Nutrients最新文献

Exposure to air pollution poses a risk to human respiratory health, and a preventive and therapeutic remedy against fine dust-induced respiratory disease is needed.

Background/objectives: The respiratory-protective effects of Lysimachia mauritiana (LM) against airway inflammation were evaluated in a mouse model exposed to a fine dust mixture of diesel exhaust particles and particulate matter with a diameter of less than 10 µm (PM10D).

Methods: To induce airway inflammation, PM10D was intranasally injected into BALB/c mice three times a day for 12 days, and LM extracts were given orally once per day. The immune cell subtypes, histopathology, and expression of inflammatory mediators were analyzed from the bronchoalveolar lavage fluid (BALF) and lungs.

Results: LM alleviated the accumulation of neutrophils and the number of inflammatory cells in the lungs and the BALF of the PM10D-exposed mice. LM also reduced the release of inflammatory mediators (MIP-2, IL-17, IL-1α, CXCL1, TNF-α, MUC5AC, and TRP receptor channels) in the BALF and lungs. Lung histopathology was used to examine airway inflammation and the accumulation of collagen fibers and inflammatory cells after PM10D exposure and showed that LM administration improved this inflammation. Furthermore, LM extract inhibited the MAPK and NF-κB signaling pathway in the lungs and improved expectoration activity through an increase in phenol red release from the trachea.

Conclusions: LM alleviated PM10D-exposed neutrophilic airway inflammation by suppressing MAPK/NF-κB activation. This study indicates that LM extract may be an effective therapeutic agent against inflammatory respiratory diseases.

Background/objectives: The impact of daily variations in habitual maternal intake on human milk (HM) composition has been poorly studied. We aimed to investigate the associations between day-to-day fluctuation in the micronutrient concentration in HM and daily maternal diet.

Methods: To this end, an observational longitudinal study was carried out. A total of 143 lactating women each compiled a five-day weighed dietary record and concomitantly expressed milk for four successive days. Maternal daily intakes of micronutrients and food groups were analyzed. Free thiamine, free riboflavin, nicotinamide, pantothenic acid, pyridoxal, folic acid, cobalamin, ascorbic and dehydroascorbic acids, retinol, alpha- and gamma-tocopherol, cholecalciferol, and calcidiol in HM were determined for each of the four investigated days. A longitudinal data analysis with generalized estimating equation models was performed.

Results: For each daily serving of meat, fish, and eggs, total vitamin D₃ levels increased by 243.2 pg/mL (p = 0.027) and selenium levels increased by 0.16 ppb (p = 0.031) in HM. For every 1 mg/day of riboflavin supplementation, free riboflavin levels in HM increased by 28.6 mcg/L (p = 0.019). Pyridoxal levels in HM increased by 6.3 mcg/L per 1 mg/day of vitamin B₆ supplementation (p = 0.001), and by 2 mcg/L per daily fruit ration (p = 0.016).

Conclusions: In conclusion, we were able to quantify the impact of the usual day-to-day variations in the diet and in the intake of commonly used supplements on the fluctuation of vitamin D, free riboflavin, pyridoxal, and selenium concentration in the milk of lactating women.

Background: Every year the global incidence of obesity increases considerably and among the factors that favor it is bisphenol A (BPA), an endocrine disruptor widely used in plastics and omnipresent in many everyday objects.

Methods: A total of 19 studies published between 2018 and 2023 that addressed the relationship between BPA exposure and obesity were included in this review in order to better understand its behavior and mechanisms of action.

Results: The studies reviewed conclude that BPA is an obesogen that alters the function of hormonal receptors, promotes metabolic syndrome, affects certain genes, etc., leading to a greater risk of developing obesity. With important emphasis on the ability to cause epigenetic changes, thus transmitting the effects to offspring when exposure has occurred during critical stages of development such as during gestation or the perinatal period.

Conclusions: There is sufficient evidence to show that BPA is a risk factor in the development of obesity. Even so, further research is necessary to exhaustively understand the causal relationship between the two in order to develop prevention measures and avoid possible future adverse effects.

Objective: This study aimed to examine the trajectories of body mass index-for-age z-score (BAZ) in preschoolers and its association with parental feeding practices, weight perception, and children's appetitive traits.

Methods: A total of 433 preschoolers and their parents from eight public kindergartens in Shanghai were assessed annually over two years. A group-based trajectory model was employed to identify distinct BAZ patterns. Logistic regression was utilized to investigate the baseline factors associated with the BAZ trajectories.

Results: Three distinct BAZ trajectories were identified among the preschoolers: "low-stable group" (n = 154, 37.3%), "moderate-stable group" (n = 214, 47.3%), and "progressive overweight and obesity group" (n = 65, 15.4%). The children perceived as overweight and obese by parents (OR = 10.57, 95% CI: 4.89-22.86), and those with lower satiety responsiveness at baseline (OR = 0.86, 95%CI: 0.76-0.97) were more likely to fall into the progressive overweight and obesity group as opposed to the moderate-stable group. Conversely, the children perceived as underweight by parents (OR = 457, 95%CI: 2.71-7.70) had a higher likelihood of being in the low-stable group rather than the moderate-stable group.

Conclusions: This study unveiled three unique body weight trajectories among preschool children. Parental perception of children's weight and lower satiety responsiveness were associated with preschoolers' subsequent weight change, while parental feeding practices were not associated.

Background: Previous studies have reported associations between fatty acids and the risk of pre-eclampsia. However, the causality of these associations remains uncertain. This study postulates a causal relationship between specific plasma fatty acids and pre-eclampsia or other maternal hypertensive disorders (PE-HTPs). To test this hypothesis, two-sample bidirectional Mendelian randomization (MR) analyses were employed to determine the causality effects.

Methods: Single-nucleotide polymorphisms associated with PE-HTPs and fatty acids were obtained from a genome-wide association study (GWAS) of European ancestry. Bidirectional MR analyses were conducted using methods such as inverse variance weighted, MR-Egger, weighted median, simple mode, and weighted mode. Sensitivity analyses, including tests for heterogeneity, horizontal pleiotropy, and co-localization, were conducted to assess the robustness of MR results.

Results: The analyses revealed causal relationships between PE-HTPs and several fatty acids, including monounsaturated fatty acid (MUFA), omega-6 fatty acid (n-6 FA), linoleic acid (LA), docosahexaenoic acid (DHA), and the PUFA/MUFA ratio. Genetically predicted higher risk of PE-HTPs was significantly associated with lower plasma n-6 FA (OR = 0.96, 95% CI: 0.93-0.99), particularly LA (OR = 0.95, 95% CI: 0.92-0.98). Conversely, increased DHA (OR = 0.86, 95% CI: 0.78-0.96) and a higher PUFA/MUFA ratio (OR = 0.86, 95% CI: 0.76-0.98) were associated with a reduced risk of PE-HTPs. Elevated MUFA levels (OR = 1.12, 95% CI: 1.00-1.25) were related to an increased risk.

Conclusions: This study provides robust genetic evidence supporting bidirectional causal relationships between PE-HTPs and specific plasma fatty acids, underscoring the critical role of fatty acid metabolism in maternal hypertensive disorders.

This review explores the understudied topic of nutritional inequality among individuals with schizophrenia, highlighting the complex interplay between diet, genetics, and mental health. Unhealthy dietary patterns, socioeconomic factors, and disordered eating behaviors contribute to malnutrition, increasing the risk of physical health issues and premature mortality. Socioeconomic factors exacerbate nutritional disparities, necessitating targeted interventions. Genetic influences on nutrient metabolism remain under-researched, although nutritional genomics shows potential for personalized interventions. Current research reveals methodological gaps, urging larger sample sizes and standardized approaches. The integration of nutrigenomics, encompassing various omics disciplines, emerges as a transformative tool. The holistic life-cycle approach to schizophrenia management underscores the vital role of nutrition, calling for personalized interventions to enhance mental health outcomes.

Background/objectives: Atherosclerosis is a chronic inflammatory disease of the arterial wall, which involves multiple cell types. Peptide OG-5 is identified from collagen hydrolysates derived from Salmo salar and exhibits an inhibitory effect on early atherosclerosis. The primary objective of this study was to investigate the impact of OG-5 on advanced atherosclerotic lesions as well as its stability during absorption.

Methods: In this study, the ApoE-/- mice were employed to establish advanced atherosclerosis model to investigate the treatment effect of peptide OG-5.

Results: The results showed that oral administration of OG-5 at a dosage of 150 mg/kg bw resulted in a 30% reduction in the aortic plaque formation area in ApoE^-/- mice with few bleeding risks. Specifically, intervention with a low dose of OG-5 (50 mg/kg bw), initiated in the early stage of atherosclerosis, continues to provide benefits into the middle and late stages without bleeding risks. Furthermore, treatment of OG-5 increased expression levels of contractile phenotype markers and reduced the accumulation of lipoprotein in VSMCs induced by ox-LDL. Peptide OG-5 could ensure transport across Caco-2 cell monolayers, exhibiting a P_app value of 1.80 × 10^-5 cm/s, and exhibited a robust stability in plasma with remaining content >70% after 8 h incubation. In vivo studies revealed that OG-5 reached maximum concentration in blood after 120 min.

Conclusion: The present results demonstrate the potential efficacy of peptide OG-5 as a promising agent for intervention in anti-atherogenesis strategies.

Numerous studies have shown that vitamin D may play an important role in modulating the inflammatory process. This study aimed to evaluate the effect of vitamin D supplementation on inflammatory markers in patients with orthopedic disorders and obesity. Thirty-three obese subjects were included in the study and were divided into two groups based on their medical condition: acute orthopedic diseases and chronic orthopedic diseases. Inclusion criteria for the research included age 18-75 years, BMI > 30 kg/m², vitamin D deficiency, and no previous vitamin D supplementation. Samples were collected before and after 3 months of 4000 IU/day vitamin D supplementation. The study used enzyme-linked immunosorbent assay (ELISA) and measured serum levels of markers such as chitinase-3-like protein 1 (YKL-40), interleukin 6 (IL-6), interleukin 17 (IL-17), tumor necrosis factor (TNF-α), and adiponectin. After 3 months of vitamin D supplementation, a statistically significant increase in vitamin D and IL-17 levels was observed in the group with acute orthopedic diseases. Similarly, after supplementation, a statistically significant increase in vitamin D, IL-6 and TNF-α levels was observed in the group with chronic orthopedic diseases. Moreover, after vitamin D supplementation, statistically significantly higher adiponectin levels were observed in the chronic orthopedic group than in the acute orthopedic group. Despite high-dose vitamin D supplementation, inflammatory markers increased in acute and chronic orthopedic conditions. Based on our study, vitamin D does not reduce inflammation in patients with orthopedic conditions and obesity.

Background: The association between coffee and pancreatic cancer risk has reported inconsistent results. Therefore, a Mendelian randomization (MR) study was undertaken to investigate the association between coffee and pancreatic cancer from a genetic perspective.

Methods: In East Asian and European populations, independent genetic variants strongly associated with coffee were chosen as instrumental variables (IVs) from relevant genome-wide association studies (GWASs). GWAS data for pancreatic cancer were obtained from the JENGER (Japanese Encyclopedia of Genetic Associations by Riken) project and GWAS catalog database. Two-sample (TSMR) and multivariable Mendelian randomization (MVMR) analyses were conducted to investigate the genetically predicted causal relationship between coffee consumption and pancreatic cancer. A fixed-effect meta-analysis was employed to aggregate estimates from the two populations to reveal the overall association.

Results: Both in East Asian and European populations, an increase in coffee intake of a cup per day was not associated with pancreatic cancer risk, regardless of coffee type (including caffeine drinks, instant coffee, decaffeinated coffee, ground coffee, etc.). The results aligned with the findings of the meta-analysis (OR = 1.100, 95%CI = 0.862-1.403, p = 0.450). Also, for coffee intake with positive results in the TSMR analysis (OR = 1.739, 95%CI 1.104-2.739, p = 0.017), consistent negative results were observed after adjusting for potential confounders (smoking traits, drinking, type 2 diabetes, body mass index) in the MVMR analyses.

Conclusions: This study found no genetically predicted causal relationship between coffee consumption and pancreatic cancer risk.

Background/Objectives: Hypomagnesemia and hypocalcemia are common conditions among older adults that may contribute to cognitive decline. However, most of the existing research has focused primarily on dietary intake rather than the actual serum levels of these nutrients or examined them separately. This study aims to investigate the relationship between hypomagnesemia, hypocalcemia, and the concurrent presence of both deficiencies in relation to cognitive performance among seniors. Methods: A total of 1220 hospitalized patients aged 60 and older were included in the analysis. The participants were categorized into four groups: those with normal serum levels of magnesium and calcium, those with hypomagnesemia, those with hypocalcemia, and those with both serum magnesium and calcium deficiencies. To evaluate the potential influence of age, sex, common comorbidities, and disturbances in magnesium and calcium levels on cognitive performance, two general linear models were employed, using the Mini-Mental State Examination (MMSE) and Clock-Drawing Test (CDT) as dependent variables. Results: After adjusting for age, sex, body mass index, and comorbidities, the mean values for the MMSE and CDT were 23.33 (95%CI: 22.89-23.79) and 5.56 (95%CI: 5.29-5.83) for the group with normomagnesemia and normocalcemia, 22.59 (95%CI: 21.94-23.24) and 5.16 (95%CI: 4.77-5.54) for the group with hypomagnesemia, 19.53 (95%CI: 18.36-20.70) and 4.52 (95%CI: 3.83-5.21) for the group with hypocalcemia, and 21.14 (95%CI 19.99-22.29) and 4.28 (95%CI 3.61-4.95) for the group with both hypomagnesemia and hypocalcemia, respectively. Magnesium and calcium deficiencies contributed to MMSE and CDT variance in the general linear models. Conclusions: Our findings indicate that in addition to age, body mass index, and chronic heart failure, both hypomagnesemia and hypocalcemia are associated with reduced cognitive performance.