat. For example, the adjusted HR for total death when substituting 150 g/week processed red meat with poultry was 0·95 (95 % CI 0·92, 0·98). We found that replacing processed red meat with poultry or fish was associated with a lower risk of total mortality and deaths due to cancer, but not deaths due to CVD.
To alleviate the re-emergence of iodine deficiency in New Zealand, two strategies, the mandatory fortification of bread with iodised salt (2009) and a government-subsidised iodine supplement for breast-feeding women (2010), were introduced. Few studies have investigated mother and infant iodine status during the first postpartum year; this study aimed to describe iodine status of mothers and infants at 3, 6 and 12 months postpartum (3MPP, 6MPP and 12MPP, respectively). Partitioning of iodine excretion between urine and breast milk of exclusive breast-feeding (EBF) women at 3MPP was determined. In total, eighty-seven mother–infant pairs participated in the study. Maternal and infant spot urinary iodine concentration (UIC) and breast milk iodine concentration (BMIC) were determined. The percentage of women who took iodine-containing supplements decreased from 46 % at 3MPP to 6 % at 12MPP. Maternal median UIC (MUIC) at 3MPP (82 (46, 157) µg/l), 6MPP (85 (43, 134) µg/l) and 12MPP (95 (51, 169) µg/l) were <100 µg/l. The use of iodine-containing supplements increased MUIC and BMIC only at 3MPP. Median BMIC at all time points were below 75 µg/l. Infant MUIC at 3MPP (115 (69, 182) µg/l) and 6MPP (120 (60, 196) µg/l) were below 125 µg/l. Among EBF women at 3MPP, an increased partitioning of iodine into breast milk (highest proportion 60 %) was shown at lower iodine intakes, along with a reduced fractional iodine excretion in urine (lowest proportion 40 %), indicating a protective mechanism for breastfed infants’ iodine status. In conclusion, this cohort of postpartum women was iodine-deficient. Iodine status of their breastfed infants was suboptimal. Lactating women who do not consume iodine-rich foods and those who become pregnant again should take iodine-containing supplements.
Inadequate nutrition during a critical period of development – as is the case during gestation and the first days of life, especially in very-low-birth-weight (VLBW) infants, can impact on neurodevelopment and favour co-morbidities. In this study, we evaluate how neurodevelopment may be affected by intra-uterine growth (IUGR) restriction and by an inadequate intake of nutritional energy during the early neonatal period. A longitudinal cohort study was conducted to analyse the nutritional contributions received during the first week of life, among a population of 396 VLBW infants. Motor, cognitive, sensory and behavioural development was assessed at 14, 25, 33 and 50 months. The association between IUGR, postnatal energy restriction and neurodevelopment was examined using multivariate logistic regression techniques. Mild cognitive delay was observed in 35·6 % of neonates with IUGR and in 24 % of those with appropriate birth weight. IUGR is associated with behavioural disorder (OR 2·60; 95 % CI 1·25, 5·40) and delayed cognitive development (OR 2·64; 95 % CI 1·34, 5·20). Energy restriction during the first week of life is associated with visual deficiency (OR 2·96; 95 % CI 1·26, 6·84) and cerebral palsy (OR 3·05; CI 95 % 1·00, 9·54). In VLBW infants, IUGR is associated with behavioural disorder, while postnatal energy restriction is significantly associated with motor disorder, infantile cerebral palsy and sensory disorder.
Spot urinary polyphenols have potential as a biomarker of polyphenol-rich food intakes. The aim of this study is to explore the relationship between spot urinary polyphenols and polyphenol intakes from polyphenol-rich food sources. Young adults (18–24 years old) were recruited into a sub-study of an online intervention aimed at improving diet quality. Participants’ intake of polyphenols and polyphenol-rich foods was assessed at baseline and 3 months using repeated 24-h recalls. A spot urine sample was collected at each session, with samples analysed for polyphenol metabolites using LC-MS. To assess the strength of the relationship between urinary polyphenols and dietary polyphenols, Spearman correlations were used. Linear mixed models further evaluated the relationship between polyphenol intakes and urinary excretion. Total urinary polyphenols and hippuric acid (HA) demonstrated moderate correlation with total polyphenol intakes (rs = 0·29–0·47). HA and caffeic acid were moderately correlated with polyphenols from tea/coffee (rs = 0·26–0·46). Using linear mixed models, increases in intakes of total polyphenols or polyphenols from tea/coffee or oil resulted in a greater excretion of HA, whereas a negative relationship was observed between soya polyphenols and HA, suggesting that participants with higher intakes of soya polyphenols had a lower excretion of HA. Findings suggest that total urinary polyphenols may be a promising biomarker of total polyphenol intakes foods and drinks and that HA may be a biomarker of total polyphenol intakes and polyphenols from tea/coffee. Caffeic acid warrants further investigation as a potential biomarker of polyphenols from tea/coffee.
Healthy Nordic diet has been beneficially associated with CHD risk factors, but few studies have investigated risk of developing CHD. We investigated the associations of healthy Nordic diet with major CHD risk factors, carotid atherosclerosis and incident CHD in middle-aged and older men from eastern Finland. A total of 1981 men aged 42–60 years and free of CHD at baseline in 1984–1989 were investigated. Diet was assessed with 4-d food recording and the healthy Nordic diet score was calculated based on the Baltic Sea Diet Score. Carotid atherosclerosis was assessed by ultrasonography of the common carotid artery intima–media thickness in 1053 men. ANCOVA and Cox proportional hazards regression analyses were used for analyses. Healthy Nordic diet score was associated with lower serum C-reactive protein (CRP) concentrations (multivariable-adjusted extreme-quartile difference 0·66 mg/l, 95 % CI 0·11, 1·21 mg/l) but not with serum lipid concentrations, blood pressure or carotid atherosclerosis. During the average follow-up of 21·6 years (sd 8·3 years), 407 men had a CHD event, of which 277 were fatal. The multivariable-adjusted hazard ratios in the lowest v. the highest quartile of the healthy Nordic diet score were 1·15 (95 % CI 0·87, 1·51) for any CHD event (Ptrend 0·361) and 1·44 (95 % CI 0·99, 2·08) (Ptrend 0·087) for fatal CHD event. We did not find evidence that adherence to a healthy Nordic diet would be associated with a lower risk of CHD or with carotid atherosclerosis or major CHD risk factors, except for an inverse association with serum CRP concentrations.
Current cancer prevention recommendations advise limiting red meat intake to <500 g/week and avoiding consumption of processed meat, but do not differentiate the source of processed meat. We examined the associations of processed meat derived from red v. non-red meats with cancer risk in a prospective cohort of 26 218 adults who reported dietary intake using the Canadian Diet History Questionnaire. Incidence of cancer was obtained through data linkage with Alberta Cancer Registry with median follow-up of 13·3 (interquartile range (IQR) 5·1) years. Multivariable Cox proportional hazards regression models were adjusted for covariates and stratified by age and sex. The median consumption (g/week) of red meat, processed meat from red meat and processed meat from non-red meat was 267·9 (IQR 269·9), 53·6 (IQR 83·3) and 11·9 (IQR 31·8), respectively. High intakes (4th Quartile) of processed meat from red meat were associated with increased risk of gastrointestinal cancer adjusted hazard ratio (AHR): 1·68 (95 % CI 1·09, 2·57) and colorectal cancers AHR: 1·90 (95 % CI 1·12, 3·22), respectively, in women. No statistically significant associations were observed for intakes of red meat or processed meat from non-red meat. Results suggest that the carcinogenic effect associated with processed meat intake may be limited to processed meat derived from red meats. The findings provide preliminary evidence towards refining cancer prevention recommendations for red and processed meat intake.
Non-communicable diseases, such as cancers and CVD, represent a major public health concern, and diet is an important factor in their development. French dietary recommendations were updated in 2017, and an adherence score, the Programme National Nutrition Santé Guidelines Score (PNNS-GS2), has been developed and validated using a standardised procedure. The present study aimed to analyse the prospective association between PNNS-GS2 and the risk of death, cancer and CVD. Our sample consisted of French adults included in the prospective NutriNet-Santé cohort (n 67 748, 75 634 and 80 269 for the risk of death, cancer and CVD, respectively). PNNS-GS2 (range: –∞ to 14·25) was calculated from the 24-h dietary records of the first 2 years of monitoring. Association between PNNS-GS2 (in quintiles, Q) and the risk of death, cancer and CVD was studied using Cox models adjusted for the main confounding factors. The sample included 78 % of women, aged on average 44·4 years (sd 14·6) with on average 6·6 (sd 2·3) dietary records. Average PNNS-GS2 was 1·5 (sd 3·4) and median follow-up was 6·6 years for cancers and 6·2 years for CVD and deaths. PNNS-GS2 was significantly associated with the risk of death (hazard ratio (HR)Q5vsQ1: 0·77 (95 % CI 0·60, 1·00), 828 cases), cancer (HRQ5vsQ1 = 0·80 (95 % CI 0·69, 0·92), 2577 cases) and CVD (HRQ5vsQ1 0·64 (95 % CI 0·51, 0·81), 964 cases). More specifically, PNNS-GS2 was significantly associated with colorectal and breast cancer risks but not prostate cancer risk. Our results suggest that strong adherence to the 2017 French dietary recommendations is associated with a lower risk of death, cancer or CVD. This reinforces the validity of these new recommendations and will help to promote their dissemination.
We aim to determine the association between Fe status and the metabolic syndrome (MetS) during menopause. Records of 1069 premenopausal and 703 postmenopausal Korean women were retrieved from the database of the fifth Korean National Health and Nutrition Examination Survey (KNHANES V 2012) and analysed. The association between the MetS and Fe status was performed using multivariable-adjusted analyses, subsequently develop a prediction model for the MetS by margin effects. We found that the risk of Fe depletion among postmenopausal women was lower than premenopausal women (PR = 0·813, 95 % CI 0·668, 0·998, P = 0·038). The risk of the MetS was 2·562-fold lower among premenopausal women with than without Fe depletion (PR = 0·390, 95 % CI 0·266, 0·571, P < 0·001). In contrast, the risk of the MetS tended to be higher among postmenopausal women with than without Fe depletion (PR = 1·849, 95 % CI 1·406, 2·432, P < 0·001). When the serum ferritin levels increased, the risk of the MetS increased in both premenopausal women and postmenopausal women. The margin effects showed that an increase in serum Hb and ferritin was associated with an increase in the risk of the MetS according to menopausal status and age group. Therefore, ferritin is the most validated and widely used Fe marker, could be a potential clinical value in predicting and monitoring the MetS during menopause. Further prospective or longitudinal studies, especially, clinically related studies on menopause and Fe status, are needed to clarify the causality between serum ferritin levels and the MetS that could offer novel treatments for the MetS.