Search Results (15,959)

Type 2 diabetes mellitus (T2D) is a major and growing global health burden that is associated with substantial cardiovascular, renal, and metabolic complications and is increasingly recognized as a systemic disorder involving multiple organs, particularly the liver. Metabolic dysfunction-associated steatotic liver disease (MASLD) affects more than half of individuals with T2D, and the two conditions have a bidirectional relationship: T2D promotes the development and progression of MASLD, including advanced fibrosis and increased liver-related mortality, while MASLD worsens insulin resistance and metabolic control, favoring the onset of T2D. In this context, the liver is increasingly viewed not only as a metabolic organ but also as an endocrine one, secreting hepatokines that act on distant tissues to regulate insulin sensitivity, inflammation, glucose metabolism, and lipid homeostasis. Through these actions, hepatokines are thought to represent one of the mechanistic links between MASLD and T2D. This narrative review summarizes current evidence on several of the most extensively studied hepatokines, including fibroblast growth factor 21, fetuin-A, fetuin-B, leukocyte cell-derived chemotaxin-2, selenoprotein P, angiopoietin-like proteins, and retinol-binding protein 4. As a distinctive feature, the review also discusses emerging pharmacological strategies targeting hepatokine pathways and evaluates how commonly used antidiabetic therapies may modulate hepatokine secretion. Full article

Policosanol (sugarcane wax alcohol), phosphatidylserine, and Ginkgo biloba leaf extract are Ministry of Food and Drug Safety (MFDS), Republic of Korea-listed functional foods for health-promoting effects. Herein, a combination of policosanol, phosphatidylserine, and G. biloba leaf extract (hereafter PPG) was investigated against metabolic stress induced by a high-cholesterol, high-galactose (HCHG) diet in hyperlipidemic and hyperglycemic zebrafish. After 9 weeks of feeding, the zebrafish following the HCHG diet co-supplemented with PPG exhibited a significant 14.1% (p < 0.02) reduction in body weight and higher zebrafish survivability compared to the HCHG-supplemented group. Significantly reduced total cholesterol (TC, 1.2-fold), triglycerides (TG, 1.4-fold), low-density lipoprotein cholesterol (LDL-C, 1.3-fold), and glucose levels (1.2-fold), along with a 1.5-fold (p = 0.003) elevated high-density lipoprotein cholesterol (HDL-C), were observed in the PPG co-supplemented group relative to the HCHG group. In addition, the HCHG-elevated plasma malondialdehyde (MDA), diminished ferric ion reduction activity (FRA), and paraoxonase (PON)-like activity significantly (p < 0.001) reverted by 1.6-fold, 1.4-fold, and 1.6-fold, respectively, by co-supplementation with PPG. Consistently, the plasma from the PPG-supplemented group showed greater ability to prevent carboxymethyllysine (CML)-induced apoptotic death, altered heart rate, and developmental deformities in zebrafish embryos. Moreover, PPG exerted significant protective effects against HCHG-induced hepatomegaly and fatty liver, accompanied by marked inhibition of hepatic interleukin (IL)-6 and reactive oxygen species (ROS) generation. Consistently, PPG supplementation inhibits ROS generation and senescence in the liver, intestine, brain, kidney, testis and ovary and protects the organ damage caused by exposure to HCHG. Similarly, in intestinal tissue, HCHG-induced fibrosis and oxidative stress were mitigated by the co-supplementation of PPG. The findings indicate that PPG is an effective combination for preventing dyslipidemia, oxidative stress, inflammation, and multi-organ damage associated with HCHG-mediated metabolic stress in zebrafish. Full article

Background/Objectives: Vitamin D is a pleiotropic substance that plays a pivotal role in the human body. Several studies have suggested sex-based differences in vitamin D metabolism. Recently, the vitamin D metabolite ratio (VMR), defined as the ratio of serum 24,25-dihydroxyvitamin D [24,25(OH)₂D] to 25-hydroxyvitamin D [25(OH)D], has been identified as a novel marker that may more accurately reflect vitamin D status than serum 25(OH)D alone. This study aimed to assess whether significant variability exists in the VMR across different demographic groups. Methods: Residual serum samples and laboratory data were collected from healthy adults who underwent health checkups at a health center in Japan. Serum concentrations of 25(OH)D₃ and 24,25(OH)₂D₃ were simultaneously measured using a fully automated liquid chromatography–tandem mass spectrometry (LC-MS/MS) system. Factors affecting the levels of 25(OH)D₃, 24,25(OH)₂D₃, and VMR were analyzed using multiple regression analysis and the stabilized inverse probability weighting method. Results: Tentative reference intervals for 24,25(OH)₂D₃ were found to be 0.3–3.0 ng/mL for males and 0.2–2.3 ng/mL for females. Those for VMR were found to be 3.0–11.8% for males and 2.5–10.4% for females, demonstrating statistically significant but moderate differences between the sexes. These differences remained significant even after adjusting for baseline covariates including 25(OH)D₃. However, the standard deviation ratios were less than 0.5. An estimated glomerular filtration rate and an age of ≥50 years were positively associated with 24,25(OH)₂D₃ and VMR, whereas diabetic status was negatively associated with these markers. Conclusions: This study revealed moderate sex-based differences in markers of vitamin D metabolism. Although further research is needed to determine whether these differences are consistent across other populations, future epidemiology and clinical interventions should take into consideration of the sex-based differences in vitamin D metabolism. Full article

Marine bacteria represent a vast and largely untapped resource for biotechnological innovation, offering solutions to global challenges in health, sustainability, and environmental conservation. The ocean’s unique conditions have driven marine bacteria to evolve diverse metabolic capabilities, resulting in the production of bioactive compounds, enzymes, and other metabolites with wide-ranging applications. Recent advances in high-throughput sequencing, metagenomics, and analytical chemistry have unlocked new opportunities for leveraging these microorganisms in fields as varied as medicine, agriculture, and bioremediation. This review highlights the role of marine bacteria in the One Health framework, showcasing their contributions to antimicrobial discovery, nutraceutical development, pathogen biocontrol, and environmental cleanup, including microplastic degradation. This review also examines emerging methodologies such as microbiome mining and advanced culturing techniques, which hold the key to realizing the full potential of marine bacteria in a sustainable bioeconomy. By bridging fundamental research with applied sciences, marine biotechnology promises to deliver transformative impacts on human, animal, and environmental health. Full article

Chronic kidney disease (CKD) represents a major global health challenge, affecting more than 10% of the population and contributing substantially to morbidity and premature mortality. Growing evidence identifies oxidative stress and mitochondrial dysfunction as central drivers of renal injury and disease progression across diverse etiologies. The kidney is one of the most mitochondria-rich organs in the body, reflecting the high bioenergetic demands required for tubular reabsorption and metabolic homeostasis. Disruption of mitochondrial oxidative phosphorylation, excessive production of reactive oxygen species (ROS), and impaired mitochondrial quality control mechanisms promote tubular injury, inflammation, and fibrosis. In particular, dysfunction of the electron transport chain, activation of NADPH oxidase isoforms—especially NOX4—and alterations in mitochondrial dynamics create a vicious cycle of oxidative damage and bioenergetic failure. Emerging evidence highlights the importance of mitochondrial quality control pathways, including fusion–fission balance, PINK1/Parkin-mediated mitophagy, and mitochondrial biogenesis regulated by PGC-1α and TFAM. Additional mechanisms include ferroptosis, epigenetic regulation, mitochondrial DNA-mediated innate immune activation, and Na⁺/K⁺-ATPase-linked redox signaling. At the translational level, redox and mitochondrial biomarkers and targeted therapies are biologically compelling, but the evidence is uneven: most candidate biomarkers remain insufficiently standardized, and direct mitochondria-targeted interventions are supported predominantly by preclinical studies or small human proof-of-concept trials. This review therefore emphasizes not only mechanistic advances but also conflicting findings, model limitations, and the barriers that currently separate experimental efficacy from clinically meaningful CKD outcomes. Full article

Background: Malnutrition is a significant clinical problem in patients with cancer, occurring not only during hospitalization but also throughout the recovery phase. It brings severe health and economic consequences, affecting patients on both physical and psychological levels. The American Society for Parenteral and Enteral Nutrition (ASPEN) and the European Society for Clinical Nutrition and Metabolism (ESPEN) emphasize the critical importance of early detection of nutritional disorders and timely intervention in oncology populations. The aim of this study was to determine the prevalence of malnutrition and factors associated with malnutrition among hospitalized Polish oncology patients and to draw attention to the need for early nutritional assessment in patients with cancer so as to ensure appropriate nutritional care. Methods: A multicenter cross-sectional study was conducted in accordance with the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) guidelines among adult patients diagnosed with cancer and undergoing oncological treatment. Data collection involved a structured survey questionnaire, anthropometric measurements, and validated screening tools: Mini Nutritional Assessment (MNA), Nutritional Risk Screening Score 2002 (NRS 2002), and Subjective Global Assessment (SGA). Results: The study group comprised 560 patients with a mean age of 55 ± 13.95 years, including 59% women and 41% men. The mean duration of illness was 3.37 years. Advanced-stage cancer was present in 43% of participants, and 66% were undergoing chemotherapy. The mean Body Mass Index (BMI) for the study group was 23.14 kg/m², with a mean MNA score of 16.23 points and a mean NRS 2002 score of 2.39 points. Based on Subjective Global Assessment, moderate malnutrition was identified in 45% of patients, whereas severe malnutrition was confirmed in 27% of the study population. Conclusions: The prevalence of malnutrition among oncology patients is high. Early screening and regular monitoring are essential for the prompt identification of patients at risk, enabling the implementation of appropriate nutritional therapy and the improvement of clinical outcomes. Full article

High-intensity interval training (HIIT) is widely recognized as an effective strategy for improving cardiorespiratory fitness and metabolic health. Beyond these physiological benefits, growing evidence indicates that HIIT may also induce beneficial immunometabolic adaptations. A key exercise-responsive metabolite in this context is lactate, which is increasingly being recognized not as a metabolic waste product but as a bioactive signaling metabolite capable of coordinating metabolic, inflammatory, and immune processes. This narrative review examines current evidence suggesting a potential role for exercise-induced lactate in immune responses associated with HIIT. We summarize the molecular pathways through which lactate may interact with immune cells, including uptake via monocarboxylate transporters (MCT1/MCT4) and SLC5A12, receptor-dependent signaling through GPR81/HCAR1, and epigenetic regulation via histone lactylation. We further discuss the cell-specific effects of lactate on macrophages, dendritic cells, neutrophils, and T lymphocytes, highlighting how these mechanisms may influence immune-cell metabolism, inflammatory regulation, and functional remodeling. A central concept emerging from the current literature is that the biological actions of lactate are highly dependent on the kinetics, duration, and physiological context of exposure. Unlike pathological lactate elevations observed in conditions such as cancer, sepsis, or mitochondrial myopathies—the latter potentially involving an exaggerated lactate response during exercise due to impaired oxidative metabolism—HIIT generates transient systemic lactate elevations as part of a coordinated neuroendocrine and metabolic response. When combined with adequate recovery, these repeated metabolic perturbations may promote hormetic adaptations characterized by improved inflammatory regulation, enhanced immune resilience, and more efficient immunometabolic homeostasis. Conversely, excessive training loads or inadequate recovery may shift these responses toward maladaptive immune stress. Overall, current evidence suggests a paradigm shift in exercise immunology in which lactate should be regarded as one component of an integrated immunometabolic signaling network rather than simply as a marker of anaerobic metabolism. Future mechanistic studies integrating lactate kinetics, immune-cell phenotyping, transporter expression, and lactate-dependent post-translational modifications are needed to clarify the extent to which lactate may contribute to exercise-induced immune remodeling and to guide the development of immunologically informed HIIT protocols. Full article

(1) Background: Mosquitoes represent major vectors of human pathogens, and their control remains a global public health priority. However, the widespread use of synthetic insecticides has resulted in environmental contamination, adverse effects on non-target organisms, and the rapid emergence of insecticide resistance. These limitations have intensified the search for sustainable botanical alternatives. (2) Methods: The present study investigated the phytochemical composition and larvicidal efficacy of flower extracts from Chrysanthemum cinerariaefolium and Oenothera biennis, alongside their nanoemulsion formulations, against the third-instar larvae of Culex pipiens. Larvicidal assays demonstrated that nanoemulsion formulations markedly enhanced bioactivity compared with conventional extracts. (3) Results: After 48 h of exposure, C. cinerariaefolium nanoemulsion exhibited the strongest toxicity (LC₅₀ = 26.63 ppm), followed by methanol (44.46 ppm), hexane (73.90 ppm), and aqueous extracts (209.99 ppm). Corresponding LC₅₀ values for O. biennis were 31.89, 80.15, 140.69, and 393.22 ppm, respectively. Biochemical analyses indicated that C. cinerariaefolium treatments strongly inhibited detoxification and digestive enzymes (esterases, GABA-T, amylase, and lipase) and suppressed antioxidant defenses (SOD, GST, CAT, and GSH). This was accompanied by a significant elevation of oxidative stress biomarkers, including lipid peroxidation and protein carbonylation. In contrast, O. biennis induced comparatively moderate biochemical responses. The phytochemical profiling utilizing GC-MS revealed the identification of forty-nine and fifty volatile components from the C. cinerariaefolium (CW-Hex) and O. biennis (BOF) n-hexane extracts, respectively, primarily consisting of oxygenated hydrocarbons, fatty acids, and their esters. Furthermore, UPLC-MS/MS-assisted profiling of methanol, ethyl acetate, and aqueous extracts identified thirty-eight metabolites for CW and thirty-one for BOF. The CW extracts were predominant in flavonoids and fatty acids while also containing cinnamic acid derivatives, phenolic acids, diterpenoids, triterpenoids, pyrethrins, phenyl ethanoids, steroids, aurones, and tannins. BOF extracts were particularly rich in flavonoids, followed by fatty acids, cinnamic acid derivatives, tannins, and steroids. (4) Conclusions: These findings demonstrate that plant-derived formulations of C. cinerariaefolium, particularly in nanoemulsion form, exert potent larvicidal activity through the disruption of metabolic and antioxidant pathways, offering a promising eco-friendly strategy for vector control. Full article

Background: Understanding the nasopharyngeal (NAS) and rectal (INT) microbiomes is critical to maintain host health. However, their functional roles in shaping microbial network structure and niche differentiation remain unexplored in most animal species, especially endangered primates. Here, we compared the NAS and INT microbiomes of golden snub-nosed monkeys (Rhinopithecus roxellana) using full-length 16S rRNA amplicon sequencing and metagenomics, focusing on taxonomic composition, functional profiles (KEGG, CAZy, PHI), and microbial co-occurrence networks. Results: Our results indicate that microbial community structure and diversity (Shannon evenness) differ significantly between the two niches. Taxonomically, both sequencing approaches consistently show that, at the relative-abundance level, NAS is dominated by genera such as Dolosigranulum and Vibrio, whereas the INT is characterized by Campylobacter, Helicobacter, and Aerococcus. Notably, metagenomic analysis indicates a relatively high abundance of potential pathogens, including Helicobacter pylori and Chlamydia psittaci. LEfSe analysis shows Dolosigranulum and Campylobacter are key microbial markers for the NAS and INT niches, respectively. KEGG pathway analysis reveals that the NAS microbiome is enriched in valine/leucine/isoleucine degradation and glutathione metabolism, while the INT microbiome is enriched in amino sugar and nucleotide sugar metabolism and ribosome pathways. At the CAZy level, all 29 differentially abundant families (e.g., GH13_29, GH103, AA3_2) were enriched in the NAS. Distinct pathogen–host interaction profiles further reflect niche-specific adaptations. Exploratory Spearman-based co-occurrence networks (in which no genus–CAZy edge survived Benjamini–Hochberg (FDR) correction) linked core commensals to KEGG pathways and CAZy families (e.g., GT35, GH0). In the INT, Campylobacter and Helicobacter form high-connectivity modules associated with pathways such as those involving the two-component system and ABC transporters. Conclusions: The nasopharyngeal and rectal microbiomes in golden snub-nosed monkeys differ not only taxonomically but also functionally, exhibiting clear spatially specialized functional differentiation. Given the small sample size (n = 8), these findings provide preliminary evidence for niche-specific microbial and functional partitioning and suggest that the nasopharynx may harbor a relatively high abundance of potential zoonotic pathogens. This study provides a basis for further exploration with a larger sample size. Full article

Background: Lifestyle behaviors and psychosocial factors are key determinants of cardiometabolic health across the life course. Beyond traditional risk factors, emerging evidence suggests that chronic stress and burnout may influence metabolic risk through behavioral pathways such as physical inactivity and poor diet. However, their joint contribution to type 2 diabetes risk in working populations remains insufficiently understood. Objectives: Our objectives were to examine the joint contribution of lifestyle habits, sociodemographic factors, and burnout to type 2 diabetes risk, and to explore potential behavioral pathways linking psychosocial stress to metabolic risk in a large adult population. Methods: A cross-sectional study was conducted in 92,480 Spanish workers undergoing routine occupational health assessments between 2021 and 2023. Type 2 diabetes risk was assessed using validated tools (FINDRISC, QDScore, CANRISK). Lifestyle indicators included adherence to the Mediterranean diet and physical activity levels; burnout was assessed using the Burnout Assessment Tool (BAT). Multivariable logistic regression models were used to evaluate associations between determinants and diabetes risk. Mediation analyses were performed to assess the contribution of lifestyle behaviors to the association between burnout and diabetes risk, and predictive performance analyses evaluated the incremental value of burnout. Results: Burnout was independently associated with a higher probability of moderate-to-high diabetes risk across all screening tools. Exploratory cross-sectional mediation analyses indicated that lifestyle behaviors, particularly physical inactivity and low adherence to the Mediterranean diet, statistically accounted for approximately 45% of the observed association. Adding burnout to the models significantly improved discrimination and reclassification of moderate-to-high diabetes-risk classification. In addition, higher diabetes risk was consistently observed among individuals from lower socioeconomic groups and those with unhealthy lifestyle profiles. Conclusions: Lifestyle behaviors and psychosocial stress were associated with estimated diabetes risk across adulthood. Burnout was independently associated with a higher probability of moderate-to-high diabetes-risk classification, with exploratory analyses suggesting that lifestyle behaviors may statistically account for part of this association. These cross-sectional findings highlight the potential relevance of considering both behavioral and psychosocial factors when studying cardiometabolic risk in working populations, while prospective studies are needed to establish temporal and causal relationships. Full article

Background: Technostress has emerged as a growing occupational health concern in increasingly digitalized workplaces. Although its psychological consequences have been extensively investigated, little is known about its potential association with metabolic health and insulin resistance. This study aimed to evaluate the relationship between technostress and insulin resistance risk using four validated surrogate markers in a large cohort of Spanish workers. Methods: A cross-sectional study was conducted among 104,175 Spanish workers who underwent routine occupational health assessments. Technostress was assessed using a 15-item questionnaire covering five technostress dimensions and was analyzed using four operational categories (low, moderate, high, and very high). Insulin resistance risk was assessed using the triglyceride–glucose (TyG) index, TyG-body mass index (TyG-BMI), the metabolic score for insulin resistance (METS-IR), and the single-point insulin sensitivity estimator (SPISE). Sociodemographic characteristics, lifestyle habits, anthropometric measurements, and biochemical parameters were also recorded. Modified Poisson regression with robust variance estimation was used to estimate crude and adjusted prevalence ratios (PRs) for increased insulin resistance risk according to technostress level. Firth penalized logistic regression was additionally performed as a sensitivity analysis to address sparse-data bias and separation. Results: Higher technostress levels were associated with progressively less favorable anthropometric and metabolic profiles. The prevalence of increased insulin resistance risk rose significantly across technostress categories for all markers evaluated (p < 0.001). For TyG, prevalence increased from 3.8% in the low technostress group to 54.3% in the very high technostress group. Corresponding increases were observed for TyG-BMI (0.2% to 78.2%), METS-IR (0.0% to 45.2%), and elevated SPISE-IR values (0.0% to 57.5%). After adjustment for age, sex, educational level, physical activity, adherence to the Mediterranean diet, and smoking status, higher technostress remained associated with a higher prevalence of increased insulin resistance risk. A clear graded cross-sectional pattern was observed, with the strongest associations found among workers reporting very high technostress. Conclusions: Higher technostress was associated with a higher prevalence of increased insulin resistance risk according to TyG, the primary outcome, with a clear graded cross-sectional pattern across technostress categories. Associations were also observed for the secondary BMI-containing indices (TyG-BMI, METS-IR, and SPISE-IR), which should be interpreted as complementary rather than independent evidence. Given the cross-sectional design and the pronounced clustering of technostress with adiposity and lifestyle characteristics, residual confounding cannot be excluded and causal inference is not possible. Full article

Recurrent vulvovaginal candidiasis (RVVC), commonly defined as ≥3 symptomatic episodes per year, affects an estimated 138 million women worldwide. This structured narrative review (PubMed/MEDLINE and open-indexed sources, January 2020–July 2026, as well as selected pre-2020 landmark studies) synthesizes epidemiological and metabolic risk factors (including SGLT2-inhibitor-associated susceptibility), host immunogenetic and vaginal microbiome mechanisms, emerging preventive pharmacotherapies, and patient-reported outcomes within a unified clinical framework. RVVC arises from interacting host, microbial, metabolic, behavioral, and iatrogenic domains—diabetes-related hyperglycemia, innate immune polymorphisms (MBL2, TLR2), altered bacterial–fungal vaginal communities, and non-albicans Candida in difficult-to-treat cases. Fluconazole maintenance remains a guideline-supported suppressive option but relapse after discontinuation is common; oteseconazole and ibrexafungerp expand prevention choices, while probiotics show inconsistent, low-certainty benefit. RVVC consistently impairs health-related quality of life, sexual function, and mental health and imposes substantial economic burden; regional data from Southeastern Europe underscore diagnostic and access gaps. We propose a multifactorial host–pathogen–microbiome model that favors individualized, diagnosis-driven management and routine incorporation of validated patient-reported outcomes. Research priorities include harmonized case definitions, head-to-head trials of new agents, validated quality-of-life instruments, longer post-treatment follow-up, and real-world cost-effectiveness evaluations. Implementation research, equitable access strategies, clinician education, and national health policy are essential to translate evidence into improved patient outcomes globally. Full article

Endocrine system hormones regulate growth, metabolism, and reproduction. These hormones often function at low concentrations, making them especially susceptible to disruption via endocrine-disrupting chemicals (EDCs) that can mimic, block, or disturb normal hormone signaling. Among these EDCs, polychlorinated biphenyls (PCBs) and per- and polyfluoroalkyl substances (PFAS) are of special concern for human health because they are persistent and bioaccumulate. In this review, we focus on effects of PCBs and PFAS on female reproduction, with emphasis on steroidogenesis, ovarian function, fertility, and assisted reproductive technology (ART) outcomes. We describe the chemical properties and exposure routes of PCBs and PFAS, and how these features explain their long half-lives and ability to transfer to the female reproductive system and fetus. Evidence suggests that both PCBs and PFAS can reduce follicle numbers, disturb oocyte quality, and increase oxidative stress and apoptosis. Human and animal data also link PCB and PFAS exposure with altered ART outcomes. Together, the literature indicates that persistent exposure to PCBs and PFAS poses a significant and long-lasting risk to female reproductive health. Full article

Functional pet foods are increasingly being developed to support host metabolism and intestinal health. Lycium barbarum polysaccharide (LBP), a major bioactive component of goji berries, has been reported to possess antioxidant, anti-inflammatory, immunomodulatory, and gut microbiota-regulatory activities; however, its effects in domestic cats remain unclear. This study investigated the effects of dietary LBP supplementation on serum metabolomic profiles and gut microbiota in adult cats. Twenty-four healthy adult Chinese domestic cats (1.50 ± 0.50 years old; 3.70 ± 0.80 kg) were allocated to four groups using a body-weight-balanced procedure (n = 6 per group): a basal diet group (C) and basal diet supplemented with 0.2% (L), 0.3% (M), or 0.4% (H) LBP. After a 1-week adaptation period, the formal feeding trial lasted 8 weeks. Growth-related indices, health scores, hematological and serum biochemical parameters, untargeted serum metabolomics, and fecal 16S rRNA sequencing were evaluated. LBP supplementation did not significantly affect body weight, average daily feed intake, body condition score, fecal score, coat score, hematological indices, or serum biochemical parameters. Metabolomic analysis showed that LBP mainly affected lipid metabolism, unsaturated fatty acid biosynthesis, branched-chain amino acid metabolism, lysine degradation, and protein digestion and absorption-related pathways. Microbiota analysis showed changes in alpha diversity, community structure, and the relative abundance of taxa such as Olsenella, Bifidobacterium, Catenibacterium, Peptoclostridium, Collinsella, and Clostridium. Correlation analysis suggested potential associations between key bacterial genera and serum metabolites related to fatty acid and amino acid metabolism. Overall, dietary LBP altered serum metabolic signatures and gut microbial composition without causing adverse effects in adult cats, These exploratory findings require confirmation in larger feline studies and do not establish an optimal supplementation level. Full article

Glyphosate is an herbicide used to control plant growth and ripen specific crops. Glyphosate exposure has been associated with cancer, metabolic and neurological diseases, and reproductive issues in humans. A common element linking these disorders could be vitamin D deficiency. However, the relationship between glyphosate exposure and vitamin D status in the general population remains unclear. This analysis focused on the association between urinary glyphosate levels and serum 25-hydroxy vitamin D [25(OH)D] concentrations in a large representative sample of U.S. adults. Data from 4284 participants in the National Health and Nutrition Examination Survey (NHANES) between 2013–2018 were analyzed. Serum 25(OH)D levels were modeled using multivariable weighted linear regression, with adjustment for age, sex, race/ethnicity, body mass index, season, education, income, physical activity, smoking, and kidney function. Urinary glyphosate concentration was inversely associated with serum 25(OH)D in both the design-based univariate weighted analysis (β = −3.537, p = 0.035) and adjusted survey-weighted models for major confounding factors (β = −4.208, p = 0.009), using Taylor linearization for variance estimation to account for the complex NHANES survey design. In stratified analysis, the relationship between total vitamin D intake and serum 25(OH)D was found to be significantly modified by glyphosate exposure, with stronger dietary dependence observed in the high-exposure tertile (β = 12.88, p < 0.0066) than in the low-exposure tertile (β = 7.41, p < 0.0165). Higher urinary glyphosate concentration was associated with lower serum 25(OH)D levels in U.S. adults, suggesting it may represent an unrecognized risk factor for vitamin D deficiency. Longitudinal and experimental studies are needed to clarify causality, the underlying mechanisms, and public health implications. Full article