Search Results (2,401)

Background/Objectives: Metabolic syndrome (MetS) increases susceptibility to myocardial ischemia/reperfusion (I/R) injury through metabolic disturbance, hypertension, and oxidative stress. This study aimed to compare the effects of liraglutide and semaglutide on post-ischemic cardiac function, oxidative stress, and histomorphological changes in rats with MetS. Methods: MetS was induced in male Wistar rats by a high-fat diet followed by low-dose streptozotocin. After confirmation of MetS, animals were treated with saline, liraglutide, or semaglutide for 6 weeks. Blood pressure, glycemia, oral glucose tolerance, and lipid profile were assessed during the protocol. In vivo cardiac function was evaluated by echocardiography, whereas ex vivo I/R injury was induced using the Langendorff technique. Cardiodynamic parameters, coronary flow, oxidative stress markers, and histological changes in the heart, liver, and pancreas were analyzed. Results: Both liraglutide and semaglutide improved the cardiometabolic profile of MetS rats, with semaglutide showing a more evident effect on body weight control. In the Langendorff model, both treatments improved post-ischemic recovery of myocardial contractility and relaxation during reperfusion. Treated animals also showed a more favorable oxidative stress profile, particularly lower superoxide anion levels and enhanced antioxidant defense. Histologically, both agents attenuated myocardial hypertrophy and collagen deposition, improved hepatic architecture by reducing inflammatory changes, and preserved pancreatic structure with less lipid accumulation and tissue injury. Conclusions: Liraglutide and semaglutide exerted significant cardioprotective and tissue-protective effects in experimental MetS complicated by myocardial I/R injury. These findings support their potential in limiting post-ischemic cardiac dysfunction and multiorgan damage in metabolically compromised conditions. Full article

Mulberry leaf is a promising plant feed resource for aquaculture, yet high inclusion limits its application due to anti-nutritional factors. Exogenous enzyme supplementation can improve the utilization efficiency of bioactive compounds in mulberry leaf-containing diets. This study aimed to evaluate the dose-dependent effects of mulberry leaf powder supplemented with a multi-enzyme premix (MLE) on growth, intestinal health, antioxidant and immune responses, as well as intestinal microbiota and metabolome in juvenile Acipenser schrenckii. Four diets containing 0%, 2%, 4% and 6% MLE were formulated for a 10-week feeding trial. Moderate MLE supplementation maintained normal growth without significantly improving growth performance relative to the control, and was associated with reduced serum triglyceride, total cholesterol and glucose, as well as improved intestinal morphology and digestive enzyme activity. Appropriate MLE supplementation was associated with changes in the Nrf2/Keap1 signaling pathway, enhanced antioxidant capacity, and upregulated anti-inflammatory gene il10. Multi-omics analysis revealed that MLE induced taxon-specific changes in the intestinal microbiota and was associated with altered metabolic profiles, enriching beneficial taxa including Priestia, Bacillus_P and Cetobacterium_A. These changes suggest a potential modulation of the microbiota–metabolite–immunity axis that may help sustain intestinal homeostasis. Nevertheless, the beneficial effects declined at the 6% inclusion level. Collectively, MLE was associated with dose-dependent protective effects on the intestinal barrier that may involve the microbiota–metabolite–immunity axis and the Nrf2/Keap1 pathway; the optimal supplementary range is preliminarily estimated at 3.5–4.5% for juvenile Acipenser schrenckii, although this estimate is based on four dietary levels and requires validation in future dose–response studies. Full article

Administrative labels such as “organic” or “pasture-fed” animal food products inadequately capture the biological complexity of dairy production systems and consequently fail to differentiate potentially meaningful associations with nutritional quality, environmental impact and consumers’ health. We developed a functional classification framework based on three measurable traits: (1) botanical diversity, (2) concentrate dependence, and (3) input intensity, and applied it to six observational and/or experimental studies from tropical Mexico (n = 109 farms across Yucatán, Chiapas, and Colima federal states). Animal production systems were categorized as: (a) biodiverse grazing (silvopastoral, organic, or traditional grazing; >15 plant species or 8–14 species with concentrate < 25% dry matter intake and no synthetic inputs) or (b) conventional (monoculture/indoor systems; <5 plant species or 6–10 species with concentrate >40% with a use of agrochemicals). Biodiverse grazing systems produced lower daily milk yields (6.1 vs. 7.7 L d⁻¹; p < 0.0001) but yielded milk with more favorable cardiovascular lipid indices: atherogenic index (AI: 1.6–2.2 vs. 1.9–2.5), thrombogenic index (TI: 2.3–2.7 vs. 2.3–3.1), and health promotion index (HPI: 0.46–0.67 vs. 0.40–0.54). Artisan cheese from biodiverse systems contained substantially higher concentrations of tocopherols (127 vs. 77 mg 100 g⁻¹ DM) and monoterpenes (460–475 vs. 111–126 ng kg⁻¹). An intensive silvopastoral system reduced enteric methane emissions by 18.2% (376 vs. 460 g d⁻¹; p < 0.05) and by 21.3% per unit dry matter intake (24.0 vs. 30.5 g kg⁻¹ DMI; p < 0.0001). Forage nutritional quality (crude protein, neutral detergent fiber, acid detergent fiber) varied by species and season, with these parameters influencing estimated methane emissions. In a C57BL/6 murine model of high-fat diet-induced obesity, milk from biodiverse silvopastoral systems attenuated body weight gain (30.5 vs. 36.8 g; p < 0.05), preserved glucose tolerance (AUC: 32,616 vs. 45,248), nearly eliminated hepatic macrovesicular steatosis, and promoted smaller adipocyte size (1863 vs. 3880 µm²; p < 0.05) compared with conventional milk. These findings suggest that functional ecological traits provide a useful framework for evaluating dairy systems, with biodiverse grazing offering a potential convergence of environmental sustainability and preclinical health benefits. Nevertheless, external validation across diverse tropical regions and direct human intervention trials remain necessary to establish generalizability, and the associations identified should be considered hypothesis-generating rather than confirmatory. Full article

Objective: Adipose tissue inflammation in obesity promotes insulin resistance and metabolic disease. The Duffy Antigen Receptor for Chemokines (DARC), a non-signaling receptor expressed on erythrocytes and on other cell types, modulates inflammation by regulating chemokine levels. Gene variants that affect DARC expression on erythrocytes are common in people of African descent. Here, we disrupted DARC expression in hematopoietic cells and adipocytes to determine the impact on obesity. Methods: DARC floxed mice were bred with vav1-Cre mice to disrupt DARC expression in hematopoietic cells (DARC^Δhemato), and with adipoq-Cre mice to disrupt DARC expression in adipocytes (DARC^Δadipo). Mice were fed a chow diet (CD) versus a high-fat diet (HFD) and studied in vivo. In vitro studies were conducted on preadipocytes isolated from wild-type (WT) and global DARC knockout mice. Results: HFD-fed DARC^Δhemato mice exhibited impaired glucose tolerance compared with WT littermates, independent of weight gain. This was associated with increased adipose tissue inflammation and systemic oxidative stress. DARC^Δadipo mice exhibited similar glucose tolerance but had subtle differences in adipose depot mass and adipocyte size compared with WT littermates. Deletion of DARC in preadipocytes had no impact on adipogenic differentiation or lipid accumulation in vitro. Similarly, endothelial-specific DARC KO mice also showed no differences in glucose tolerance compared with WT. Conclusions: DARC disruption in hematopoietic cells is associated with adipose tissue inflammation and alters glucose homeostasis during diet-induced obesity, accompanied by reduced circulating levels of several DARC-binding chemokines. The relevance of these findings to human DARC genetic variants and obesity-related metabolic disease warrants further investigation. Full article

Metabolic syndrome came to the attention of the scientific community several decades ago, and its definition has undergone multiple changes over time. It is currently defined by the coexistence of hypertension, central obesity, dyslipidemia, and impaired glucose metabolism, with insulin resistance, chronic inflammation, and oxidative stress representing important underlying pathophysiological mechanisms. The latter two processes are major promoters of the onset and progression of atherosclerosis. In parallel, many individuals develop metabolic dysfunction-associated steatotic liver disease (MASLD), formerly called non-alcoholic fatty liver disease (NAFLD). Growing evidence indicates that MASLD may interact bidirectionally with cardiovascular, renal, and metabolic dysfunction and may contribute to cardiometabolic risk. These observations have prompted proposals for a broader cardio–reno–hepato–metabolic axis. However, MASLD is not currently included in the established cardiovascular-kidney-metabolic (CKM) definition or staging system, and its incorporation remains an evolving conceptual extension. Prediabetes is a reversible condition characterized by abnormal glucose levels that do not meet the diagnostic criteria for diabetes. The American Diabetes Association defines prediabetes as glycated hemoglobin (HbA1c) = 5.7–6.4%, fasting plasma glucose = 100–125 mg/dL, or two-hour plasma glucose during an oral glucose tolerance test = 140–199 mg/dL. This comprehensive review examines traditional and genetic risk determinants, shared pathophysiological mechanisms, diagnostic strategies, clinical manifestations, emerging phenotypes, circulating microRNAs as non-invasive biomarkers, complications, and the principal therapeutic strategies, including diet, exercise, and pharmacotherapy. Particular attention is given to the recent approvals of resmetirom and semaglutide for metabolic dysfunction-associated steatohepatitis and to the expanding roles of sodium-glucose cotransporter 2 (SGLT2) inhibitors, glucagon-like peptide-1 (GLP-1) receptor agonists and non-steroidal mineralocorticoid receptor antagonists. Cardiovascular, renal, metabolic, and hepatic disorders are frequently present in the same patient. Other individuals may develop this high-risk cluster over time. The aim of this article is to define the interplay between different metabolic conditions and to outline the best approach to diagnosis, monitoring, and effective integrated therapy. Full article

This study examined the effects of dietary carbohydrate levels on growth performance, immune response, and antioxidant capacity of male giant freshwater prawn Macrobrachium rosenbergii. Prawns with an initial body weight of 15.04 ± 0.08 g were fed for 9 weeks on five isonitrogenous, isolipidic diets formulated to contain 10%, 15%, 20%, 25%, and 30% carbohydrate (designated CHO10–CHO30). Weight gain rate and specific growth rate rose from CHO10 to CHO20 and then declined (peak in CHO20); broken-line regression of weight gain rate estimated the optimal dietary carbohydrate level at approximately 19.36% under the present experimental conditions. Moderate carbohydrate inclusion (15–20%) enhanced hepatopancreatic total antioxidant capacity (T-AOC), superoxide dismutase (SOD) and catalase (CAT) activities together with the transcription of cu/znsod, cat and glutathione peroxidase (gsh-px), whereas levels ≥ 25% lowered these defenses and raised hepatopancreatic malondialdehyde (MDA). High-carbohydrate diets also increased hemolymph glucose, triglyceride, total cholesterol and low-density lipoprotein cholesterol, progressively altered the mRNA expression of genes involved in the Toll-like receptor (TLR)/myeloid differentiation primary response 88 (MyD88) signaling pathway (upregulated tlr, myd88, relish and tumor necrosis factor; downregulated inhibitor of NF-κB alpha (IκB-α)), and altered the expression of apoptosis-related genes (downregulated B-cell lymphoma 2 (bcl-2), upregulated caspase-3). These results suggest that M. rosenbergii has an estimated optimal dietary carbohydrate level of approximately 19.36% under the present experimental conditions; intakes at or above 25% are associated with compromised hepatopancreatic health and growth, likely through the induction of oxidative stress, altered transcription of TLR/MyD88 pathway-related genes, and changes in apoptosis-related gene expression. Full article

Diabetes mellitus is a long-term metabolic disease associated with elevated glucose levels in blood and still constitutes one of the major public health issues worldwide. Inhibition of carbohydrate-digesting enzymes like α-amylase and α-glucosidase has been found to be effective in controlling postprandial hyperglycemia. The current study focused on designing, synthesis, characterization, and evaluation of novel 2,4-thiazolidinedione derivatives (D1–D5) as potent antidiabetic drugs utilizing combined in silico, in vitro, and in vivo techniques. Results from drug-likeness and ADME analyses indicated that all synthesized derivatives met Lipinski’s rule of five and had desirable pharmacokinetics properties along with reduced toxicity. Molecular docking against maltase-glucoamylase (human; PDB ID: 3TOP) protein showed good binding affinities of both D1 and D5 derivatives (−7.74 and −7.40 kcal/mol respectively) due to stable interactions with catalytic residues of enzymes. Inhibition of enzymes in vitro showed that D1 and D5 had the highest inhibitory activities of all synthesized derivatives, with IC₅₀ of 33.86 ± 2.1 and 37.55 ± 1.7 μM against α-amylase and 29.81 ± 3.2 and 32.43 ± 1.2 μM against α-glucosidase, respectively. Cytocompatibility tests on L6 myoblast cells proved that the lead compounds were well tolerated. In addition, studies in a model of Drosophila melanogaster induced by a high-sugar diet revealed a significant decrease in the level of glucose concentration depending on the dose, especially for D1 and D5, indicating their antihyperglycemic activity in vivo. Thus, these data confirm that D1 and D5 can be regarded as promising lead compounds for the development of new antidiabetics acting via inhibition of carbohydrate-metabolizing enzymes. 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: 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

Background: Although dietary fat and carbohydrates are major determinants of gut microbiota composition, their interactive effects across changing dietary monosaccharide-to-lard energy ratios remain incompletely understood. This study descriptively examined treatment-level cecal microbiome profiles across dietary gradients in which lard (L) was progressively replaced with glucose (G) or fructose (F). Methods: A carbohydrate-free, lard-rich control diet was formulated, and lard was progressively replaced with glucose or fructose while maintaining a constant protein-to-energy ratio. Cecal contents from eight rats per dietary group were pooled in equal amounts, yielding one composite microbiome sample per treatment. Pooled samples were characterized by shotgun metagenomic sequencing. Sequencing/classified read counts (CRs) and relative abundance (RA) were treated as complementary sequencing-derived representations rather than measures of absolute bacterial abundance. Microbiome outcomes were interpreted descriptively at the treatment level. Results: Across the pooled treatment profiles, CRs and RA showed non-linear patterns and did not consistently change in parallel, providing complementary descriptions of treatment-level taxonomic responses. CR patterns indicated a combined effect of L and monosaccharide content, with several mixed L–monosaccharide diets showing lower CRs than both the L_6.03 reference and the lard-free endpoints. Differences between the G and F series were most apparent at low L and high monosaccharide levels, particularly under lard-free conditions, although their magnitude and direction varied among taxa. Hierarchical clustering and exploratory correlation networks provided complementary descriptions of treatment-level community organization. Conclusions: The pooled treatment-level microbiome profiles revealed non-linear responses to changing dietary L–monosaccharide composition, with CRs and RA providing partly different information on taxonomic patterns. Differences between the G and F series were most apparent at low L and high monosaccharide levels, particularly under lard-free conditions. Full article

The Chinese longsnout catfish is a typical carnivorous fish with a relatively weak ability to utilize glucose. However, the genomic basis for its glucose metabolic adaptation remains unclear. In this study, we used comparative genomics methods to systematically analyze the evolutionary characteristics of glucose metabolism-related genes in the Chinese longsnout catfish, focusing on gene family evolution, patterns of expansion and contraction, and selective pressures. The results indicate that glucose metabolism-related genes have undergone significant reshaping during evolution. Genes involved in glucose digestion, absorption, and insulin signaling pathways demonstrate a tendency toward contraction, while those associated with protein and lipid metabolism exhibit expansion. This pattern is consistent with the species’ long-term adaptation to a high-protein, high-fat diet. Comparative analysis further revealed that, compared to fish with different dietary habits, certain key genes involved in glycolysis in the Chinese longsnout catfish exhibit a reduction in copy number. Molecular evolutionary analysis showed that key genes involved in glycolysis and gluconeogenesis (including hexokinase 2 (hk2), phosphofructokinase, muscle/platelet (pfkm/p)) exhibit signs of accelerated evolution or positive selection. Notably, the PFK gene family exhibits complex evolutionary characteristics resulting from the combined effects of gene contraction, rapid evolution, and positive selection. In summary, this study reveals the genomic evolutionary basis for the glucose metabolic adaptation of the Chinese longsnout catfish and identifies the PFK gene family as a key candidate for elucidating its unique glucose metabolic characteristics. Full article

The study compares the effects of policosanol (Poli), atorvastatin (Ator), and their combination (Poli+Ator) in mitigating high-cholesterol and high-galactose (HCHG) diet-induced metabolic stress and organ damage in zebrafish. After 22 weeks of feeding, the lowest survival probability was observed in the Ator-supplemented group (0.64). In comparison, the Poli and Poli+Ator-supplemented groups showed higher survival probabilities of 0.76 and 0.71, respectively. Compared with Poli, Ator supplementation had a greater effect in mitigating HCHG-induced dyslipidemia. Nonetheless, Poli+Ator demonstrated a significantly greater effect than Ator and Poli in reducing total blood cholesterol (TC), triglycerides (TG), and low-density lipoprotein cholesterol (LDL-C), and in elevating the HDL-C/TC ratio. No significant effect of Ator supplementation was observed on the HCHG-induced elevations in blood glucose and malondialdehyde (MDA) levels or the diminished sulfhydryl content; however, Poli alone and Poli+Ator significantly improved blood glucose, MDA, and sulfhydryl content. Consistently, the non-significant effect of Ator on the amputated tail fin regeneration was substantially improved by the Poli+Ator supplementation. In addition, Poli and Poli+Ator markedly reduce liver steatosis, neutrophil infiltration, and interleukin (IL)-6 production, while inhibiting the generation of oxidative species and senescent-positive cells in the kidney and preventing intestinal fibrosis. Also, Poli and Poli+Ator substantially minimize HCHG-triggered oxidative stress in reproductive organs, enhance spermatozoa count in the testis and substantially improve the embryo-producing ability of zebrafish. The study outlines the beneficial effect of Poli and Poli+Ator in mitigating HCHG-induced dyslipidemia, organ damage, and reproductive health. Full article

Metformin is a widely prescribed antidiabetic agent with pleiotropic effects extending beyond glycemic control, including anti-inflammatory and antioxidant actions. However, its impact on cytokine signaling and ferroptosis-related pathways in brown adipose tissue (BAT) remains poorly characterized. Here, we examined the transcriptional and metabolic responses to metformin in brown adipocytes and in a diet-induced obesity model. Differentiated brown adipocytes were treated with metformin and analyzed by RNA sequencing and RT-qPCR. C57BL/6 male mice fed a high-fat diet (HFD) were administered metformin to assess systemic metabolic parameters and BAT-specific responses, with validation by histology, RT-qPCR, and Western blot. Transcriptomic profiling identified differentially expressed genes enriched in cytokine–cytokine receptor interaction and ferroptosis-related KEGG pathways. Metformin modulated the expression of multiple inflammatory cytokine genes and upregulated antioxidant and ferroptosis defense-related genes, including the glutathione biosynthesis genes Gclc and Gclm, together with Hmox1, Gpx4, Nfe2l2 (Nrf2), and Slc7a11. Among these, Gpx4 showed the most consistent upregulation across mRNA and protein levels in BAT. In HFD-fed mice, metformin improved glucose tolerance and elevated the expression of antioxidant and ferroptosis-related genes in BAT, consistent with the in vitro findings. Together, these results indicate that metformin coordinately modulates antioxidant and ferroptosis defense-related gene expression in BAT, suggesting a tissue-protective transcriptional program under metabolic stress. Our findings identify candidate immunometabolic and ferroptosis-related targets of metformin in BAT and provide a basis for further mechanistic investigation of its tissue-specific actions beyond glycemic control. Full article

Background: Mitigation of systemic inflammation may support the achievement of healthy lives and well-being. The American Heart Association recently proposed “Life’s Essential 8” (LE8) lifestyle metric for evaluating cardiovascular health (CVH) status; however, most existing studies have been limited to populations in the United States. This study examined the association between the LE8 score and high-sensitivity C-reactive protein (hs-CRP) levels in Korean adults. Methods: A nationwide sample of 18,500 adults was analyzed. The LE8 score was calculated based on four health behaviors (diet, physical activity, smoking, and sleep health) and four biometric health factors (body mass index, blood lipids, blood glucose, and blood pressure). The LE8 scores were categorized into three groups: 80–100 (ideal CVH), 50–79 (intermediate CVH), and 0–49 (poor CVH). The hs-CRP levels were classified as <3 mg/L or ≥3 mg/L. Logistic regression models were used for the analysis. Results: Among the participants, 21.9%, 67.3%, and 10.9% had ideal, intermediate, and poor CVH, respectively. In the logistic regression models, the adjusted OR (95% CI) for the association between LE8 categories and hs-CRP ≥ 3 mg/L was 1.94 (1.56–2.40) for the intermediate group and 3.21 (2.41–4.28) for the poor group, respectively, compared with the ideal group. Conclusions: Poor CVH status assessed by the LE8 lifestyle health metric was associated with high hs-CRP levels. The study findings suggest that future longitudinal studies are required to establish the temporal relationship between the LE8 and hs-CRP. Full article

Obesity is a multifactorial disorder with increasing global prevalence, highlighting the importance of identifying early-life factors that may influence long-term metabolic outcomes. While metformin is widely used to improve metabolic dysfunction in adulthood, whether neonatal exposure to this drug modifies adult responses to subsequent dietary challenges remains poorly understood. This exploratory study evaluated whether intraperitoneal metformin administration during the neonatal period alters adult metabolic responses to hyperlipidic diet (HL) exposure in Wistar rats. Following weaning and sex determination, male offspring (n = 80) were included in the study and distributed among four experimental groups, i.e., saline–normolipidic (SAL-NL), saline–high-fat (SAL-HL), metformin–normolipidic (MET-NL), and metformin–high-fat (MET-HL), with 20 animals per group. From postnatal days 1 to 12, animals received daily intraperitoneal saline or metformin (100 mg/kg/day). From days 60 to 90, animals were fed normolipidic or hyperlipidic diets. Body mass, food intake, glucose tolerance (GTT), and insulin tolerance (ITT) were assessed. Neonatal metformin exposure was associated with reduced body mass gain in MET-HL animals compared to SAL-HL, while food intake differed according to dietary condition. Metformin-treated animals also exhibited improved insulin sensitivity, reflected by higher kITT values, while no significant differences were observed in glucose tolerance. These preliminary findings suggest that neonatal metformin administration may influence adult metabolic responses to dietary challenge. Further studies are required to elucidate the mechanisms and long-term implications of this early-life intervention. Full article