Search Results (845)

Background: Thallium is a metal that is ubiquitous in our natural environment. Despite its potential for high toxicity, thallium is understudied and not regulated in food. The California Department of Public Health was alerted to a household cluster of elevated urine thallium levels noted among a mother (peak 5.6 µg/g creatinine; adult reference: ≤0.4 µg/g creatinine) and her three young children (peak 10.5 µg/g creatinine; child reference: ≤0.8 µg/g creatinine). Objectives: This case report identifies questions raised after a public health investigation linked a household’s thallium exposure to a commercially available food product. We provide an overview of the public health investigation. We then explore concerns, such as gaps in toxicological data and limited surveillance of thallium in the food supply, which make management of individual and population exposure risks challenging. Methods: We highlight findings from a cross-agency investigation, including a household exposure survey, sampling of possible environmental and dietary exposures (ICP-MS analysis measured thallium in kale chips at 1.98 mg/kg and 2.15 mg/kg), and monitoring of symptoms and urine thallium levels after the source was removed. We use regulatory and research findings to describe the challenges and opportunities in characterizing the scale of thallium in our food supply and effects of dietary exposures on health. Discussion: Thallium can bioaccumulate in our food system, particularly in brassica vegetables like kale. Thallium concentration in foods can also be affected by manufacturing processes, such as dehydration. We have limited surveillance data nationally regarding this metal in our food supply. Dietary reviews internationally show increased thallium intake in toddlers. Limited information is available about low-dose or chronic exposures, particularly among children, although emerging evidence shows that there might be risks associated at lower levels than previously thought. Improved toxicological studies are needed to guide reference doses and food safety standards. Promising action towards enhanced monitoring of thallium is being pursued by food safety agencies internationally, and research is underway to deepen our understanding of thallium toxicity. Full article

We recently reported that phospholipase A2 (PLA2)-mediated production of prostaglandins within the ventromedial hypothalamus (VMH) plays a critical role in systemic glucose homeostasis. However, the role of PLA2 in the VMH in regulating food intake is still unclear. Here, we attempted to investigate the role of PLA2 in regulating food intake and body weight in male mice. We injected an adeno-associated virus encoding short hairpin RNA (AAV-shRNA) targeting cytosolic phospholipase A2 (shPla2g4a) into the VMH. We assessed food intake, body weight, oxygen consumption, glucose tolerance, and insulin sensitivity. Three weeks after the AAV injection, the shPla2g4a group exhibited increased food intake and body weight gain compared to controls (shSCRM). Energy expenditure, oxygen consumption, and respiratory quotient (RQ) were comparable between groups. Our findings suggest that the cPLA2-mediated pathway in the VMH is critical for feeding behavior and maintaining energy homeostasis. Further investigation is needed to elucidate the underlying mechanisms. Full article

The available literature data indicate that obestatin, a peptide derived from the preproghrelin precursor, may modulate neuroendocrine function, particularly in appetite regulation and somatotrophic/gonadotrophic pathways. This review synthesizes animal studies assessing the influence of obestatin on central neuroendocrine systems. Obestatin has been shown to affect the hypothalamic appetite-regulating center through neuropeptides such as neuropeptide Y and agouti-related peptide, yet findings remain inconsistent between species. In rodents, its effects on food intake and energy balance are inconclusive, whereas sheep models demonstrate significant alterations in orexigenic gene expression and peptide immunoreactivity. Regarding the somatotrophic axis, obestatin showed no significant effect on growth hormone (GH) secretion in rodents; however, in sheep, it modulated growth hormone-releasing hormone and somatostatin mRNA expression, elevated pituitary GH synthesis, and increased circulating GH levels. Studies involving the gonadotrophic axis demonstrated the presence of obestatin in Leydig and pituitary cells, with in vitro evidence suggesting its ability to modulate intracellular pathways implicated in gonadoliberin, luteinizing hormone, and follicle-stimulating hormone release. The collective findings discussed in this article indicate that obestatin interacts with multiple hypothalamic–pituitary axes, though its effects vary depending on species and experimental conditions. This review highlights the complexity of obestatin’s central actions and the need for further research to elucidate its functional relevance in neuroendocrine regulation. Full article

The thyroid gland plays a crucial role in regulating metabolism and supporting development through the production of the hormones T4 and T3. These hormones are essential during childhood for nervous system myelination, physical growth, puberty, skeletal and dental maturation, and overall metabolic balance. In early infancy, when the hypothalamic–pituitary–thyroid axis is still immature, thyroid dysfunction can result in a range of long-term complications. The metabolism and action of thyroid hormones depend not only on iodine but also on other vital micronutrients, particularly selenium (Se). This narrative review aims to comprehensively examine the role of selenium in maintaining thyroid health from fetal life through adolescence. Selenium is a key micronutrient involved in thyroid development, hormone synthesis, antioxidant defense, and immune regulation, especially during pregnancy and childhood. Inadequate selenium levels may contribute to the onset, progression, and clinical management of various thyroid disorders, particularly hypothyroidism and autoimmune thyroid diseases. Although scientific evidence supports selenium’s critical functions in hormone metabolism and antioxidant protection, public awareness and monitoring of selenium intake remain insufficient. Beyond the need for further research, there is an urgent call for integrated public health strategies, ranging from sustainable, food-based approaches to targeted clinical screening and educational programs. Promoting awareness of selenium’s importance and incorporating selenium status into maternal and pediatric care protocols could play a significant role in preventing deficiencies and supporting long-term endocrine and neurodevelopmental health. Full article

Background/Objectives: Obesity is increasingly recognized as a global health concern due to its association with metabolic disorders and gut microbiota dysbiosis. While probiotics offer promise in regulating gut microbiota and improving host metabolism, strain-specific effects remain underexplored, particularly for canine-derived probiotics. This study aimed to isolate and characterize a novel probiotic strain, Ligilactobacillus animalis LA-1, and evaluate its anti-obesity effects and underlying mechanisms using a high-fat diet (HFD)-induced obese mouse model. Methods: LA-1 was isolated from the feces of a healthy dog and assessed for probiotic potential in vitro, including gastrointestinal tolerance, bile salt hydrolase activity, cholesterol-lowering capacity, and fatty acid absorption. Male C57BL/6J mice were fed either a standard chow diet or an HFD for 16 weeks, with HFD mice receiving oral LA-1 supplementation (2 × 10⁹ CFU/day). Multi-omics analyses, including 16S rRNA gene sequencing, short-chain fatty acid (SCFA) quantification, and untargeted liver metabolomics, were employed to investigate the effects of LA-1 on gut microbiota composition, metabolic pathways, and obesity-related phenotypes. Results: LA-1 supplementation significantly alleviated HFD-induced weight gain, hepatic lipid accumulation, and adipose tissue hypertrophy, without affecting food intake. It improved serum lipid profiles, reduced liver injury markers, and partially restored gut microbiota composition, decreasing the Firmicutes/Bacteroidetes ratio and enriching SCFA-producing genera. Total SCFA levels, particularly acetate, propionate, and butyrate, increased following LA-1 treatment. Liver metabolomics revealed that LA-1 modulated pathways involved in lipid and amino acid metabolism, resulting in decreased levels of acetyl-CoA, triglycerides, and bile acids. Conclusions: L. animalis LA-1 exerts anti-obesity effects via gut microbiota modulation, enhanced SCFA production, and hepatic metabolic reprogramming. These findings highlight its potential as a targeted probiotic intervention for obesity and metabolic disorders. Full article

In placental mammals, the co-option of vertebrate orthologous ATP1B4 genes has profoundly altered the properties of the encoded BetaM proteins, which function as bona fide β-subunits of Na,K-ATPases in lower vertebrates. Eutherian BetaM acquired an extended Glu-rich N-terminal domain resulting in the complete loss of its ancestral function and became a skeletal and cardiac muscle-specific component of the inner nuclear membrane. BetaM is expressed at the highest level during perinatal development and is implicated in gene regulation. Here we report the long-term consequences of Atp1b4 ablation on metabolic parameters in adult mice. Male BetaM-deficient (Atp1b4−/Y) mice have remarkably lower body weight and adiposity than their wild-type littermates, despite higher food intake. Indirect calorimetry shows higher energy expenditure (heat production and oxygen consumption) with a greater spontaneous locomotor activity in Atp1b4−/Y males. Their lower respiratory exchange ratio suggests a greater reliance on fat metabolism compared to their wild-type counterparts. Consistently, Atp1b4−/Y KO mice exhibit enhanced β-oxidation in skeletal muscle, along with improved glucose and insulin tolerance. These robust metabolic changes induced by Atp1b4 disruption demonstrate that eutherian BetaM plays an important role in regulating adult mouse metabolism. This demonstrates that bypassing the co-option of Atp1b4 potentially reduces susceptibility to obesity. Thus, Atp1b4 ablation leading to the loss of evolutionarily acquired BetaM functions serves as a model for a potential alternative pathway in mammalian evolution. Full article

Over the past decades, bile acids have been recognized as important signaling molecules with significant roles in metabolic health and disease. Many of their beneficial effects are mediated through the activation of the Takeda G protein-coupled receptor 5 (TGR5), a G protein-coupled receptor ubiquitously expressed in both humans and animals. Upon activation, TGR5 stimulates adenylate cyclase, leading to increased cyclic adenosine monophosphate (cAMP) levels and subsequent activation of protein kinase A (PKA). PKA then phosphorylates and activates several downstream signaling pathways, including exchange protein directly activated by cAMP (EPAC), extracellular signal-regulated kinase 1/2 (ERK1/2), and protein kinase B (AKT). Through these pathways, TGR5 acts as a key molecular link between bile acid signaling and the regulation of energy metabolism. TGR5 activation has been associated with body weight loss in obese models, primarily by reducing food intake, enhancing thermogenesis in adipose tissue and muscle to increase energy expenditure, and improving insulin secretion. This review highlights recent advances in our understanding of TGR5 biology and critically examines its therapeutic potential, limitations, and controversies in the context of energy metabolism, offering new perspectives and opportunities for treating metabolic disorders. Full article

Sweet taste plays a pivotal role in human dietary behavior and metabolic regulation. With the increasing incidence of metabolic disorders linked to excessive sugar intake, the development and accurate evaluation of new sweeteners have become critical topics in food science and public health. However, the structural diversity of sweeteners and their complex interactions with sweet taste receptors present major challenges for standardized sweetness detection. This review offers a comprehensive and up-to-date overview of sweet taste transmission mechanisms and current detection methods. It outlines the classification and sensory characteristics of both conventional and emerging sweeteners, and explains the multi-level signaling pathway from receptor binding to neural encoding. Key detection techniques, including sensory evaluation, electronic tongues, and biosensors, are systematically compared in terms of their working principles, application scope, and limitations. Special emphasis is placed on advanced biosensing technologies utilizing receptor–ligand interactions and nanomaterials for highly sensitive and specific detection. Furthermore, an intelligent detection framework integrating molecular recognition, multi-source data fusion, and artificial intelligence is proposed. This interdisciplinary approach provides new insights and technical solutions to support precise sweetness evaluation and the future development of healthier food systems. Full article

Background High-sensitivity C-reactive protein (hs-CRP) is a protein that indicates inflammation and the risk of cardiovascular diseases. The intake of dietary amino acids can influence immune and inflammatory reactions. However, studies on the relationship between dietary amino acids and hs-CRP, especially in children, remain scarce. Methods This cross-sectional study analyzed data from the Nutrition and China Children and Lactating Women Nutrition and Health Survey (2016–2019), focusing on 3514 children (724 with elevated hs-CRP ≥ 3 mg/L and 2790 with normal levels). Dietary information was gathered via a food frequency questionnaire, and hs-CRP levels were obtained from blood samples. Boruta algorithm and propensity scores were used to select and match dietary factors and sample sizes. Machine learning (ML) algorithms and logistic regression models assessed the link between amino acid intake and elevated hs-CRP risk, adjusting for age, sex, BMI, and lifestyle factors. Results The odds ratios (ORs) for elevated hs-CRP were significant for several amino acids, including Ile, Leu, Lys, Ser, Cys, Tyr, His, Pro, SAA, and AAA, with values ranging from 1.10 to 2.07. The LightGBM algorithm was the most effective in predicting elevated hs-CRP risk, achieving an AUC of 0.927. Tyrosine, methionine, cysteine, and proline were identified as important features by SHAP analysis and logistic regression. The intake of Ser, Cys, Tyr, and Pro showed a linear increase in the risk of elevated hs-CRP, especially in individuals with low protein intake and normal weight (p < 0.1). Conclusions Intake of amino acids like Ser, Cys, Tyr, and Pro significantly impacts hs-CRP levels in children, indicating that regulating these could help prevent inflammation-related diseases. This study supports future dietary and health management strategies. This is first large-scale ML study linking amino acids to pediatric inflammation in China. The main limitations are the cross-section design and the use of self-reported dietary data. Full article

Sweet sensing is a fundamental sensory experience that plays a critical role not only in food preference, reward and dietary behaviour but also in glucose metabolism. Sweet taste receptors (STRs), composed of a heterodimer of taste receptor type 1 member 2 (T1R2) and member 3 (T1R3), are now recognised as being widely distributed throughout the body, including the gastrointestinal tract. Preclinical studies suggest these receptors are central to nutrient and glucose sensing, detecting energy availability and triggering metabolic and behavioural responses to maintain energy balance. Both internal and external factors tightly regulate their signalling pathways, and dysfunction within these systems may contribute to the development of metabolic disorders such as obesity and type 2 diabetes (T2D). Functional magnetic resonance imaging (fMRI) has provided valuable insights into the neural mechanisms underlying sweet sensing by mapping brain responses to both lingual/oral and gastrointestinal sweet stimuli. This review highlights key findings from fMRI studies and explores how these neural responses are modulated by metabolic state and individual characteristics such as body mass index, habitual intake and metabolic health. By integrating current evidence, this review advances our understanding of the complex interplay between sweet sensing, brain responses, and health and identifies key gaps and directions for future research in nutritional neuroscience. Full article

Background/Objectives: High sodium consumption increases the risk of hypertension and cardiovascular disease. Although food remains the primary source of intake, elevated sodium levels in drinking water can further contribute to excessive intake, particularly in populations already exceeding recommendations. This review examines the extent to which national drinking water standards account for sodium-related health risks and aims to inform discussion on the need for enforceable, health-based sodium limits. Methods: National standards for unbottled drinking water in 197 countries were searched for using the WHO 2021 review of drinking water guidelines, the FAOLEX database, and targeted internet and AI searches. For each country, data were extracted for the document name, year, regulatory body, regulation type, sodium limit (if stated), and rationale. Socio-geographic data were sourced from World Bank Open Data. A descriptive analysis was conducted using Microsoft Excel. Results: Standards were identified for 164 countries. Of these, 20% (n = 32), representing 30% of the global population, had no sodium limit. Among the 132 countries with a sodium limit, 92% (n = 121) adopted the WHO’s palatability-based guideline of 200 mg/L. Upper limits ranged from 50 to 400 mg/L. Only twelve countries (9%) cited health as a rationale. Three countries—Australia, Canada, and the United States—provided a separate recommendation for at-risk populations to consume water with sodium levels below 20 mg/L. Conclusions: Globally, drinking water standards give inadequate attention to sodium’s health risks. Most either lack sodium limits or rely on palatability thresholds that are too high to protect health. Updating national and international standards to reflect current evidence is essential to support sodium reduction efforts. Health-based sodium limits would empower communities to better advocate for safe water. Amid rising water salinity, such reforms must be part of a broader global strategy to ensure universal and equitable access to safe, affordable drinking water as a basic human right. Full article

Fermented foods represent an intricate ecosystem that delivers live microbes and numerous metabolites, influencing gut health. In this review, we explore how complex microbial communities and metabolites generated during food fermentation modulate the gut microbiome and affect human health. We discuss fermentation-induced biochemical transformations, including enhanced fiber fermentability; nutrient availability; and the synthesis of bioactive metabolites such as short-chain fatty acids, exopolysaccharides, bacteriocins, and modified polyphenols. We describe the dynamic microbial ecology of fermented foods, influenced by ingredient variations, highlighting its effect on health-related metabolic outcomes. Fermented products when consumed transiently introduce beneficial microbes and bioactive compounds into the gut, thereby boosting microbial diversity, resilience, and barrier function. We review clinical and preclinical studies to substantiate the roles of fermented foods in immune regulation, metabolic homeostasis, cognitive function, and inflammation mitigation. Individual variability in response to fermented foods has been emphasized, underscoring the potential for personalized nutrition strategies informed by advanced omics technologies. By integrating microbial ecology, metabolomics, and clinical evidence, this review positions fermented food intake as a strategic dietary intervention for microbiome modulation and health promotion. Full article

Obesity and metabolic disorders remain major global health concerns, traditionally attributed to excessive caloric intake and poor diet quality. Recent studies emphasize that the timing of meals plays a crucial role in determining metabolic health. This review explores chrononutrition, a growing field that examines how food intake patterns interact with endogenous circadian rhythms to influence energy balance, glucose and lipid metabolism, and cardiometabolic risk. The circadian system, which includes a central clock in the suprachiasmatic nucleus and peripheral clocks in metabolic tissues, regulates physiological functions on a 24 h cycle. While light entrains the central clock, feeding schedules act as key synchronizers for peripheral clocks. Disrupting this alignment—common in modern lifestyles involving shift work or late-night eating—can impair hormonal rhythms, reduce insulin sensitivity, and promote adiposity. Evidence from clinical and preclinical studies suggests that early time-restricted eating, where food intake is confined to the morning or early afternoon, offers significant benefits for weight control, glycemic regulation, lipid profiles, and mitochondrial efficiency, even in the absence of caloric restriction. These effects are particularly relevant for populations vulnerable to circadian disruption, such as adolescents, older adults, and night-shift workers. In conclusion, aligning food intake with circadian biology represents a promising, low-cost, and modifiable strategy to improve metabolic outcomes. Integrating chrononutrition into clinical and public health strategies may enhance dietary adherence and treatment efficacy. Future large-scale studies are needed to define optimal eating windows, assess long-term sustainability, and establish population-specific chrononutritional guidelines. Full article

Zn is a trace element necessary for the functioning of about 300 enzymes. It plays a biochemical, structural, and regulatory role. It participates in the immune response, proper functioning of the endocrine system, and regulation of gene expression. Its deficiencies are most often caused by the mismatch between dietary intake and the body’s needs. Bioavailability of zinc depends on interactions with other food components. Phytates negatively affect this element’s absorption, whereas proteins, peptides, and amino acids increase its bioavailability. It has been proven that organic forms of zinc are better absorbed than inorganic compounds, like zinc oxide and sulfate. Amino acid combinations with zinc can use amino acid transporters in the absorption process. Estimation of Zn bioavailability and bioaccessibility are based on in vivo and in vitro studies, each having their advantages and disadvantages. The current review aims to gather and summarize recent research on the dietary role of Zn, especially data on bioavailability from food substances promoting/inhibiting absorption, and the latest methods for determining the level of bioavailability of this nutrient. Full article

Ultraprocessed foods (UPFs), now dominant in global diets, pose health risks that go beyond poor nutrition due to the synergistic effects of compounds in their ultracomplex industrial formulations. This narrative review aims to provide researchers and health professionals in the field of cancer with updated and critical information, as they are often unaware of the complex and evolving evidence linking UPFs to carcinogenesis. The review discusses potential mechanisms through which UPFs may contribute to cancer development, including harmful additives, neo-formed contaminants, and packaging-derived substances, as well as the displacement of protective nutrients found in whole foods. Despite limitations in establishing direct causality, epidemiological studies consistently associate high UPF intake with increased incidence of various cancers, notably colorectal, breast, and pancreatic cancers. These findings reflect a broader paradigm shift in nutritional epidemiology, recognizing that food processing is an essential dimension of diet-related health risks. To mitigate the impact of UPFs, the review emphasizes the need for preventive strategies that integrate clear dietary guidelines, regulatory measures on food labeling and additives, and public education campaigns. Successful international experiences in regulating marketing and improving transparency serve as important references. Moreover, eliminating corporate influence and conflicts of interest is crucial to ensure that public health, rather than industry agendas, guides nutrition policy. As scientific research advances to clarify the mechanisms of action and synergistic effects of harmful compounds in UPFs, coordinated efforts are needed to reduce their consumption and ultimately alleviate the global cancer burden. Full article