Metabolic Products Research Articles

Novel insights into the role of gut microbiota and its metabolites in diabetic chronic wounds.

Wounds in patients with diabetes present significant physical and economic challenges due to impaired healing and prolonged inflammation, exacerbated by complex interactions between microbes. Especially, the development and healing of diabetic foot ulcers (DFUs) remain an urgent clinical problem. The human gut harbors a vast microbial ecosystem comprising intestinal flora and their metabolic products. Recent advancements in research have illuminated the concept of the "gut-skin axis," revealing intricate relationships between gut microbiota, microbiota-derived metabolites, and various skin diseases, including DFUs. This review aims to unravel the formation and healing process of DFUs in the context of the gut-skin axis. We reviewed the current research progress worldwide regarding to the gut-skin axis, compared and discussed significant changes in the microbiota colonizing the skin and gut in patients with DFUs. The roles of microbiota-derived metabolites such as lipopolysaccharides, short-chain fatty acids, and trimethylamine-N-oxide in the development of DFUs are highlighted. We also reviewed treatment strategies currently employed in clinical practice and identified potential therapeutic targets such as probiotics for treating DFUs. The need for more comprehensive experimental designs to elucidate the intricate relationship between gut microbiota and its metabolites in the context of DFUs are therefore highlighted.

Targeting glycolysis: exploring a new frontier in glioblastoma therapy

Glioblastoma(GBM) is a highly malignant primary central nervous system tumor that poses a significant threat to patient survival due to its treatment resistance and rapid recurrence.Current treatment options, including maximal safe surgical resection, radiotherapy, and temozolomide (TMZ) chemotherapy, have limited efficacy.In recent years, the role of glycolytic metabolic reprogramming in GBM has garnered increasing attention. This review delves into the pivotal role of glycolytic metabolic reprogramming in GBM, with a particular focus on the multifaceted roles of lactate, a key metabolic product, within the tumor microenvironment (TME). Lactate has been implicated in promoting tumor cell proliferation, invasion, and immune evasion. Additionally, this review systematically analyzes potential therapeutic strategies targeting key molecules within the glycolytic pathway, such as Glucose Transporters (GLUTs), Monocarboxylate Transporters(MCTs), Hexokinase 2 (HK2), 6-Phosphofructo-2-Kinase/Fructose-2,6-Biphosphatase 3 (PFKFB3), Pyruvate Kinase Isozyme Type M2 (PKM2), and the Lactate Dehydrogenase A (LDHA). These studies provide a novel perspective for GBM treatment. Despite progress made in existing research, challenges remain, including drug penetration across the blood-brain barrier, side effects, and resistance. Future research will aim to address these challenges by improving drug delivery, minimizing side effects, and exploring combination therapies with radiotherapy, chemotherapy, and immunotherapy to develop more precise and effective personalized treatment strategies for GBM.

Metabolomics and Lipidomics Reveal the Metabolic Disorders Induced by Single and Combined Exposure of Fusarium Mycotoxins in IEC-6 Cells

Deoxynivalenol (DON), fumonisin B1 (FB1), and zearalenone (ZEN) are typical fusarium mycotoxins that occur worldwide in foodstuffs, posing significant health hazards to humans and animals. Single and combined exposure of DON, FB1, and ZEN leads to intestinal toxicity but the toxicology mechanism research is still limited. In this study, we explored the cytotoxicity effects of DON, FB1, ZEN, and their combination in rat intestinal epithelial cell line 6 (IEC-6) cells. Cell viability results showed that the cytotoxicity potency ranking was DON > ZEN > FB1. Furthermore, both DON + FB1 and DON + ZEN presented synergism to antagonism effects based on a combination index (CI)-isobologram equation model. Integrated metabolomics and lipidomics was adopted to explore cell metabolism disorders induced by fusarium mycotoxin exposure. A total of 2011 metabolites and 670 lipids were identified. An overlap of 37 and 62 differential compounds was confirmed after single and combined mycotoxin exposure by multivariate analysis, respectively. Some of the differential compounds were endocellular antioxidants and were significantly downregulated in mycotoxin exposure groups, indicating metabolic disorders as well as antioxidant capacity damage in cells. Pathway enrichment analysis annotated ethanol metabolism production of ROS by CYP2E1 was mainly involved in the disturbance of DON, FB1, and ZEN. The results obtained in this study help to define the toxicity effects of DON, FB1, and ZEN singly and in co-existence, providing an important scientific basis for combined risk recognition of mycotoxin contamination.

Sirtuin activators as an anti-aging intervention for longevity

Sirtuins are a family of NAD+-dependent class III histone deacetylases that regulate histones and other proteins. The mammalian sirtuins comprise seven members that have a role in energy metabolism, DNA repair, inflammation, cell survival, apoptosis, cellular senescence, oxidative stress, and mitochondrial production. Sirtuin modulation may have beneficial effects on aging and age-related diseases; thus, attracting a growing interest in discovering small molecules modifying their activity. A class of compounds both natural and chemically synthesized has emerged as sirtuin activators. This review discusses mammalian sirtuins in aging, the small molecules that activate sirtuins, modulation of sirtuin activity, and its impact in alleviating the effects of aging.

Limosilactobacillus reuteri fermented brown rice alleviates anxiety improves cognition and modulates gut microbiota in stressed mice

Chronic stress disrupts gut microbiota homeostasis, contributing to anxiety and depression. This study explored the effects of Limosilactobacillus reuteri fermented brown rice (FBR) on anxiety using an ICR mouse chronic mild stress (CMS) model. Anxiety was assessed through body weight, corticosterone levels, neurotransmitter profiles, and behavioral tests. A four-week FBR regimen reduced corticosterone, restored neurotransmitters like gamma-aminobutyric acid (GABA) and serotonin, and improved anxiety-related behaviors. Metagenomic (16S rRNA) and metabolomic analyses revealed enhanced amino acid metabolism, energy metabolism, and short-chain fatty acid (SCFA) production in FBR-treated mice. FBR-enriched beneficial gut bacteria, aligning the microbiota profile with that of non-stressed mice. FBR also modulated GABA receptor-related gene expression, promoting relaxation. Network pharmacology identified quercetin, GABA, glutamic acid, phenylalanine, and ferulic acid as bioactive compounds with neuroprotective potential. These findings highlight FBR’s potential as a gut-brain axis-targeted therapeutic for anxiety and stress-related disorders.

Blastocyst-Derived Lactate as a Key Facilitator of Implantation

The blastocyst develops a unique metabolism that facilitates the creation of a specialized microenvironment at the site of implantation characterized by high levels of lactate and reduced pH. While historically perceived as a metabolic waste product, lactate serves as a signaling molecule which facilitates the invasion of surrounding tissues by cancers and promotes blood vessel formation during wound healing. However, the role of lactate in reproduction, particularly at the implantation site, is still being considered. Here, we detail the biological significance of the microenvironment created by the blastocyst at implantation, exploring the origin and significance of blastocyst-derived lactate, its functional role at the implantation site and how understanding this mediator of the maternal–fetal dialogue may help to improve implantation in assisted reproduction.

Emerging Concepts in Periprosthetic Joint Infection Research: The Human Microbiome.

Microorganisms, including bacteria, fungi, and viruses, that reside on and within the human body are collectively known as the human microbiome. Dysbiosis, or disruption in the microbiome, has been implicated in several disease processes, including asthma, obesity, autoimmune diseases, and numerous other conditions. While the Human Microbiome Project (HMP) and the generation of descriptive studies it inspired established correlations between characteristic patterns in the composition of the microbiome and specific disease phenotypes, current research has begun to focus on elucidating the causal role of the microbiome in disease pathogenesis. Within the field of orthopaedic surgery, researchers have proposed the concept of a "gut-joint axis" by which the intestinal microbiome influences joint health and the development of diseases such as osteoarthritis and periprosthetic joint infection (PJI). It is theorized that intestinal dysbiosis increases gut permeability, leading to the translocation of bacteria and their metabolic products into the systemic circulation and the stimulation of proinflammatory response cascades throughout the body, including within the joints. While correlative studies have identified patterns of dysbiotic derangement associated with osteoarthritis and PJI, translational research is needed to clarify the precise mechanisms by which these changes influence disease processes. Additionally, an emerging body of literature has challenged the previously held belief that certain body sites are sterile and do not possess a microbiome, with studies identifying distinct microbial genomic signatures and a core microbiome that varies between anatomic sites. A more thorough characterization of the joint microbiome may have profound implications for our understanding of PJI pathogenesis and our ability to stratify patients based on risk. The purpose of this review was to outline our current understanding of the human microbiome, to describe the gut-joint axis and its role in specific pathologies, including PJI, and to highlight the potential of microbiome-based therapeutic interventions in the field of orthopaedics.

Minimally invasive measurement of carotid artery and brain temperature in the mouse.

Brain temperature is tightly regulated and reflects a balance between cerebral metabolic heat production and heat transfer between the brain, blood, and external environment. Blood temperature and flow are critical to the regulation of brain temperature. Current methods for measuring in vivo brain and blood temperature are invasive and impractical for use in small animals. This work presents a methodology to measure both brain and arterial blood temperature in anesthetized mice by MRI using a paramagnetic lanthanide complex: thulium tetramethyl-1,4,7,10-tetraazacyclododecane-1,4,7,10-tetraacetic acid (TmDOTMA-). A phase-based imaging approach using a multi-TE gradient echo sequence was used to measure the temperature-dependent chemical shift difference between thulium tetramethyl-1,4,7,10-tetraazacyclododecane-1,4,7,10-tetraacetic acid methyl protons and water, and from this calculate absolute temperature using calibration data. In a series of mice in which core body temperature was held stable but at different values within the range of 33° to 37°C, brain temperature away from the midline was independent of carotid artery blood temperature. In contrast, midline voxels correlated with carotid artery blood temperature, likely reflecting the preponderance of larger arteries and veins in this region. These results are consistent with brain temperature being actively regulated. A limitation of the present implementation is that the spatial resolution in the brain is coarse relative to the size of the mouse brain, and further optimization is required for this method to be applied for finer spatial scale mapping or to characterize focal pathology.

Hepatic metabolism and ketone production in metabolic dysfunction-associated steatotic liver disease.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is present in 25-35% of individuals in the United States. The purpose of this review is to provide the contextual framework for hepatic ketogenesis in MASLD and to spotlight recent advances that have improved our understanding of the mechanisms that drive its development and progression. Traditionally, hepatic ketogenesis has only been considered metabolically during prolonged fasting/starvation or with carbohydrate deplete ketogenic diets where ketones provide important alternative energy sources. Over the past 2 years, it has become increasingly clear from preclinical rodent and human clinical studies that hepatic ketogenic insufficiency is a key contributor to the initiation and progression of MASLD. A more thorough understanding of the metabolic dysregulation that occurs between the liver and extrahepatic tissues has significant potential in the development of innovative nutritional and pharmacological approaches to the treatment of MASLD.

The malic acid inhibiting inflammation in ankylosing spondylitis by interfering M1 macrophage polarization

Ankylosing spondylitis (AS) is a motor system immune disease with significant genetic characteristics, resulting in joint fusion, deformity, rigidity, seriously affecting the quality of life of patients. Inflammatory bowel disease (IBD), characterized by intestinal mucosal damage and inflammatory changes, the most common extra-articular manifestation of AS. Due to the limitations of the application of therapeutic drugs, it is urgent to look for new mechanisms and strategies to effectively inhibit AS inflammation is. The content of malic acid (MA) was significantly decreased in peripheral blood of AS patients, and it was significantly negatively correlated with C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR). MA dramatically alleviated spinal damage and intestinal inflammation in mouse models of AS induced by β-1, 3-glucan solution. Mechanically, MA suppressed the NF-κB pathway by inhibiting polarization of M1-type macrophages, thereby alleviating spinal and intestinal inflammation. From the perspective of material metabolism, this study explored the mechanism by which MA, an intermediate product of glucose metabolism, reducing M1 polarization of macrophages to inhibit AS inflammation, providing a reliable basis for the pathogenesis research and precise targeted treatment of AS in the later stage.

Metabolic changes during evolution of Sjögren's in both an animal model and human patients.

Sjögren's (SS) involves salivary and lacrimal gland dysfunction. These studies examined metabolic profiles in the B6. Il14α transgene mouse model of SS and a cohort of human SS patients at different stages of disease. In B6. Il14α mice, products of glucose and fatty acid were common at 6 months of age, while products of amino acid metabolism were common at 12 months of age. Treating B6. Il14α mice with the glycolysis inhibitor 2-deoxyglucose from 6 to 10 months of age normalized salivary gland secretions, dacryoadenitis, hypergammaglobulinemia and physical performance, while treatment from 10 to 14 months of age failed to improve any of the clinical manifestations. Similarly, SS patients at an early stage of disease showed high glycolysis. SS patients with long-standing disease utilized predominantly amino acid metabolism, like B6. Il14α mice at 10-12 months of age. Additional studies are suggested to further define metabolic activities at the various disease stages.

Integrating microfluidic and bioprinting technologies: advanced strategies for tissue vascularization.

Tissue engineering offers immense potential for addressing the unmet needs in repairing tissue damage and organ failure. Vascularization, the development of intricate blood vessel networks, is crucial for the survival and functions of engineered tissues. Nevertheless, the persistent challenge of ensuring an ample nutrient supply within implanted tissues remains, primarily due to the inadequate formation of blood vessels. This issue underscores the vital role of the human vascular system in sustaining cellular functions, facilitating nutrient exchange, and removing metabolic waste products. In response to this challenge, new approaches have been explored. Microfluidic devices, emulating natural blood vessels, serve as valuable tools for investigating angiogenesis and allowing the formation of microvascular networks. In parallel, bioprinting technologies enable precise placement of cells and biomaterials, culminating in vascular structures that closely resemble the native vessels. To this end, the synergy of microfluidics and bioprinting has further opened up exciting possibilities in vascularization, encompassing innovations such as microfluidic bioprinting. These advancements hold great promise in regenerative medicine, facilitating the creation of functional tissues for applications ranging from transplantation to disease modeling and drug testing. This review explores the potentially transformative impact of microfluidic and bioprinting technologies on vascularization strategies within the scope of tissue engineering.

Dietary Calcium-to-Phosphorous Ratio, Metabolic Risk Factors and Lipid Accumulation Product, Skeletal Muscle Mass, and Visceral Fat Area Among Healthy Young Individuals.

Numerous studies have revealed the role of low dietary calcium-to-phosphorous ratio and low bone health. However, its possible role in visceral adiposity, skeletal muscle mass (SMM), and metabolic parameters has not been investigated before. Therefore, the aim of the current cross-sectional study was to evaluate the relation between dietary calcium-to-phosphorous ratio, metabolic risk factors, SMM, and visceral fat area (VFA) among physically active young individuals. In the current study, the sample was composed of 391 healthy young individuals (e.g.,205 men and 186 women), aged between 20 and 35years old, who were engaged in moderate physical activity for at least 4hr per week and were recruited thorough cluster sampling from seven sport clubs. Anthropometric measurements were performed, and VFA and SMM index (SMI) were calculated. Biochemical assays were also performed by standard kits. Data were analyzed by one-way analysis of variance, analysis of co-variance, and multinomial logistic regression analysis using SPSS software. Those in the fourth quartile of dietary calcium-to-phosphorous ratio were more likely to have lower VFA (odds ratio [OR] = 0.98; 95% confidence interval [CI] [0.97, 0.99]; p = .023) and a nonsignificantly higher SMI (OR = 1.15; 95% CI [0.99, 1.34]; p = .058) after adjustment for the effects of confounders (e.g.,age, gender, body mass index, physical activity level, dietary energy intake). Also, being in the third quartile of dietary calcium-to-phosphorous ratio made the subjects more susceptible to have lower insulin concentration (OR = 0.99; 95% CI [0.88, 0.93]; p = .026) in the adjusted model. The findings of the current study revealed that a higher dietary calcium-to-phosphorous ratio in the habitual diet was negatively associated with visceral adiposity and insulin concentrations and higher SMM among physically active young individuals. Further interventional studies are required to confer causality that was not inferable in the current study because of cross-sectional design.

Combined effects of climate stressors and soil arsenic contamination on metabolic profiles and productivity of rice (Oryza sativa L.).

Rice productivity and quality are increasingly at risk in arsenic (As) affected areas, challenge that is expected to worsen under changing climatic conditions. Free-Air Concentration Enrichment experiments revealed that eCO2, eO3, and eTemp, whether acting individually or in combination with low and high As irrigation, significantly impact rice yield and grain quality. Elevated CO₂ significantly increased shoot biomass, with minimal impact on root biomass, except under low As irrigation conditions. In contrast, eTemp alone reduced both shoot and root biomass, though the effect was not significant; eO₃ alone had little to no effect. Combined climatic stressors showed slight positive effects on growth. Under low As irrigation, eCO2 and eO3 promoted root growth but reduced shoot growth, while eTemp significantly suppressed both. High As irrigation exacerbated yield reductions, with the most severe decline observed under eTemp (66%), followed by eCO2 (48%), eO3 (36%), and their combination (35%). Arsenic irrigation, whether low or high, reduced macro and micronutrient concentrations in rice grains, with calcium being sole exception, remaining stable or even increasing. Sugar metabolites decreased under eCO2, eO3, and eTemp, but increased with As irrigation. Interestingly, climatic variables generally reduced grain As levels, high As irrigation combined with eCO2 exposure resulted in elevated grain As. This poses a dual concern: increased cancer risk due to As but potential benefit for individuals with diabetes, as the higher amylose content contributes to lower glycemic index. However, rice grown under high As irrigation exhibited significant nutritional imbalances, being rich in maltose and amylose but deficient in organic acids, phytosterols, fatty acids, organosilicons, and carboxylic acids. These findings underscore the dual threat of climate change and As contamination to rice productivity and quality. Developing resilient rice varieties with low grain As content is essential to ensure sustainable agricultural production and nutritional security in As affected regions.

Nitrogen stress-induced modulation of antimicrobial and antioxidant activities in Aphanothece sp.: Insights from phytochemical profiling and molecular docking

The modulation of nutrient availability represents a critical factor influencing the metabolic pathways and production of bioactive compounds in algae. This study aimed to examine the impact of nitrogen stress on the antimicrobial and antioxidant properties, phytochemical composition, and molecular docking assessments of the cyanobacterium Aphanothece sp. The results demonstrated that Aphanothece sp. when cultivated under conditions of nitrogen deficiency, exhibited markedly elevated antimicrobial and antioxidant activity compared to the control. The minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC) values of the extracts obtained from algae on E. coli ATCC 25922 were found to be 25 mg mL−1 when the sample was grown in nitrogen medium and 6.25 mg mL−1 when grown in a nitrogen-free medium. The IC50 value obtained from DPPH free radical scavenging assay changed from 137.30 ± 16.22 mg mL−1 to 20.07 ± 1.55 mg mL−1 in nitrogen-free medium. According to the results of GC–MS analysis, the major components in the extract obtained from the algae grown in the nitrogen-free environment were 13,16-Octadecadiynoic acid, methyl ester (35.10 %) and Hexadecanoic acid, methyl ester (22.65 %), while the major components in the extract obtained from the algae grown in nitrogen-containing medium were Protopine (65.68 %) and 3,6,9,12,15-Pentaoxabicyclo(15.3.1)henicosa-1(21),17,19-triene-2,16-dione (12.15 %). The findings suggest a range of binding energies and interaction profiles for the compounds in the extracts with their molecular targets, which may have implications for their potential significance in therapeutic applications. The results of this study indicate that nitrogen stress can be employed as a strategic tool to enhance the production of valuable bioactive compounds in Aphanothece sp., thereby underscoring its potential applications in biotechnology and drug development.

Identification of biomarkers associated with ferroptosis in macrophages infected with Mycobacterium abscessus using bioinformatic tools.

Mycobacterium abscessus is a rapidly growing nontuberculous mycobacterium that causes severe pulmonary infections. Recent studies indicate that ferroptosis may play a critical role in the pathogenesis of M. abscessus pulmonary disease. We obtained gene expression microarray data from the Gene Expression Omnibus database, focusing on THP-1-derived macrophages infected with M. abscessus and uninfected controls. Differentially expressed genes related to ferroptosis were identified through weighted gene co-expression network analysis and the "limma" package, followed by gene set variation analysis and gene set enrichment analysis for enrichment assessment. To explore regulatory network relationships among hub genes, we constructed RBP-mRNA, ceRNA, and TF-mRNA networks. Additionally, a protein-protein interaction network was built, and functional enrichment analyses were conducted for the hub genes. The diagnostic value of these genes was assessed using receiver operating characteristic curves. Six differentially expressed genes associated with ferroptosis were identified in M. abscessus infection. The receiver operating characteristic curves demonstrated that these genes had excellent predictive value for the infection. Functional enrichment analysis showed that these genes were involved in immune responses, inflammation, cellular metabolism, cell death, and apoptosis. Pathway enrichment analysis revealed significant enrichment in pathways related to apoptosis, inflammation, and hypoxia. The RBP-mRNA network highlighted significant interactions between hub genes and key RNA-binding proteins, while the ceRNA network predicted that miRNAs and lncRNAs regulate ferroptosis-related genes NACC2 and ITPKB. Furthermore, interactions between the hub gene HSD3B7 and transcription factors LMNB1 and ASCL1 may promote ferroptosis in macrophages by influencing iron metabolism and reactive oxygen species production, contributing to the M. abscessus infection process. Our findings identified biomarkers linked to ferroptosis in M. abscessus infection, providing new insights into its pathogenic mechanisms and potential therapeutic strategies.

Description of Veillonella absiana sp. nov., isolated from pig faeces.

Two Gram-stain-negative cocci anaerobes were isolated from pig faeces and designated as strains YH-vei2232T and YH-vei2233. Phylogenetic analysis using 16S rRNA gene sequences revealed that the isolates were most closely related to Veillonella rogosae KCTC 5967T, with 97.0% similarity. Analysis of housekeeping gene sequences (rpoB) revealed the strain formed a sub-cluster within the genus Veillonella. The average nucleotide identities between the two isolates and the most closely related strains within genus Veillonella were <75.0%. The major fatty acids were Summed Feature 8 and C16 : 1 ω9c. The cell wall peptidoglycan contained meso-diaminopimelic acid. The major metabolic end products of isolates were propionic and acetic acids. The genomic DNA G+C contents of both strains were 40.1 mol%. The chemotaxonomic, phenotypic and phylogenetic properties of YH-vei2232T (=KCTC 25748T=NBRC 116427T) and YH-vei2233 (=KCTC 25749=NBRC 116428) suggest that they represent a novel species of the genus Veillonella, for which the name Veillonella absiana sp. nov. is proposed.

Insect hypovirulence-associated mycovirus confers entomopathogenic fungi with enhanced resistance against phytopathogens

ABSTRACT Mycoviruses can alter the biological characteristics of host fungi, including change virulence or pathogenicity of phytopathogens and entomopathogenic fungi (EPF). However, most studies on the mycoviruses found in EPF have focused on the effects of the viruses on the virulence of host fungi towards insect pests, with relatively few reports on the effects to the host fungi with regard to plant disease resistance in hosts. The present study investigated the effects of the mycovirus Beauveria bassiana chrysovirus 2 (BbCV2) virus infection on host biological characteristics, evaluated antagonistic activity of BbCV2 against two phytopathogenic fungi (Sclerotinia sclerotiorum and Botrytis cinerea), and transcriptome analysis was used to reveal the interactions between viruses and hosts. Our results showed that BbCV2 virus infection increased B. bassiana‘s growth rate, spore production, and biomass, it also enhanced the capacity of host fungi and their metabolic products to inhibit phytopathogenic fungi. BbCV2 virus infection reduced the contents of the two pathogens in tomato plants significantly, and transcriptome analysis revealed that the genes related to competition for ecological niches and nutrition, mycoparasitism and secondary metabolites in B. bassiana were significantly up-regulated after viral infection. These findings indicated that the mycovirus infection is an important factor to enhance the ability of B. bassiana against plant disease after endophytic colonization. We suggest that mycovirus infection causes a positive effect on B. bassiana against phytopathogens, which should be considered as a potential strategy to promote the plant disease resistance of EPF.

Biochemical Processes During Cheese Ripening

Cheese ripening entails specific biochemical changes that occur under certain conditions during storage. These changes allow different cheese varieties to develop their unique characteristics. The ripening process is influenced by both primary and secondary biochemical events. These are driven by coagulating enzymes, milk's natural enzymes, and the enzymes of both starter and non-starter microflora. The main biochemical events during cheese ripening include proteolysis, lipolysis, and the metabolism of citrate and lactate. Secondary biochemical reactions then process the primary metabolic products, such as lactic acid, fatty acids, and amino acids. This leads to the formation of volatile compounds like alcohols, aldehydes, ketones, acids, lactones, phenols, esters, and sulfur compounds, which play a crucial role in determining the cheese's quality. These processes give each cheese type its distinctive features, like aroma, taste, color, texture, and pore structure, influencing consumer preferences. This review provides insights into the biochemical events that occur during the cheese ripening period.

Role of Abscisic Acid in the Whole-Body Regulation of Glucose Uptake and Metabolism.

Abscisic acid (ABA) is a hormone with a long evolutionary history, dating back to the earliest living organisms, of which modern (ABA-producing) cyanobacteria are likely descendants, which existed long before the separation of the plant and animal kingdoms, with a conserved role as signals regulating cell responses to environmental challenges. In mammals, along with the anti-inflammatory and neuroprotective function of ABA, nanomolar ABA regulates the metabolic response to glucose availability by stimulating glucose uptake in skeletal muscle and adipose tissue via an insulin-independent mechanism and increasing metabolic energy production and also dissipation in brown and white adipocytes. Chronic ABA intake of micrograms per Kg body weight improves blood glucose, lipids, and morphometric parameters (waist circumference and body mass index) in borderline subjects for prediabetes and metabolic syndrome. This review summarizes the most recent in vitro and in vivo data obtained with nanomolar ABA, the involvement of the receptors LANCL1 and LANCL2 in the hormone's action, and the importance of mammals' endowment with two distinct hormones governing the metabolic response to glucose availability. Finally, unresolved issues and future directions for the clinical use of ABA in diabetes are discussed.