Abstract

Childhood obesity remains a major public health issue globally. Understanding how early-life dietary, lifestyle, socioeconomic, and environmental factors shape obesity risk is critical for designing targeted prevention strategies. This study aimed to identify distinct early-life cluster patterns among Australian children and examine their associations with longitudinal obesity outcomes from ages 4–15 years. Data came from the Longitudinal Study of Australian Children (LSAC) Birth cohort (N = 5107). An analytic sample of 4246 children with complete data at Wave 2 (aged 2–3) was analysed. Latent Class Analysis (LCA) was applied to identify early-life clusters, and body mass index (BMI) categories, underweight, normal weight, overweight, and obesity, were tracked across Waves 3–8 (ages 4–15). Chi-square tests and multinomial logistic regression (adjusted for maternal employment, neighbourhood safety, child screen time) examined associations between clusters and obesity outcomes. Four clusters were identified: (1) Risky Diet & Socioeconomically Disadvantaged, (2) Healthy Diet & Urban Affluent, (3) Mixed Diet & Moderate SEP Large Families, and (4) Healthy & Wealthy Metro Families. Children in Cluster 1 had persistently higher obesity prevalence (rising from 9% at age 4–5 to 17% at age 14–15), whereas Cluster 4 maintained the lowest (2–4%). Adjusted models showed significantly higher odds of obesity in Cluster 1 across all waves (AOR 2.4–7.5; p < 0.01). Distinct socio-dietary clusters established in early childhood predict divergent obesity outcomes up to age 15. Interventions addressing early nutrition, socioeconomic disadvantage, and environmental inequities are crucial to mitigate long-term obesity risk.

Abstract

Background: Sarcopenic obesity (SO), the coexistence of low muscle mass and excess adiposity, poses a major challenge for healthy aging. Resistance exercise is known to mitigate muscle loss, yet long-term interventions comparing different modalities remain scarce. This study explored the efficacy of power training (PT) versus multicomponent training (MT) and no-exercise control (CG) on muscle and fat parameters in older women with SO.

Methods: A 32-week randomized controlled trial was conducted with 40 community-dwelling women aged ≥65 years diagnosed with SO according to EWGSOP2 and ESPEN criteria. Participants were assigned to PT, MT, or CG. Both training groups performed supervised 50-minute sessions three times per week. Primary outcomes included appendicular skeletal muscle mass index (ASMI) and body fat percentage (BF%), while secondary outcomes were visceral fat (VF), gait speed (GS), timed up and go (TUG), and five-times sit-to-stand test (5STS). Nutritional intake was assessed at baseline to control for dietary effects.

Results: PT induced significant improvements in ASMI (+0.36 ± 0.34 kg/m², p = 0.039), BF% (−6.9 ± 6%, p = 0.002), and VF (p = 0.044), with large effect sizes (Cohen’s d > 0.8). Functional gains were notable in GS (p = 0.018), TUG (p = 0.005), and 5STS (p < 0.001), outperforming MT. Remarkably, 35.7% of PT participants no longer met diagnostic criteria for SO after the intervention. No adverse events were reported, and adherence exceeded 85%.

Conclusions: Long-term power training was more effective than multicomponent or no exercise in enhancing muscle mass, reducing fat, and improving functional performance in older women with SO. Its capacity to reverse SO in one-third of participants supports PT as a feasible, safe, and clinically relevant first-line strategy for managing sarcopenic obesity in aging populations.

Abstract

This study aimed to determine the critical stage of fat deposition in Shaziling pigs and to identify key candidate genes and regulatory pathways associated with lipid metabolism. A total of 60 Shaziling pigs were slaughtered at 60d, 90d, 120d, and 180d. Growth performence, carcass traits, adipocyte morphology, fatty acid composition, and transcriptomic profiles of backfat tissue were analyzed to characterize phenotypic and molecular changes during fat deposition. The period between 90d and 120d represents a critical stage of accelerated fat deposition in Shaziling pigs, accompanied by significant increases in fat percentage, adipocyte area, and alterations in fatty acid profiles(P<0.05). Gene expression analysis revealed significant alterations in key adipogenic regulators, including CCAAT/enhancer-binding protein alpha (C/EBPα), fatty acid synthase (FAS), acetyl-CoA carboxylase (ACC), Forkhead Box O1 (FOXO1) and sterol regulatory element-binding protein 1c (SREBP-1c) (P<0.05). Transcriptomic analysis identified 362 differentially expressed genes (DEGs) between 90d and 120d, with 106 DEGs enriched in lipid metabolism-related pathways, such as Tumor necrosis factor-alpha (TNF-α), Phosphoinositide 3-kinase–protein kinase B (PI3K–Akt), Peroxisome proliferator-activated Receptor (PPAR), Nuclear factor kappa-light- chain-enhancer of activated B cells (NF-κB), and FOXO signaling pathways.Integration of protein interaction and co-expression networks highlighted FBJ murine osteosarcoma viral oncogene homolog (FOS), Jun proto-oncogene (JUN), Jun B proto-oncogene (JUNB), Bone morphogenetic protein 6 (BMP6), Suppressor of cytokine signaling 3 (SOCS3), and Interleukin 6 (IL6) as candidate regulators significantly associated with carcass fat percentage and backfat thickness. These findings demonstrate that 90–120d is a pivotal stage for fat deposition in Shaziling pigs and reveal candidate genes and pathways involved in lipid metabolism. The results provide new insights into the genetic regulation of lipid metabolism in IPBs and offer potential targets for improving meat quality and nutritional value.

Abstract
The development of natural, multi-mechanistic anti-obesity strategies remains a critical need in nutritional science. While lactic acid bacteria (LAB) show probiotic promise, their full potential, particularly regarding non-viable forms and metabolites, is not fully realized. This study establishes a complete pipeline from strain screening to practical application, highlighting their multifunctional role in lipid metabolism. We performed comprehensive in vitro screening of LAB strains (including Lactiplantibacillus plantarum, Pediococcus acidilactici, Enterococcus faecalis, and Ligilactobacillus animalis) for cholesterol assimilation and bile salt deconjugation. Genomic analysis of selected strains confirmed functional genes and importantly, revealed an absence of virulence factors, ensuring their safety profile. Beyond conventional probiotics, we systematically investigated live bacteria, heat-inactivated cells (postbiotics), and capsular polysaccharide (CPS). The application and efficacy were then rigorously evaluated in vivo across diverse models of obesity (obese mice, laying hens). The results demonstrated that administration of these multifunctional LAB preparations significantly alleviated obesity phenotypes, improved blood lipid profiles, and reduced hepatic steatosis. Crucially, we confirmed that the beneficial effects were not exclusive to live bacteria, as inactivated forms and purified CPS also exhibited substantial lipid-modulating activities, underscoring a multi-factorial mechanism of action. In conclusion, our findings unveil the robust anti-obesity properties of the selected LAB strains. We demonstrate that the beneficial effects are mediated through multiple forms—live, inactivated, and their bioactive metabolites. This holistic study, from in vitro screening to multi-model in vivo validation, provides a solid scientific foundation for developing novel LAB-based strategies, including next-generation postbiotics, for combating obesity and metabolic syndromes.