**AWARDS ISSUED PRIOR TO JANUARY 20, 2025, WERE FUNDED UNDER PREVIOUS ADMINISTRATIONS AND MAY NOT REFLECT THE PRIORITIES AND POLICIES OF THE CURRENT ADMINISTRATION.** DURING EMBRYONIC-TO-POST-HATCH TRANSITION IN CHICKEN, THERE IS A DRAMATIC METABOLIC SWITCH FROM, THE EMBRYO DERIVING OVER 90% OF ENERGY FROM YOLK-LIPID OXIDATION TO, THE NEONATAL CHICK LIVER UPREGULATING NEW LIPID SYNTHESIS (LIPOGENESIS). INTERESTINGLY, A SIMILAR METABOLIC MILIEU IS EVIDENT IN FATTY LIVER HEMORRHAGIC SYNDROME (FLHS) IN POULTRY LAYERS AND NON-ALCOHOLIC FATTY LIVER DISEASE (NAFLD) IN MICE AND HUMANS, BUT ALONG WITH THE TOXIC EFFECTS OF OXIDATIVE STRESS AND INFLAMMATION. INEFFICIENT EMBRYONIC-TO-POST-HATCH TRANSITION IS ALSO A SIGNIFICANT SOURCE OF MORTALITY AND ECONOMIC LOSS TO THE POULTRY INDUSTRY. WE HYPOTHESIZE THAT THE OPTIMAL RELATIONSHIP BETWEEN MITOCHONDRIAL LIPID-OXIDATION AND LIPOGENESIS IN THE LIVER CONTRIBUTES TO THE HEALTHY EMBRYONIC-TO-POST-HATCH SWITCH. DISRUPTING THIS RELATIONSHIP WILL RESULT IN SYMPTOMS OF FATTY LIVER DISEASE, IN TURN LEADING TO INEFFICIENT EMBRYONIC-TO-POST-HATCH TRANSITION AND LOSSES IN PRODUCTIVITY. OUR OBJECTIVE 1 WILL CHARACTERIZE THE ADAPTABILITY OF THE CENTRAL MITOCHONDRIAL NETWORKS AND LIPOGENESIS IN THE LIVER DURING EMBRYONIC-TO-POST-HATCH TRANSITION. OBJECTIVE 2 WILL TEST THE HYPOTHESIS THAT THE MAL-ADAPTABILITY OF THE HEPATIC MITOCHONDRIAL METABOLIC NETWORKS CONTRIBUTE TO METABOLIC DYSFUNCTION IN SMALL-EGG DERIVED EMBRYOS AND CHICKS FROM YOUNGER FLOCKS, COMPARED TO THEIR LARGER AND OLDER COUNTERPARTS. HERE, WE ALSO HYPOTHESIZE THAT BRANCHED CHAIN AMINO ACIDS (BCAAS) WILL POSITIVELY IMPACT THE REMODELING OF MITOCHONDRIAL LIPID METABOLISM AND LIPOGENESIS. THE INVESTIGATION OF THE ROLE OF BCAAS IS UNDER THE PREMISE THAT BCAAS CLOSELY INTERACT WITH AND REGULATE SEVERAL ASPECTS OF MITOCHONDRIAL LIPID METABOLISM. TOWARDS THESE OBJECTIVES, WE WILL INTEGRATE METABOLIC PROFILING BY STATE-OF-THE-ART TECHNIQUES IN STABLE ISOTOPE-BASED MASS SPECTROMETRY (MS) AND NUCLEAR MAGNETIC RESONANCE (NMR), WITH GENE PROFILES FROM RNA-SEQUENCING. THIS STRATEGY WILL HELP US IDENTIFY CENTRAL MECHANISMS PROMOTING THE OPTIMAL CROSSTALK BETWEEN MITOCHONDRIAL FUNCTION, LIPOGENESIS AND HEPATO-CELLULAR STRESS. THIS IN TURN WILL HELP FORMULATE NUTRITIONAL, HORMONAL OR GENETIC STRATEGIES TO OPTIMIZE THE HATCHLING HEALTH. THE IMPACT OF THESE STUDIES WILL BE TOWARDS TARGETING MITOCHONDRIAL FUNCTION AS A NEW PARADIGM TO IMPROVE POULTRY PRODUCTION AND ECONOMICS, SPECIFICALLY BY A) OPTIMIZING THE METABOLIC HEALTH OF THE EMBRYONIC AND HATCHLING LIVER, B) IDENTIFYING METABOLIC MECHANISMS WHICH CAN HELP PREVENT THE ONSET OF FATTY LIVER SYNDROMES.