This study aimed to investigate the effects of partially replacing corn with rice in the diet and supplementing with cellulase on growth performance, pork quality, and gut microbiota of growing–finishing pigs. A total of 64 healthy pigs (68.03 ± 1.59 kg) were randomly assigned into four groups: CON (basal diet), ASE (basal diet + 20,000 IU/g cellulase), RICE (the basal diet replaced 50% of corn with rice), RASE (the basal diet replaced 50% of corn with rice + 20,000 IU/g cellulase). The results indicated that dietary rice and cellulase, either individually or in combination, had no significant effects (p > 0.05) on the FBW, ADG, ADFI, and F/G of pigs. However, the dietary rice markedly increased the intramuscular fat (IMF) content (p < 0.05). Furthermore, gut microbiota profiling indicated that Papillibacte were enriched in the RICE group and positively associated with IMF content. Metabolomic analysis revealed substantial differences in fecal metabolites among the treatment groups. The RICE group exhibited reduced levels of Zygadenine, Carpaine, and Rhodioloside E, which were negatively correlated with both IMF content and Papillibacter. In conclusion, dietary rice can promote IMF deposition by modulating gut microbiota and host metabolism, without compromising the growth performance of pigs.

Obesity arises from dysregulation of central nervous system and peripheral energy homeostasis pathways. To maintain metabolic balance, neural circuits in the brain integrate nutritional signals from central and peripheral systems to correct deviations in energy supply and expenditure. Hence, elucidating the core neurobiological mechanisms of metabolic regulation and how alterations in these pathways contribute to obesity and related metabolic disorders is therefore of critical importance. Notably, neurotrophins not only support neuronal growth, development and function, but also play key roles in sensing nutritional status and regulating energy metabolism. Here, we summarize the potential mechanisms by which neurotrophins in key metabolic organs, including the hypothalamus, adipose tissue, pancreas islet, liver, skeletal muscle and intestine, sense nutritional signals and regulate energy homeostasis. Furthermore, we also further highlight the clinical application prospects and translational strategies for activating, inhibiting and stratifying interventions that target neurotrophins and their receptors. Finally, we outline outstanding issues related to neurotrophins mediated nutritional regulation of lipid metabolism, providing a reference for the design of therapeutic interventions against obesity.