Nutri-Score of Meat, Fish, and Dairy Alternatives: A Comparison between the Old and New Algorithm.

Nutri-Score is a front-of-pack label that visualizes the nutritional quality of food products from most healthy (A, dark green) to least healthy (E, red). However, concerns have been raised about discrepancies between Nutri-Score labels and dietary recommendations. Therefore, the Nutri-Score algorithm has recently been adapted. To investigate the effect of the new algorithm, the Nutri-Score of plant-based meat, fish, and dairy alternatives (n = 916) was calculated with the old and new algorithms. In addition, the nutritional values of meat and milk alternatives with Nutri-Score labels A and B were compared under the old and new conditions and subsequently assessed for alignment with the criteria of Dutch dietary guidelines. The new algorithm resulted in a reduction in the number of products with labels A and B, ranging from 5% (cold cuts alternatives) to 55% (milk alternatives). The nutritional composition of products with labels A and B improved for meat alternatives (lower energy and saturated fatty acid contents; higher protein content) and milk alternatives (lower energy, salt, and sugar contents; higher protein and fiber contents). Overall, the new Nutri-Score algorithm is more in line with the Dutch dietary guidelines for plant-based meat and dairy alternatives, though challenges remain with respect to micronutrient (iron, calcium, vitamin B12), salt, and protein contents.

Cross-Sectional Study to Map Nutritional Quality of Meat, Fish, and Dairy Alternatives in Dutch Supermarkets According to the Dutch Food-Based Dietary Guidelines and Nutri-Score.

Due to a growing challenge to feed the world's population and an increased awareness to minimize the impact of our food choices on climate change, a more plant-based diet has gained popularity with a growing number of plant-based products on the market. To stimulate a plant-based diet that also improves long-term health, data are needed to monitor whether these products are healthy alternatives to animal-based foods. Therefore, this study inventoried 916 plant-based meat, fish, and dairy alternatives from eight Dutch supermarkets. The nutritional quality of each product was assessed by (1) the Dutch food-based dietary guidelines and (2) the Nutri-Score. The results show that over 70% of meat, fish, and dairy alternatives have an A/B Nutri-Score (indicating high nutritional quality), but do not comply with the Dutch dietary guidelines. This is mainly due to high salt and low vitamin B12 and iron content (meat and fish alternatives) or low protein and calcium levels (dairy alternatives). In conclusion, the majority of plant-based products are nutritionally not full alternatives of the animal-based equivalents; however, there are still opportunities for reformulation. To aid the consumer in making healthy plant-based food choices, a better alignment between the Nutri-Score and the recommended dietary guidelines is needed.

Fermented Infant Formula Increases Ileal Protein Digestibility and Reduces Ileal Proteolytic Activity Compared with Standard and Hydrolyzed Infant Formulas in Piglets.

BACKGROUND: An infant formula that contained milk fermented by the bacteria Bifidobacterium breve and Streptococcus thermophilus (Lactofidus) was reported to alleviate functional digestive symptoms in infants. It was hypothesized that improved protein digestibility of the fermented infant formula could contribute to this effect. OBJECTIVE: The aim of this study was to evaluate the protein digestibility of a specific fermented (FF), a standard (SF), and an extensively hydrolyzed protein (HF) formula. METHODS: Four-week-old piglets (n = 7) were fitted with a T-cannula at the terminal ileum and received each formula in a Latin square design. FF, SF, and HF contained 11.7%, 9.3%, and 11.9% (w/w) crude protein; 1.5%, 5.4%, and 5.6% (w/w) fiber; and had a casein/whey ratio of 60:40, 50:50, and 0:100 per kilogram of powder, respectively. Ileal digesta were collected and analyzed for amino acids and proteolytic activity. RESULTS: FF had a significantly higher apparent ileal crude protein digestibility (92.1% ± 1.0%) than SF and HF (84.4% ± 1.0% and 83.9% ± 0.9%, respectively). FF also had a significantly higher dry matter digestibility than SF and HF. The ileal crude protein flow of FF was significantly lower than that of SF and HF. The ileal flow of FF total proteolytic activity was significantly lower than that of SF but not significantly different from that of HF (412 ± 163 kU/8 h vs. 1530 ± 163 and 703 ± 156 kU/8 h, respectively). CONCLUSIONS: The FF in piglets had a significantly higher apparent ileal crude protein digestibility than the SF and HF and displayed lower ileal proteolytic activity than the SF. Both effects may contribute to the alleviation of functional gastrointestinal symptoms reported in infants fed fermented infant milk formula.

Expression profiling of claudins in the human gastrointestinal tract in health and during inflammatory bowel disease.

BACKGROUND: Claudins, being part of the tight junction protein family, partially determine the integrity and paracellular permeability of the intestinal epithelium. The aim of this study was twofold. First, the authors set out to create an overview of claudin mRNA expression along the proximal-distal axis of the healthy human intestine. Second, the authors aimed to analyze expression levels of claudins in patients with active and inactive inflammatory bowel diseases (IBD) such as Crohn's disease or ulcerative colitis (UC). METHODS: mRNA expression levels of claudins were determined in gastrointestinal biopsies from healthy patients as well as patients diagnosed with IBD using SybrGreen real-time PCR. RESULTS: Claudins show distinct expression patterns throughout the gastrointestinal tract. Some claudins show a proximal expression pattern, such as CLDN18 which is solely expressed in the stomach, and CLDN2 and -15 that are predominantly expressed in the proximal parts of the gastrointestinal tract. Other claudins, such as CLDN3, -4, -7 and -8, are predominantly expressed in the distal parts of the gastrointestinal tract or show a ubiquitous expression pattern throughout the entire gastrointestinal tract, which is the case for CLDN12. In addition, we show that changes in claudin expression in IBD are dependent on gastrointestinal location and inflammatory activity. CONCLUSIONS: This study provides detailed mRNA expression patterns of various claudins throughout the human gastrointestinal tract. Analysis of expression levels of claudins in patients with CD, active and inactive UC shows that changes in expression are confined to specific intestinal segments and strongly depend on inflammatory activity.

Involvement of claudin 3 and claudin 4 in idiopathic infantile hypercalcaemia: a novel hypothesis?

BACKGROUND: Idiopathic infantile hypercalcaemia (IIH) is a rare disease that generally resolves spontaneously between the age of 1 and 3 years. Similar symptoms may occur in patients suffering from Williams-Beuren syndrome (WBS), which is caused by a microdeletion on chromosome 7. Two of the genes, named CLDN3 and CLDN4, located within this region are members of the claudin family that has been shown to be involved in paracellular calcium (Ca(2+)) absorption. Based on the hemizygous loss of CLDN3 and CLDN4 in WBS and the function of these genes in paracellular Ca(2+) transport, we hypothesized that mutations in CLDN3 or CLDN4 could also be involved in IIH. METHODS: Biochemical characteristics, including calciotropic hormone levels, were obtained from three typical IIH patients. CLDN3 and CLDN4 sequences were also analysed in these patients. The major intestinal Ca(2+) transporter TRPV6 was also screened for the presence of mutations, since hypercalcaemia in IIH and WBS has been shown to result from intestinal hyperabsorption. All three patients were also analysed for the presence of deletions or duplications using a single-nucleotide polymorphism (SNP) array for genomic DNA. RESULTS: The serum Ca(2+) levels of patients were 2.9, 3.3 and 3.8 mmol/L (normal <2.7 mmol/L). Levels of 25-hydroxyvitamin D(3) and 1,25-dihydroxyvitamin D(3) were normal, parathyroid hormone (PTH) and PTH-related peptide (PTHrP) levels were appropriately low. Sequencing of coding regions and intron-exon boundaries did not reveal mutations in CLDN3, CLDN4 and TRPV6. Identified SNPs were not correlated with the disease phenotype. A SNP array did not reveal genomic deletions or duplications. CONCLUSIONS: Biochemical analysis did not reveal inappropriate levels of calciotropic hormones in IIH patients in this study. Furthermore, based on the lack of mutations in CLDN3, CLDN4 and TRPV6, we conclude that IIH is neither caused by mutations in these candidate genes nor by deletions or duplications in the genome of these patients.

Murine TNF(DeltaARE) Crohn's disease model displays diminished expression of intestinal Ca2+ transporters.

BACKGROUND: Patients suffering from Crohn's disease (CD) show increased incidence of low bone mineral density. Investigating this complication is difficult because the exact etiology of CD remains elusive. Mice carrying a deletion in the tumor necrosis factor (TNF) AU-rich elements (ARE) are reported as a model for human CD and are characterized by elevated TNF-alpha levels and inflammations in the terminal ileum. To evaluate whether these mice have a Ca(2+) handling problem, this study analyzed the Ca(2+) homeostasis in heterozygous TNF(DeltaARE) mice (TNF(DeltaARE/+)) in comparison to wildtype littermates. METHODS: Beside serum Ca(2+) and vitamin D levels, the expression of Ca(2+) transporters was analyzed in intestine, kidney and bone using quantitative real-time PCR, Western blot and immunohistochemistry. Bone scans were performed to measure bone parameters. RESULTS: Ca(2+) transporters in duodenum (TRPV6, calbindin-D(9K), PMCA1b) and kidney (TRPV5, calbindin-D(28K), NCX1) showed significantly reduced mRNA expression levels in TNP(DeltaARE/+) mice, except for renal TRPV5. In bone, only calbindin-D(9K) mRNA displayed a significant down-regulation. These findings were supported by declined duodenal calbindin-D(9K) and renal calbindin-D(28K) protein values. Likely, this down-regulation of Ca(2+) transporters in TNP(DeltaARE/+) mice is mediated by the 58 +/- 9% reduction in serum 1,25(OH)(2)D(3) levels. Diminished expression of Ca(2+) transporters combined with unchanged serum Ca(2+) levels assumes Ca(2+) loss from bone to compensate for the body's overall Ca(2+) shortage. Indeed, microcomputed tomography scanning demonstrated reduced trabecular and corticol bone thickness and volume in TNF(DeltaARE/+) mice. This finding is further supported by increased total deoxypyridinoline in serum. CONCLUSIONS: Our results imply that TNF(DeltaARE/+) mice have a disturbed Ca(2+) homeostasis characterized by reduced duodenal and renal Ca(2+) transporters, diminished 1,25(OH)(2)D(3) levels, and increased bone resorption associated with profound bone abnormalities.

Prednisolone-induced Ca2+ malabsorption is caused by diminished expression of the epithelial Ca2+ channel TRPV6.

Glucocorticoids, such as prednisolone, are often used in clinic because of their anti-inflammatory and immunosuppressive properties. However, glucocorticoids reduce bone mineral density (BMD) as a side effect. Malabsorption of Ca2+ in the intestine is supposed to play an important role in the etiology of low BMD. To elucidate the mechanism of glucocorticoid-induced Ca2+ malabsorption, the present study investigated the effect of prednisolone on the expression and activity of proteins responsible for active intestinal Ca2+ absorption including the epithelial Ca2+ channel TRPV6, calbindin-D(9K), and the plasma membrane ATPase PMCA1b. Therefore, C57BL/6 mice received 10 mg/kg body wt prednisolone daily by oral gavage for 7 days and were compared with control mice receiving vehicle only. An in vivo 45Ca2+ absorption assay indicated that intestinal Ca2+ absorption was diminished after prednisolone treatment. We showed decreased duodenal TRPV6 and calbindin-D(9K) mRNA and protein abundance in prednisolone-treated compared with control mice, whereas PMCA1b mRNA levels were not altered. Importantly, detailed expression studies demonstrated that in mice these Ca2+ transport proteins are predominantly localized in the first 2 cm of the duodenum. Furthermore, serum Ca2+ and 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] concentrations remained unchanged by prednisolone treatment. In conclusion, these data suggest that prednisolone reduces the intestinal Ca2+ absorption capacity through diminished duodenal expression of the active Ca2+ transporters TRPV6 and calbindin-D(9K) independent of systemic 1,25(OH)2D3.

Age-dependent alterations in Ca2+ homeostasis: role of TRPV5 and TRPV6.

Aging is associated with alterations in Ca2+ homeostasis, which predisposes elder people to hyperparathyroidism and osteoporosis. Intestinal Ca2+ absorption decreases with aging and, in particular, active transport of Ca2+ by the duodenum. In addition, there are age-related changes in renal Ca2+ handling. To examine age-related changes in expression of the renal and intestinal epithelial Ca2+ channels, control (TRPV5+/+) and TRPV5 knockout (TRPV5-/-) mice aged 10, 30, and 52 wk were studied. Aging of TRPV5(+/+) mice resulted in a tendency toward increased renal Ca2+ excretion and significantly decreased intestinal Ca2+ absorption, which was accompanied by reduced expression of TRPV5 and TRPV6, respectively, despite increased serum 1,25(OH)2D3 levels. Similarly, in TRPV5-/- mice the existing renal Ca2+ loss was more pronounced in elder animals, whereas the compensatory intestinal Ca2+ absorption and TRPV6 expression declined with aging. In both mice strains, aging resulted in a resistance to 1,25(OH)2D3 and diminished renal vitamin D receptor mRNA levels, whereas serum Ca2+ levels remained constant. Furthermore, 52-wk-old TRPV5-/- mice showed severe hyperparathyroidism, whereas PTH levels in elder TRPV5+/+ mice remained normal. In 52-wk-old TRPV5-/- mice, serum osteocalcin levels were increased in accordance with the elevated PTH levels, suggesting an increased bone turnover in these mice. In conclusion, downregulation of TRPV5 and TRPV6 is likely involved in the impaired Ca2+ (re)absorption during aging. Moreover, TRPV5-/- mice likely develop age-related hyperparathyroidism and osteoporotic characteristics before TRPV5+/+ mice, demonstrating the importance of the epithelial Ca2+ channels in Ca2+ homeostasis.

Polymorphisms in genes encoding acetylsalicylic acid metabolizing enzymes are unrelated to upper gastrointestinal health in cardiovascular patients on acetylsalicylic acid.

BACKGROUND: As acetylsalicylic acid is metabolized by UDP-glucuronosyltransferase 1A6 (UGT1A6) and cytochrome P450 2C9 (CYP2C9), interindividual differences in activity of these enzymes may modulate the effects and side-effects of acetylsalicylic acid. The objective of this study was to assess whether polymorphisms in UGT1A6 and CYP2C9 genes are related to the prevalence of upper gastrointestinal symptoms in cardiovascular patients using acetylsalicylic acid for secondary prevention of ischaemic heart disease. METHODS: Blood samples were taken from acetylsalicylic acid using patients admitted to the Coronary Care Unit. Dyspepsia-related health was evaluated at week 2, using a validated upper gastrointestinal complaint questionnaire. A subset of 160 patients responded to a survey and were eligible to participate in this study. DNA was isolated and UGT1A6 and CYP2C9 genotypes were determined using polymerase chain reaction restricted fragment length polymorphism techniques. RESULTS: Seventy per cent of the patients returned the questionnaire. UGT1A6 and CYP2C9 variant polymorphisms were found in 103 (63%) and 56 (35%) patients, respectively. There was no association between gastrointestinal symptoms and UGT1A6 (OR = 0.80, 95% CI = 0.41-1.56) or CYP2C9 polymorphisms (OR = 0.85, 95% CI = 0.44-1.67). CONCLUSIONS: There was no association between polymorphisms in genes encoding for acetylsalicylic acid metabolizing enzymes on the prevalence of gastric complaints in cardiovascular patients on acetylsalicylic acid.

Time- and dose-dependent effects of curcumin on gene expression in human colon cancer cells.

BACKGROUND: Curcumin is a spice and a coloring food compound with a promising role in colon cancer prevention. Curcumin protects against development of colon tumors in rats treated with a colon carcinogen, in colon cancer cells curcumin can inhibit cell proliferation and induce apoptosis, it is an anti-oxidant and it can act as an anti-inflammatory agent. The aim of this study was to elucidate mechanisms and effect of curcumin in colon cancer cells using gene expression profiling. METHODS: Gene expression changes in response to curcumin exposure were studied in two human colon cancer cell lines, using cDNA microarrays with four thousand human genes. HT29 cells were exposed to two different concentrations of curcumin and gene expression changes were followed in time (3, 6, 12, 24 and 48 hours). Gene expression changes after short-term exposure (3 or 6 hours) to curcumin were also studied in a second cell type, Caco-2 cells. RESULTS: Gene expression changes (>1.5-fold) were found at all time points. HT29 cells were more sensitive to curcumin than Caco-2 cells. Early response genes were involved in cell cycle, signal transduction, DNA repair, gene transcription, cell adhesion and xenobiotic metabolism. In HT29 cells curcumin modulated a number of cell cycle genes of which several have a role in transition through the G2/M phase. This corresponded to a cell cycle arrest in the G2/M phase as was observed by flow cytometry. Functional groups with a similar expression profile included genes involved in phase-II metabolism that were induced by curcumin after 12 and 24 hours. Expression of some cytochrome P450 genes was downregulated by curcumin in HT29 and Caco-2 cells. In addition, curcumin affected expression of metallothionein genes, tubulin genes, p53 and other genes involved in colon carcinogenesis. CONCLUSIONS: This study has extended knowledge on pathways or processes already reported to be affected by curcumin (cell cycle arrest, phase-II genes). Moreover, potential new leads to genes and pathways that could play a role in colon cancer prevention by curcumin were identified.