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Nutritional interventions, either by controlling dietary energy (DE) or supplementing rumen-protected choline (RPC) or both, may mitigate negative postpartum metabolic health outcomes. A companion paper previously reported the effects of DE density and RPC supplementation on production and health outcomes. The objective of this study was to examine the effects of DE and RPC supplementation on the expression of hepatic oxidative, gluconeogenic, and lipid transport genes during the periparturient period. At 47 ± 6 d relative to calving (DRTC), 93 multiparous Holstein cows were randomly assigned in groups to dietary treatments in a 2 × 2 factorial of (1) excess energy (EXE) without RPC supplementation (1.63 Mcal of NE L /kg of dry matter; EXE−RPC); (2) maintenance energy (MNE) without RPC supplementation (1.40 Mcal of NE L /kg dry matter; MNE−RPC); (3) EXE with RPC supplementation (EXE+RPC); and (4) MNE with RPC supplementation (MNE+RPC). To achieve the objective of this research, liver biopsy samples were collected at −14, +7, +14, and +21 DRTC and analyzed for mRNA expression (n = 16/treatment). The interaction of DE × RPC decreased glucose-6-phosphatase and increased peroxisome proliferator-activated receptor α in MNE+RPC cows. Expression of cytosolic phosphoenolpyruvate carboxykinase was altered by the interaction of dietary treatments with reduced expression in EXE+RPC cows. A dietary treatment interaction was detected for expression of pyruvate carboxylase although means were not separated. Dietary treatment interactions did not alter expression of carnitine palmitoyltransferase 1A or microsomal triglyceride transfer protein. The 3-way interaction of DE × RPC × DRTC affected expression of carnitine palmitoyltransferase 1A, glucose-6-phosphatase, and peroxisome proliferator-activated receptor α and tended to affect cytosolic phosphoenolpyruvate carboxykinase. Despite previously reported independent effects of DE and RPC on production variables, treatments interacted to influence hepatic metabolism through altered gene expression. [ABSTRACT FROM AUTHOR]

The digestive physiology of young chickens is characterized by inefficient digestion and absorption of fat due to a low level of natural endogenous lipase production. These evidences have increased the interest on the use of emulsifiers to improve utilization of fats in young chickens and growth performance of broiler. The effect of a synthetic emulsifier on growth performance, meat quality, caecum microbial count, plasma metabolites and hepatic apolipoprotein gene expression was investigated in male broiler chicks. A total of 600 one-day-old ROSS 308 broiler chicks were assigned to 2 experimental groups consisting of 15 pens with 20 birds/ per pen each, to compare the different dietary treatments: control diet (CTR) or diet supplemented with AVI-MUL TOP (AMT) at 1 g/kg from day 0 to 12, 0.75 g/kg from day 12 to 22 and 0.5 g/kg from day 22 to 44. Growth performance was determined on days 0, 12, 22, and 44. At the end of the trial (day 44), one chick from each pen was chosen on body weight (BW) basis and sacrificed and samples of blood, liver, caecum content and breast were collected for analysis. AMT supplementation increased BW on days 12 and 22 ( P  = 0.02; P  = 0.02) and ADG from day 0 to 12 ( P  = 0.02), while reduced FCR from day 22 to 44 ( P  = 0.047) and from day 0 to 44 ( P  = 0.02). AMT supplementation modified carcass and meat characteristics, increasing dressing percentage ( P  = 0.01) and b* (yellowness) ( P  = 0.01) compared to control group. Moreover, AMT dietary supplementation increased total cholesterol ( P  = 0.02) and HDL cholesterol ( P  = 0.02) plasma concentrations. No differences between the two treatments were observed in caecum microbial counts and hepatic apolipoprotein gene expression. In conclusion, our findings show that AMT supplementation to broiler chicks may have a beneficial effect on growth performances (BW, ADG and FCR) and carcass dressing and may affect meat colour (b* yellowness) and lipid metabolism (cholesterol and HDL). [ABSTRACT FROM AUTHOR]