Background: Natural differences in running capacities among rats remain poorly understood, and the mechanisms driving these differences need further investigation. Methods: Twenty male Sprague-Dawley (SD) rats were selected. High and low running capacity rats were identified using Treadmill Exhaustion Tests. Peripheral blood was collected for serum isolation, followed by metabolomics analysis using LC-MS/MS. Data were preprocessed, and principal component analysis (PCA) and partial least squares-discriminant analysis (PLS-DA) were applied to identify metabolic profile differences. Significant metabolites were screened, and pathway enrichment analysis was conducted using the KEGG database to determine key metabolic pathways. Forty SD rats (equal male and female) were randomly divided into an ITP group (24.29 mg/kg.bw) and a control group. Running capacity was assessed after one week of continuous treatment. Results: Three independent measurements showed consistent differences in running capacity. A total of 519 differential metabolites were identified, with 255 up-regulated and 264 down-regulated. KEGG pathway analysis revealed significant enrichment of the Purine Metabolism pathway (ITP-ATP ) in the high running capacity group (P< 0.05). The ITP-treated group exhibited significantly higher running capacity than controls (P< 0.05), confirming the efficacy of dietary ITP supplementation. Conclusion: The running capacity of rats is influenced by the ITP-ATP pathway,and exogenous ITP administration through dietary intervention significantly improves running ability.

Food preparation methods markedly influence the glycemic index (GI) of carbohydrate‐rich staple foods, impacting postprandial glycemic control and associated health risks. We aim to systematically review and quantify how common cooking methods influence the GI of staple carbohydrate foods to inform dietary advice and food policy particularly in high‐diabetes‐prevalence regions like Asia‐Pacific. We conducted a systematic review and random‐effects meta‐analysis of 35 in vivo human trials ( n ≈ 580) comparing GI across boiling, baking, frying, steaming, pressure‐cooking, and refrigerated (“cook‐chill”) preparation methods for rice, potatoes, corn, sweet potatoes, cassava, bread, pasta, and lentils. Data were pooled using DerSimonian–Laird random‐effects models, and subgroup analyses were performed according to food type and preparation method. Boiling produced an intermediate GI (63.1; 95% CI 59.2–67.0). Baking (71.5) and frying (72.8) raised GI, while steaming (59.9) and pressure‐cooking (58.7) lowered it. Refrigeration followed by reheating (“cook‐chill”) yielded the lowest GI (46.3). Subgroup analyses confirmed consistent effects across rice, potatoes, bread, and legumes. Cooking practices substantially alter the GI of carbohydrate‐rich foods. Promoting steaming, pressure‐cooking, and refrigeration with reheating as everyday preparation strategies may reduce the glycemic impact of staple foods, with cook‐chill methods showing the largest reductions in GI compared with boiling. These findings have direct implications for dietary guidance in Asia‐Pacific populations, where rice and tubers predominate, supporting behavioral nutrition interventions, policy reforms in school/institutional catering, and the development of region‐specific low‐GI convenience foods to combat rising diabetes rates.

Introduction: Ginseng's bioactive components can cross the placental barrier and influence offspring through lactation; however, their effects on development remain unclear. Methods: This study used specific pathogen-free (SPF) Sprague-Dawley rats, divided into four groups: control, 31.3 mg/kg·bw, 125 mg/kg·bw, and 500 mg/kg·bw. Ginseng extract was administered by gavage during gestation and lactation. Maternal body weight, offspring growth, developmental milestones, sensory-motor abilities, learning-memory performance, and tissue pathology were assessed. Results: We found that female rats in the 500 mg/kg·bw group exhibited smoother, glossier fur from day 36 onward. Offspring in this group showed increased escape behavior and hyperactivity between postnatal days 5–11. Significant maternal weight loss occurred in the 125 mg/kg·bw and 500 mg/kg·bw groups. In the 500 mg/kg·bw group, female offspring exhibited delayed incisor eruption and temporary weight loss, which recovered post-weaning. Righting reflex times were shortened in the 31.3 mg/kg·bw group but prolonged in the 500 mg/kg·bw group. Female offspring in the 31.3 mg/kg·bw group displayed increased forelimb suspension time and greater running endurance. Male offspring in the 125 mg/kg·bw group demonstrated improved target quadrant latency and spatial exploration. Conclusion: These results suggest that ginseng extract has dose-dependent and sex-specific effects on maternal physiology and offspring development.

Caffeine is among the world's most widely consumed psychoactive substances, yet its potential to interact with the endocrine system, particularly as an estrogen mimic, remains ambiguous and inadequately characterized using validated in vivo models. Our objective is to definitively assess the intrinsic estrogenic activity of caffeine and its potential interaction with a reference estrogen using the standardized OECD 440 uterotrophic bioassay. Immature female Sprague-Dawley rats (n = 10/group) were administered vehicle, caffeine (10, 20, or 40 mg/kg/day), 17β-estradiol (positive control), or estradiol combined with caffeine for three consecutive days. Uterine wet and blotted weights were measured 24 h post-final dose, and the uterotrophic response was evaluated. As expected, estradiol treatment provoked a robust uterotrophic response, increasing uterine wet weight over 4-fold and blotted weight over 3.7-fold compared to controls (P < 0.001). In contrast, caffeine alone at all tested doses failed to produce any significant increase in uterine weight, indicating a lack of intrinsic estrogenic activity. Notably, co-administration of caffeine with estradiol significantly attenuated the estradiol-induced response, reducing wet weight by approximately 33% and blotted weight by 25% (P < 0.05). These findings demonstrate that caffeine is not an estrogen agonist in this validated in vivo model. Co-administration with estradiol significantly reduced the uterotrophic response, suggesting a potential interaction that warrants further mechanistic investigation.