Abstract
INTRODUCTION: This study investigated the physiological, biochemical, and molecular shifts in male Mule ducks during an assisted-feeding period and the subsequent recovery phase following the cessation of overfeeding. While assisted-feeding is known to induce significant hepatic changes, the timeline and extent of the liver's capacity to return to a basal state remain critical areas of inquiry. METHODS: Male Mule ducks were subjected to a period of assisted-feeding followed by a recovery phase where they returned to an ad libitum diet. We monitored body weight and liver mass, analyzed plasma metabolic markers (including lipids and liver enzymes), and evaluated hepatic composition. Molecular analysis was conducted to assess gene expression related to lipogenesis, inflammation, and apoptosis, while antioxidant enzyme activities and hypoxia markers were measured to determine cellular stress levels. RESULTS: Assisted-feeding significantly increased body weight, liver mass, and hepatic steatosis, accompanied by a sharp rise in plasma markers such as triglycerides, cholesterol, and liver enzymes (ALAT, LDH, ALP). At the molecular level, there was a marked upregulation of genes involved in lipogenesis (scd1, dgat2), inflammation (TNFα, IL8), and apoptosis. Furthermore, increased activities of antioxidant enzymes (SOD, Cat, GPX1) and markers of hypoxia (HIF-1α, HIF-2α) indicated significant metabolic load and cellular stress. Following the cessation of overfeeding, most physiological and biochemical parameters, including liver mass and enzyme levels, returned to control values within 20 to 29 days. Notably, while hepatic alterations were fully abolished, abdominal fat remained significantly higher in ex-force-fed ducks compared to the control group. CONCLUSION: The study demonstrates that hepatic steatosis induced by assisted-feeding in Mule ducks is a highly reversible process. Despite triggering significant oxidative stress, hypoxia, and inflammatory responses, the avian liver exhibits a remarkable regenerative capacity, returning to its basal physiological and molecular state within 29 days of returning to a standard diet.