Heat stress, high stocking density, and feed safety risks are common features of modern intensive poultry production and collectively disrupt metabolic homeostasis in chickens. These stressors promote oxidative stress, lipid metabolic dysfunction, and inflammatory activation, ultimately reducing growth performance and overall health. This review summarizes current evidence on the effects of major stressors under intensive farming conditions on lipid metabolic homeostasis, redox balance, and immune regulatory networks, with particular emphasis on the supplementation strategies and physiological effects of chlorogenic acid (CGA) in chickens. Available studies indicate that CGA may regulate lipid metabolic homeostasis through adenosine monophosphate-activated protein kinase (AMPK)-related signaling pathways, enhance antioxidant defenses mediated by nuclear factor erythroid 2 related factor 2 (Nrf2), and suppress inflammatory responses associated with nuclear factor κB (NF-κB), thereby contributing to protective regulation at multiple levels.

The global poultry industry faces escalating challenges in animal welfare and production efficiency in the post-antibiotic era. Feed intake, a crucial determinant of growth, is frequently suppressed under stress, forming a key bottleneck for sustainable production. The microbiota–gut–brain (MGB) axis provides a novel framework to understand this complex regulation. Short-chain fatty acids (SCFAs), produced from dietary fiber by gut microbiota, serve as vital chemical messengers within this axis, modulating hypothalamic feeding centers and systemic metabolism. This review summarizes SCFA biosynthesis and kinetics in poultry and examines their neural, humoral, and immune pathways to the brain. Emphasis is placed on receptor-mediated signaling, epigenetic regulation, energy sensing, and neuroimmune modulation through which SCFAs regulate feeding and reduce inflammation. Practical strategies—such as substrate engineering, microbiota modulation, and exogenous regulators—are discussed to enhance SCFA levels and poultry health. Future directions include multi-omics integration, novel additives, and predictive models to advance antibiotic-free nutrition.

High-stocking-density (HD) environments can trigger systemic inflammatory responses, consequently impairing broiler growth. Given the broad anti-inflammatory properties of aspirin eugenol ester (AEE), this study investigated the effects of AEE supplementation on growth performance, immune organ indices, serum immunoglobulin levels, and hypothalamic inflammation-related markers in HD broilers. A total of 528 one-day-old male Arbor Acres (AA) broilers were randomly assigned to four groups: ND, HD, ND-AEE, and HD-AEE (ND, 14 birds/m²; HD, 22 birds/m²), with six replicate cages per treatment group over a 42-day experimental period. The results revealed that AEE significantly improved the growth performance of HD broilers. Immune organ indices, serum immunoglobulin levels, and the expression of spleen inflammatory factors was associated with the organismal inflammatory response, which manifested primarily during the late growth phase. On Day 35, AEE significantly suppressed (p < 0.05) the relative mRNA expression of p21-activated kinase 1 (PAK1) in the hypothalamus of HD broilers. On Day 42, AEE significantly reduced the relative mRNA expression of PAK1, p38 mitogen-activated protein kinase (p38MAPK), cyclooxygenase-2 (COX-2), prostaglandin E synthase 1 (mPGES-1), and interleukin-1β (IL-1β) (p < 0.05), while significantly elevating the relative mRNA expression of growth hormone-releasing hormone (GHRH) (p < 0.05). Collectively, these findings demonstrate that AEE mitigates high-density rearing-induced hypothalamic inflammation and is associated with downregulated mRNA expression of PAK1 and its downstream targets in the p38MAPK/COX-2 axis. This gene expression profile correlates with improved growth and immune function in high-density-stressed broilers, suggesting a potential regulatory link that requires further validation at the protein and functional levels.

This study evaluated whether chlorogenic acid (CGA) attenuates hepatic injury in broilers under high stocking density (HSD). A total of 216 experimental male Arbor Acres broilers were assigned to normal density without CGA (ND; 14 birds/m²), high density without CGA (HD; 22 birds/m²), normal density with 0.1% CGA (NDCGA), or high density with 0.1% CGA (HDCGA) groups, with six cages per treatment. CGA was supplied from day 7 to 42. At 42 d, live-weight densities were 35.00, 50.25, 34.48, and 49.38 kg/m², respectively. Compared with their corresponding normal-density groups, the high-density groups had lower body weights at 21, 28, 35, and 42 d, and lower average daily gain (ADG) during days 21–42 (p < 0.05), whereas CGA did not significantly alter body weight or ADG within either stocking density (p > 0.05). At 35 and 42 d, the HD group had lower hepatic T-AOC, SOD, and CAT activities and higher MDA content than the ND group (p < 0.05). Compared with the HD group, the HDCGA group had higher T-AOC and CAT activities and lower MDA content at both ages, and higher SOD activity at 42 d (p < 0.05). Qualitative histological and transcript-level alterations were evident at 28 d. Compared with HD, the HDCGA group showed treatment-associated shifts in AMPK, SREBP1, ACACA, PLA2G4A, COX-2, ALOX5, and NOX5 mRNA abundance (p < 0.05). Under the experimental conditions, 0.1% CGA was associated with partial attenuation of HSD-related hepatic oxidative, lipid-metabolic, and inflammatory disturbances without a significant growth response.