Search Results (385)

Metabolic syndrome is a disorder of energy metabolism characterized by persistently high prevalence and significant medical and economic burden on society. An effective animal model that closely replicates the key features of the syndrome in humans is essential for evaluating therapeutic strategies aimed at improving health outcomes. High-calorie diet-induced animal models of metabolic syndrome are preferred by many research groups for studying its pathogenesis, prevention and therapy. However, there are numerous variations in the types and proportions of carbohydrates and/or fats in the diets used. In 2015, our research team developed a diet-induced model of metabolic syndrome in young adult male Wistar rats that was based on adding 17% animal fat and 17% fructose to the standard rat chow and 10% fructose to the drinking water. This model reliably induced the morphometric and biochemical alterations that represent the core diagnostic features of the syndrome in humans. Since its initial introduction, we have utilized the high-fat high-fructose diet-induced model of metabolic syndrome/obesity in ten experimental studies. The current paper provides a protocol for applying the model, presents its repeatability and discusses the variability in the morphometric, biochemical, histopathological, immunohistochemical, and behavioral data of 10 experimental studies on Wistar rats. Full article

Background/Objectives: Food cravings are common with high-palatability foods that are high in sugar and/or fat. Food cues can strongly induce food craving, and heightened food cue reactivity is associated with eating disorders and obesity. Sweet taste signalling is suggested to be an important regulator of appetite and food intake, with sensory-metabolic mismatch potentially relevant for the food craving experience. This study investigated the interaction between taste and food cues and food craving in healthy people with and without ingestion of a sugary drink. Methods: This study had a randomised crossover design with 47 healthy individuals who participated in two experimental trials. Fasted individuals were exposed to food cues, and food craving pre- and post-exposure was measured via a newly validated method using handgrip force as a response modality. This was followed either by ingestion (ingestion trial) or mouth rinse (mouth rinse trial) of a sugary drink and reassessment of food cue craving responses. Continuous interstitial glucose monitoring was performed using a glucose sensor inserted into the upper arm, and a blood sample for leptin levels was taken. Results: A strong food craving response to food cues was bound to the fasted state, while ingestion of a sugary drink blunted food cue reactivity and reduced craving levels. Mouth rinse induced a stable increase in food craving, which reached a maximum after food cues. Interstitial glucose levels over the after-trial periods (incremental area under the curve, iAUC) were significantly higher for the rinse trial day than for the ingestion trial day, which may suggest higher carbohydrate/sugar intake after the rinse trial, while craving levels were associated with iAUC in the rinse trial. Conclusions: Outcomes indicate that taste/flavour in connection with food cues may generate an error signal experienced as food craving, whereas receipt of sugars, with concomitant physiological responses, reduces the signal and diminishes food craving. These results highlight the importance of sensory-metabolic mismatch in the food craving experience. Full article

Numerous hypotheses have been proposed to explain the origin of Alzheimer’s disease (AD), a chronic neurodegenerative disorder that currently has no curative treatment. These hypotheses include the abnormal accumulation of β-amyloid and hyperphosphorylated Tau, degeneration of cholinergic neurons associated with chronic neuroinflammation and oxidative stress, and dysregulation of lipid and carbohydrate metabolism. oleanolic acid (OA), a pentacyclic triterpenoid widely distributed across plant species, has demonstrated anti-inflammatory and antioxidant activities, anti-aggregation properties, together with regulatory effects on carbohydrate and lipid metabolism. Given the diversity of hypotheses proposed for AD and its multifactorial nature, the pleiotropic actions of OA positions it as a promising candidate for preventive and therapeutic strategies. This review compiles evidence on OA and selected synthetic derivatives, analyzing their impact across the major mechanistic hypotheses of AD pathogenesis. Collectively, these findings support OA as a promising candidate to address protein aggregation, metabolic imbalance, and neuroinflammation in AD. Full article

Introduction: Immune dysfunction plays a significant role in Metabolic syndrome, contributing to both insulin resistance and chronic low-grade inflammation. This immune dysfunction is characterized by overproduction of inflammatory cytokines among which of primary importance are tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and (MCP-1), whereas others such as interferon gamma (IFN-γ), IL-17A, and the anti-inflammatory IL-10 appear to be of secondary importance. Cytokines also play a significant role in Post-COVID disorders contributing to prolonged immune dysregulation and persistent subclinical inflammation. However, their role in the newly emerging metabolic disorders following infection remains poorly defined. Methods and materials: In the current study 78 patients (26 men and 52 women) were included, divided into two groups—group 1 (individuals with newly diagnosed carbohydrate disorders after proven COVID-19 or Post-COVID group; n = 35) and group 2 (COVID-19 negative persons with Metabolic Syndrome; n = 33). They were further divided into several subgroups according to type of metabolic disorder present. Standard biochemical, hormonal and immunological parameters were measured using ELISA and ECLIA methods, as well as some indices for assessment of insulin resistance were calculated using the corresponding formula. Results: Patients from both groups demonstrate similar metabolic parameters including BMI and unadjusted lipid and uric acid levels (p > 0.05). After adjustment for age, sex, and BMI revealed significant differences, Post-COVID status independently predicted higher fasting glucose, HbA1c, total cholesterol, LDL-cholesterol, triglycerides, uric acid, and insulin-resistance indices, indicating substantially impaired glycemic and metabolic control beyond traditional risk factors. Furthermore, the Post-COVID cohort demonstrated marked cytokine dysregulation, with significantly elevated levels of TNF-α, IFN-γ, IL-17A, and IL-10 after adjustment. Conclusions: The observed changes in both metabolic and immune parameters studied among the two groups show many similarities, but some significant differences have also been identified. Together, these findings indicate that Post-COVID metabolic dysfunction is characterized by inflammation-driven dyslipidemia, heightened oxidative stress, and persistent immune activation, distinguishing it from classical Metabolic syndrome. Full article

Background: Glycated hemoglobin (HbA1c) is a parameter commonly used in clinical practice to assess glycemic control in patients with diagnosed diabetes. Hyperglycemia is a strong risk factor for developing cardiovascular (CV) disease. Although there is some evidence that this parameter could also help assess CV health in patients without known carbohydrate metabolism disorders, this is not entirely clear. The purpose of this study was to investigate the relationship between HbA1c and selected echocardiographic parameters in patients without diabetes. Methods: This study was a retrospective analysis of data from 59 patients (females: 72.88%) with a mean age of 54.82 ± 17.34 years without any features of acute illness or exacerbation of chronic diseases hospitalized in the Department of Internal Medicine, Angiology and Physical Medicine of the Medical University of Silesia in Katowice (Poland) in the period between June 2022 and May 2024. Only individuals with HbA1c levels and who have undergone transthoracic echocardiography were included in the analysis. Spearman’s rank correlation test was used for statistical analysis, and a multivariate analysis model was then constructed (adjusted for age, sex, body mass index, low-density lipoprotein cholesterol, systolic blood pressure, hypertension, and smoking). Results: In univariate analysis, HbA1c was found to be significantly correlated with selected parameters relating to left ventricular dimensions and mass, left atrial dimensions, right ventricular systolic function, mitral inflow profile parameters, and tissue Doppler echocardiography. Multivariate analysis did not confirm a significant association between HbA1c and the assessed echocardiographic parameters. Conclusions: Although HbA1c significantly correlates with some echocardiographic parameters, the observed relationships are entirely explained by confounding variables. Full article

The rising global prevalence of obesity and metabolic disorders calls for innovative dietary strategies that can modulate key enzymatic pathways involved in lipid and carbohydrate metabolism. This study uncovers the effects of sulforaphane (SFN)-rich broccoli-derived formulations—including liquid and lyophilised forms, as well as two commercial prototypes, Sulforaphan^® BASIC and Sulforaphan^® SMART, the latter being characterised by the inclusion of an enteric-coated myrosinase enzyme designed to enhance the in situ conversion of glucosinolates (GSL) into bioactive isothiocyanates (ITC)—on lipid and carbohydrate metabolism in 3T3-L1 adipocytes. Across the formulations, total GSL content ranged widely, with GS0 showing the highest levels. Functionally, all SFN-rich formulations significantly reduced intracellular triglyceride content, with the SMART formulation achieving the strongest reduction (11% compared with untreated controls). Across enzymatic assays, we recorded that every formulation inhibited lipoprotein lipase and α-glucosidase activities, with Sulforaphan^® BASIC and Sulforaphan^® SMART leading to moderate inhibition (40–50%). The potent effect of SMART formulation may be associated with the presence of enteric-coated myrosinase, which enhances the conversion of GSL into bioactive ITC. The gathered evidence provides further insights into the potential of bioactive compounds in cruciferous foods to modulate metabolic health, underscoring their potential role in complementary therapeutic strategies for obesity and its comorbidities. Full article

Watercore disease, a physiological disorder in pineapple (Ananas comosus), manifests during late fruit development. Affected fruits develop water-soaked flesh and reduced storability. (1) Background: To explore underlying molecular mechanisms, comparative proteomic profiling was conducted in this study. (2) Methods: Data-independent acquisition (DIA) strategy was employed for comparative analysis between the resistant germplasm “35-1” and the susceptible germplasm “29-3”, as well as between the healthy and diseased “Paris”. (3) Results: Resistant (“35-1”) versus susceptible (“29-3”) germplasm analysis revealed differentially expressed proteins (DEPs) and unique proteins (SEPs) enriched in cell walls, secretory vesicles, and apoplast, functioning in cell wall loosening, hormone response, isoflavonoid biosynthesis, and farnesyl diphosphate biosynthesis. Healthy versus diseased “Paris” pulp analysis showed DEPs/SEPs enrichment in ribosomal small subunit biogenesis. These proteins form a central regulatory network potentially orchestrating tRNA synthesis, tubulin biosynthesis, and other carbohydrate metabolism. Partial protein overlap occurred in germplasm- and disease-derived differences. Resistant germplasm (“35-1”) and healthy “Paris” accumulated stress-responsive/resistant proteins and cell wall-modifying enzymes (e.g., phenylalanine ammonia-lyase, raffinose synthase, expansins, and mannan hydrolase). Susceptible germplasm (“29-3”) and diseased “Paris” exhibited prominent stress-responsive protein accumulation, such as alcohol dehydrogenase, 1-aminocyclopropane-1-carboxylate oxidase, and hypoxia-induced protein. (4) Conclusions: This comparative proteomics study identifies pineapple watercore resistance/susceptibility-associated proteins, providing a molecular basis for resistant germplasm development and disorder control. Full article

Metabolic syndrome, a collective term for lipid and carbohydrate disorders in the organism, is the primary cause of type 2 diabetes mellitus development and its associated systemic side effects. The current approach for the medical treatment of this condition usually requires multiple medications, targeting multiple pathophysiological pathways. A promising drug class in that regard is the dual PPARα/γ agonists, which impact both lipid and carbohydrate metabolism, yet to this day the vast majority of them have not passed the clinical trials, due to potential toxicity risks. In the present study we synthesized and tested a series of monoterpene-substituted (S)-2-ethoxy-3-(4-(4-hydroxyphenethoxy)phenyl)propanoic acids as potentially effective and safe novel dual PPARα/γ agonists. In vitro studies showed that nearly all of the tested compounds were sufficiently active towards both PPARα and PPARγ. All compounds were tested in vivo, using C57BL/6 A^y/_a mice with T2DM symptoms, in order to evaluate their impact on carbohydrate and lipid metabolism. The most promising of them was found to be compound 5h, containing a cumin fragment, which showed pronounced hypoglycemic activity by boosting tissue insulin sensitivity and hypolipidemic effects manifested by reductions in fat tissue mass and blood triglyceride levels, while simultaneously displaying a relatively safe profile. Full article

Background: Type 2 diabetes (T2DM) and prediabetes are growing public health problems worldwide. Oxidative stress plays a key role in the pathogenesis and progression of carbohydrate metabolism disorders. Metformin is an antidiabetic drug that significantly affects the oxidative-antioxidant balance. This study aimed to compare serum total antioxidant capacity (TAC) in individuals with T2DM, prediabetes, and healthy controls, and to assess the impact of dietary factors and metformin treatment on antioxidant parameters. Methods: The study involved 49 adults (aged 40–70 years) assigned to three groups: those with T2DM (n = 19), those with prediabetes (n = 12), and healthy controls (n = 18). Serum TAC was assessed using three spectrophotometric assays: DPPH, ABTS, and FRAP. A nutritional assessment was performed based on a three-day dietary recall, analysed using DietetykPro software. Statistical analyses included Kruskal–Wallis tests with post hoc corrections and Spearman correlation. Results: The prediabetes group demonstrated the lowest TAC values across all tests, while individuals with T2DM demonstrated higher levels using the ABTS and FRAP tests, which may reflect group-specific factors such as treatment or metabolic regulation. The differences between groups showed moderate to large effect sizes, including η² = 0.24 for ABTS, η² = 0.14 for DPPH and η² = 0.13 for FRAP, indicating biologically meaningful alterations in antioxidant capacity. Negative correlations were observed between antioxidant activity, as measured by the DPPH test, and body weight (p = 0.0095) and BMI (p = 0.0381), indicating that increased body weight may impair serum antioxidant capacity. After applying the FDR correction, significant correlations were observed between ABTS values and vitamin B5 (p = 0.0004, q = 0.0135), omega-6 (p = 0.0042, q = 0.0220), phosphorus (p = 0.0009, q = 0.0328), calcium (p = 0.0024, q = 0.0176) and zinc (p = 0.0012, q = 0.0138) intake. Other associations with anthropometric and dietary variables were observed as non-significant trends. Conclusions: The prediabetes group exhibited lower TAC, indicating a redox profile that differs from both healthy individuals and those with T2DM. Dietary quality, including adequate intake of selenium, could support antioxidant defence mechanisms, whereas excess body weight and high intake of omega-6 may impair them. The results also suggest that metformin may modulate TAC, supporting adaptive responses to oxidative stress in T2DM. These findings highlight the potential importance of dietary and pharmacological interventions in maintaining oxidative-antioxidant balance in metabolic disorders. Full article

Cassava fiber (CF) is a novel dietary fiber extracted from cassava by-products. To investigate its anti-obesity mechanism, obesity was induced in mice through a high-fat diet (HFD). Dietary supplementation with 10% CF significantly reduced body weight, body fat, triglycerides, low-density lipoprotein cholesterol, total cholesterol, and fasting blood glucose in mice. CF effectively ameliorated hepatic steatosis and adipocyte hypertrophy, increased the villus height-to-crypt depth ratio, enhanced mucus secretion by intestinal goblet cells, down-regulated the expression of ileal lipid absorption-related genes (NPC1L1, CD36, and FABP2), and up-regulated the short-chain fatty acid receptor GPR43, collectively improving intestinal health. Compared to HFD mice, CF altered the gut microbiota: it increased beneficial Actinobacteria (including Bifidobacterium and Blautia) and decreased Proteobacteria (including Desulfovibrio) (p < 0.05). Functional analysis showed that the HFD mice microbiota was enriched in genes linked to disease (e.g., lipid metabolism disorders, cancer, antibiotic resistance), whereas CF-enriched microbiota had genes for energy, carbohydrate, and pyruvate metabolism. Compared to microcrystalline cellulose, CF and MCC both alleviated HFD-induced obesity. In summary, cassava fiber helped prevent obesity in mice by modulating gut microbes, strengthening the gut barrier, and improving host metabolic balance. Full article

Objective: This narrative review summarizes current evidence on the associations between ultra-processed food (UPF) consumption, childhood and adolescent obesity, and functional gastrointestinal disorders (FGIDs), and examines the metabolic, inflammatory, microbial, and gut–brain mechanisms underlying these links. Methods: A comprehensive search of PubMed and Scopus identified articles published between January 2010 and September 2025. Eligible studies included human research in individuals aged 0–18 years; adult studies were considered when contributing relevant mechanistic insights. Of 335 records screened, 112 studies met the inclusion criteria and were synthesized narratively according to methodological appropriateness. Results: High UPF intake was consistently associated with increased adiposity, metabolic dysregulation, and greater cardiometabolic risk in youth. Children with overweight or obesity showed a higher prevalence of FGIDs compared with their normal-weight peers. Mechanistic evidence suggests that UPFs, rich in refined carbohydrates, unhealthy fats, and additives, may promote gut microbiota dysbiosis, impair intestinal barrier integrity, alter motility, and induce low-grade inflammation, thereby disrupting gut–brain signaling and contributing to FGID symptoms. Early-life and maternal UPF exposure may further increase susceptibility to metabolic and gastrointestinal disturbances through epigenetic and microbiome-mediated pathways. Conclusions: UPFs emerge as a shared etiological factor for obesity and FGIDs in childhood. This review contributes an integrated synthesis of epidemiological and mechanistic data while highlighting key research gaps, particularly the need for standardized methodologies and pediatric interventional studies to strengthen the evidence base. Full article

Food has a massive influence on the gut microbiota and is one of the most useful therapeutic levers in disease. Recent developments have highlighted how macronutrient balance, food format, and functional ingredients can regulate microbial diversity, metabolism, and host physiology in companion animals such as dogs and cats. This narrative review condenses evidence on the bidirectional gut microbiota–diet connection and on nutritional therapy for gastrointestinal, metabolic, renal, hepatic, and immune-mediated disorders. Protein-based diets including high or hydrolyzed protein, omega-3 acids, fermentative fiber, and probiotics can positively affect microbial composition, stimulate short-chain fatty acid synthesis, and enhance intestinal barrier functions. Conversely, excess fats or refined carbohydrates may cause dysbiosis, inflammation, and metabolic imbalances. Numerous studies have shown that therapeutic nutrition—e.g., low-protein renoprotective, hepatoprotective antioxidants, and allergen-elimination diets—holds enormous potential for treatment. In addition, fecal microbiota transplantation (FMT) can be used as an additive therapy for resistant gastrointestinal illnesses. Despite these developments, constraints remain in terms of standardization, study duration, and species-specific data, especially for cats. This review underscores dietary modification as a clinically actionable tool for microbiota-targeted therapy and calls for integrative, multi-omics research to translate microbiome modulation into precision nutrition for companion animals. Full article

Ammonia is a key water quality factor limiting shrimp aquaculture. Intestinal health is closely associated with the nutrition, metabolism and immunity of shrimp. However, the response characteristics of the shrimp intestine to ammonia stress under seawater and low-salinity environments remain unclear. In this study, the shrimp Litopenaeus vannamei reared in seawater (salinity 30) or low-salinity (salinity 3) water were subjected to ammonia stress for 14 days, respectively. The changes in intestinal morphology, antioxidant capacity, immune response, energy metabolism, and microbial community were systematically investigated. The results showed that ammonia stress induced intestinal tissue damage in both seawater and low-salinity cultured shrimp, characterized by epithelial cell detachment and mucosal structural disruption. At the molecular level, ammonia stress triggered intestinal stress responses by interfering with key physiological processes such as antioxidant defense and endoplasmic reticulum stress. This process further led to varying degrees of disorders in physiological functions, including immune regulation, inflammatory response, and autophagic activity. In addition, ammonia stress disrupted the homeostatic balance of intestinal energy metabolism by affecting the expression of genes related to glucose metabolism, the tricarboxylic acid (TCA) cycle, and mitochondrial respiratory chain. In addition, ammonia stress increased the diversity of intestinal microbiota and caused microbial dysbiosis by increasing harmful bacteria (e.g., Vibrio) and decreasing beneficial bacterial groups (e.g., Bacillus). Ammonia stress generally enhanced intestinal microbiota chemotaxis. Specifically, predicted functions of microbiota in seawater-cultured shrimp showed increased carbohydrate, linoleic acid, and cofactor/vitamin metabolism; in low-salinity-cultured shrimp, functions including protein digestion/absorption, flavonoid/steroid hormone biosynthesis, and glycosaminoglycan degradation were reduced. These results revealed that ammonia stress compromised shrimp intestinal health by disrupting mucosal structure, triggering stress responses, and disturbing immune function, energy metabolism, and microbial homeostasis. Notably, low-salinity cultured shrimp exhibited more pronounced intestinal stress responses and greater physiological vulnerability than seawater-cultured counterparts. Full article

Horses maintained under traditional management systems and dependent on natural forages are often exposed to seasonal and compositional variations that can affect metabolic homeostasis. This study examined associations between forage nutrient composition and metabolic–morphometric indicators in horses from four agroecologically distinct regions of northwestern Romania. Eighty-eight horses managed under semi-extensive rural conditions underwent clinical examination, body condition scoring (BCS), cresty neck scoring (CNS), and fasting blood sampling. Forage samples (n = 34) from daily rations were analyzed for fermentable carbohydrate content, while serum insulin, leptin, and adiponectin were quantified using validated equine-specific ELISA assays. Forage composition varied substantially among regions, influencing both endocrine and morphometric outcomes. Horses consuming carbohydrate-rich forages exhibited higher insulin (0.95–219 μIU/mL) and leptin concentrations (925–28,190 pg/mL), accompanied by elevated BCS and CNS scores, whereas adiponectin levels tended to decrease with increasing carbohydrate content. These findings demonstrate that naturally occurring variation in forage quality can significantly influence metabolic regulation in horses managed under low-input, traditional systems. Integrating forage nutrient evaluation with clinical and endocrine assessments provides a practical framework for identifying animals at risk of metabolic dysfunction and guiding nutritional strategies to mitigate the incidence of laminitis and related disorders. Full article

Tomato fruit malformation causes substantial yield and economic losses, but its molecular mechanisms are not well understood. This study compared floral traits of WT ‘QT57’ and malformed-fruit mutant ‘QT2’, integrated transcriptomic data, and qRT-PCR analysis to screen key candidate genes, and analyzed the pectinase gene family. The results found the ‘QT2’ mutant differed from WT ‘QT57’ in flower and fruit development. Expression analysis of CLAVATA-WUSCHEL pathway genes preliminarily validated the compensatory mechanism of SlCRCa and SlCRCb in ‘QT2’ malformed fruit. Six pectinase genes were identified as key candidates via RNA-seq and qRT-PCR analysis. Transcriptomic and qRT-PCR analyses of the pectinase gene family revealed their potential role in regulating tomato fruit malformation. Family analysis showed 34 pectinase genes distributed unevenly across 12 chromosomes. Subcellular localization confirmed SlPL7 in the nucleus and SlPME9 in the cell membrane/endoplasmic reticulum. The PL and PME genes were evolutionarily close, suggesting a potential functional overlap. Gibberellin-responsive elements were found in most pectinase genes. Pectinase genes may regulate tomato fruit malformation through the gibberellin-WUS pathway, carbohydrate metabolism, or cell wall metabolic disorder. This pathway provides new targets gene for the precise regulation of fruit malformation and offers significant reference value for practical production. Full article