The use of contaminated cereals in fermentation processes can elicit a marked response from yeasts in the presence of mycotoxins, as indicated by the production of defense compounds such as peroxidase (PO) and glutathione (GSH) to reduce mycotoxin damage. The objective of this study was to investigate the effect of fortifying GSH and PO levels in alcoholic fermentation as a strategy for reduce concentration deoxynivalenol (DON) during the brewing process. The QuEChERS method was validated for quantifying the mycotoxin and estimating reduction. Fermentation was conducted in a reactor containing 20 mL of synthetic wort inoculated with Saccharomyces cerevisiae (0.115 g). The reduction of DON was evaluated using a 24-1 fractional factorial design with the following independent variables: GSH concentration (0-50 mg L-1), PO activity (0-0.4 U mL-1), fortification time (0-48 h), and DON concentration (0.1-0.3 µg mL-1). The results of reducing the concentration of DON in experimental planning ranged from 76,2% to non-detection of mycotoxin, significantly, with PO activity as a significant variable. Fortification with GSH and PO was significant in the decrease of DON when it was at a higher level, increasing by 39% compared to the control. Supplementation with GSH and PO demonstrated in this study indicates the effectiveness of DON reduction in the evaluated contamination levels.

Pancreatogenic diabetes mellitus (type 3c diabetes mellitus, T3cDM) is an underrecognized form of secondary diabetes resulting from pancreatic exocrine disease, including chronic pancreatitis and pancreatic resection. It is frequently misclassified as type 2 diabetes mellitus, leading to delayed diagnosis and suboptimal management. We present a case of a 57-year-old female with a history of chronic alcoholic pancreatitis status post partial pancreatectomy who presented with severe uncontrolled hyperglycemia and medication nonadherence. Laboratory evaluation revealed a serum glucose of 668 mg/dL, hemoglobin A1c of 19%, and a low C-peptide level with normal insulin levels while receiving exogenous insulin, consistent with impaired endogenous insulin secretion and pancreatogenic diabetes. Despite repeated counseling and multiple attempts to optimize insulin therapy, the patient persistently refused insulin administration, resulting in refractory hyperglycemia throughout hospitalization. This case highlights the diagnostic challenges of distinguishing pancreatogenic diabetes from type 2 diabetes mellitus in patients with underlying pancreatic disease and emphasizes the importance of recognizing characteristic clinical features, including prior pancreatic injury and reduced endogenous insulin production. Early identification of T3cDM is essential because its pathophysiology and management differ substantially from type 2 diabetes mellitus and often require early insulin-based therapy to improve glycemic control and reduce long-term metabolic complications.

Alcoholic ketoacidosis (AKA) is a metabolic disturbance triggered by excessive alcohol intake and fasting, typically presenting as a high-anion-gap metabolic acidosis with ketosis. We report a severe case of AKA with extreme hyperlactatemia, in which the patient developed shock and disseminated intravascular coagulation, emphasizing early recognition and timely intervention.

Yeast derivative products (YDPs) are widely employed in modern oenology as technological tools to modulate fermentation performance, improve wine stability, and enhance sensory quality. Derived mainly from Saccharomyces cerevisiae and, more recently, even from non-Saccharomyces yeasts, YDPs encompass a heterogeneous group of products including inactivated yeasts, autolysates, yeast protein extracts, yeast hulls, and mannoproteins, which composition and functionality depend on yeast strain and manufacturing process. Despite their extensive use, a comprehensive understanding of the relationships among YDP composition, mechanisms of action, and oenological performance remains limited. In this context, this review aims to provide a critical and integrated overview of YDPs, covering their technological applications throughout the winemaking process. Particular attention is devoted to their role in fermentation management (alcoholic, malolactic and secondary fermentations), as well as to their antioxidant capacity. Their contribution to wine stabilization, including colloidal equilibrium, and tartaric, protein, and color stability, together with their impact on sensory properties was also explored. The multifactorial mechanisms underlying YDP activity, such as nutrient supply, adsorption of inhibitory compounds, release of polysaccharides and peptides, and redox modulation, are discussed to rationalize their technological effects. Overall, YDPs emerge as versatile tools that can support both wine quality improvement and process sustainability. Their effectiveness, however, is closely linked to wine and application conditions, highlighting the need for a more targeted and mechanistic approach to their use. Advancing the understanding of structure-function relationships will be essential to optimize their application and to foster the development of precision oenology strategies.

Non-Saccharomyces played a crucial role in huangjiu brewing. To explore the influence of aroma-producing Rhodotorula mucilaginosa H04, huangjiu samples fermented with S. cerevisiae (CK) and produced through co-fermentation with R. mucilaginosa and S. cerevisiae (COF) were evaluated. The total organic acid and amino acid content in COF were significantly reduced (P < 0.05). E-tongue revealed that the umami response value of the COF samples was highest and the sourness was lowest (P < 0.05). The esters and alcohols were significantly enhanced in the COF, endowing floral, fruity, and alcoholic aroma of huangjiu (P < 0.05). ROAV analysis identified that pentanal (-4.3 kcal/mol) and decanal (-6.4 kcal/mol) showed strong binding energy with OR1A1 through hydrogen bonding and hydrophobic interactions. Correlation analysis revealed that using R. mucilaginosa altered the relative abundance of microbial community, especially that of bacterial communities. Co-fermentation with R. mucilaginosa and S. cerevisiae significantly had improved the flavor quality of huangjiu by enhancing key aroma compounds, optimizing taste attributes, and modulating microbial community structure.

Age is a risk factor for severity and progression of Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD), yet its specific contributions to liver injury and molecular alterations remain unclear. Current animal models often overlook this variable. This study investigates how aging influences MASLD progression in a murine model, focusing on histological, biochemical, and transcriptomic differences. Young (2-month-old) and middle-aged (10-month-old) C57BL/6N male and female mice were fed chow (CD) or high-fat diet (HFD) for 20 weeks. Metabolic and biochemical parameters were assessed, and liver tissue analyzed by histology and RNA sequencing. Differentially expressed genes were identified with Limma, followed by gene ontolgy enrichment. Translational relevance was evaluated using the MASLD Human Proximity Score (MHPS). Middle-aged males developed insulin resistance and more severe hepatic injury than young males after HFD. Histological and biochemical assessments confirmed advanced disease in middle-aged mice, with extensive lipid accumulation, hepatocellular hypertrophy, inflammation and fibrosis. Females showed milder damage. Diet was the main determinant of transcriptomic changes in males: young HFD mice activated tissue remodeling pathways, whereas middle-aged mice showed inflammatory activation and reduced energy metabolism. In females, transcriptomic responses were attenuated, with metabolic and stress-related changes restricted mostly to young HFD animals. MHPS ranked the middle-aged male model highest in similarity to human MASLD. Age is a critical determinant of hepatic responses to dietary stress, with sex-specific modulation. The middle-aged male model closely mirrors human MASLD, providing a more relevant preclinical platform to improve patient stratification and therapeutic discovery.

Metabolic dysfunction and alcohol exposure drive steatotic liver disease, yet how ethanol intersects with metabolic steatohepatitis remains incompletely defined. Our iterative model examined how ethanol ingestion alters high-fat, -fructose, and -cholesterol (FFC)-driven liver injury, identifying MetALD-relevant features. A pilot study in male and female C57BL/6J mice compared chow diet (CD), FFC, CD+ethanol (E), and FFC+E on high-glucose/fructose (sugar) water (SW) at 6, 16, and 24 weeks. A redesigned study lowered glucose/fructose exposure, modified ethanol acclimation, and tested five male cohorts, CD, CD+SW, FFC+SW, CD+SW+E, FFC+SW+E, at 16 and 24 weeks. In the pilot study, FFC-dominant hepatomegaly, aminotransferase elevation, steatosis, chemokine induction, and fibrosis, without additive ethanol effects were observed. In the redesigned model, FFC drove weight gain, hepatomegaly, steatosis, aminotransferase elevation, and Ccl2/Timp1-associated fibroinflammatory remodeling. However, ethanol selectively modified collagen-positive fibrotic remodeling and lipid-droplet architecture. At 16 weeks, FFC+SW+E increased collagen area compared with FFC+SW despite lower body/liver mass and no additive aminotransferase response. BODIPY morphometry showed enlarged lipid-droplets in both FFC groups, but FFC/ethanol demonstrated reduced lipid-droplet area. In contrast, hepatic triglycerides increased with FFC but did not differ between FFC+SW and FFC+SW+E, supporting altered lipid-storage architecture rather than lipid accumulation or steatosis. Cxcl1 was induced by ethanol in CD mice but not uniformly upregulated on FFC. By 24 weeks, fibrosis, alpha smooth muscle actin staining, qPCR markers, and NanoString immune profiles converged between FFC groups. Thus, chronic ethanol in a MetALD mouse model selectively modifies collagen-positive fibrotic remodeling, lipid-storage and inflammatory features of FFC-driven liver injury.

Astringency is an important mouthfeel attribute in many beverages, yet its neurophysiological correlates remain poorly understood. It also remains unclear how beverage matrix shapes frontal hemodynamic responses to astringency over time. This study used functional near-infrared spectroscopy (fNIRS) to characterize prefrontal hemodynamic responses to proanthocyanidin (PAC)-induced astringency in three matrices: water, ethanol, and red wine. To capture temporal aspects of the perceptual experience, responses were assessed separately during the induction and aftertaste phases. Sensory evaluation showed that perceived astringency increased with PAC concentration, although both the magnitude and time course of this increase varied across matrices. During the induction phase, frontal HbO responses were generally limited and less consistent. By contrast, the aftertaste phase was associated with broader and stronger prefrontal HbO responses. Region-of-interest analysis further revealed distinct matrix-related response patterns in channels corresponding anatomically to the orbitofrontal cortex (OFC), frontopolar area (FPA), and dorsolateral prefrontal cortex (DLPFC), suggesting that lingering astringency may involve distributed evaluative processing rather than a simple representation of perceived intensity. Overall, prefrontal HbO responses to astringency differed between the induction and aftertaste phases and varied across beverage matrices. This work extends current understanding of astringency as a matrix-sensitive sensory process and provides useful neurophysiological evidence concerning the frontal hemodynamic correlates of persistent mouthfeel attributes in food systems.

Survival depends on adaptive decision-making wherein the benefits of seeking food are weighed against the risk of threats, a process influenced by internal states like hunger. Highly palatable, calorie-dense foods, such as a high-fat-containing diet (HFD), potently drive feeding even in the absence of hunger. However, it remains unclear whether approach-avoidance conflict is shaped by the interaction between hunger state, motivation for rewards of differing palatability, and the lasting effects of chronic high-fat diet exposure (cHFD). Here, we examined how hunger, reward value, and cHFD exposure affect behavioral strategies for resolving approach-avoidance conflict. We established a modified platform-mediated avoidance (PMA) task where mice resolve conflict between approaching a reward and avoiding a footshock. In this task, we systematically manipulated three key variables: (1) hunger state [via 6-hour (6h) vs. 23-hour (23h) food restriction], (2) reward type (sucrose vs. a high-fat liquid (HF-reward)), and (3) diet history (cHFD vs. control diet). We found that hunger, reward value, and diet pre-exposure shaped conflict resolution. Hunger increased risk-taking, with 23h food-restricted mice seeking more rewards than mice with limited 6h food restriction. Similarly, HF-reward increased approach behavior even under 6h food restriction. Importantly, cHFD pre-exposure robustly suppressed reward-seeking during conflict, overriding the motivational effects of both hunger and acute reward value. These findings highlight the interaction between internal states (e.g., hunger), reward value, and environmental factors (e.g., diet) in shaping behavior during conflict.

As one of the most common liver diseases, non-alcoholic fatty liver disease (NAFLD) has attracted widespread international attention given its rising incidence. The current mainstay of treatment for NAFLD is controlled diet with controlled exercise. Significantly, the development of NAFLD is proposed to be related to the liver-gut axis. The gut barrier function may be disrupted in the case of gut microbial dysbiosis, which may increase the entry of bacteria, lipopolysaccharides and endotoxins into the liver, causing an inflammatory response, increasing the load on the liver, and triggering lipid deposition, thereby advancing the progression of NAFLD. Simultaneously, liver injury can further alter intestinal permeability, inducing systemic inflammatory response, creating a vicious cycle that may subsequently exacerbate the development of NAFLD. Accordingly, the present review focused on the exploration of the relationship between the liver-gut axis and NAFLD, dissection of the biological mechanism of NAFLD induced by liver-gut axis dysfunction, and comprehensive elucidation of the research progress of Chinese medicine on the regulation of the liver-gut axis for treating NAFLD. It is expected that these findings may provide fresh and insightful evidence for the development of suitable preventive and therapeutic strategies of NAFLD.