Effects of varying levels of dietary protein and net energy on growth performance, nitrogen balance and faecal characteristics of growing-finishing pigs

This experiment was conducted to evaluate the effects of dietary protein and net energy (NE) levels on growth performance, nutrient digestibility, nitrogen metabolism, and faecal microbiota of growing-finishing pigs. Eighteen crossed barrows were randomly allocated into one of three dietary treatments: high protein + high NE diet, low protein + high NE diet, and low protein + low NE diet. The whole experiment lasted 90 days and was divided into three phases (phase I: 25-50 kg; phase II: 50-75 kg; phase III: 75-105 kg). All pigs were individually housed in a metabolism cage and subjected to four-day total faeces and urine collection period at the end of each phase. There was no significant difference in growth performance, nutrient digestibility, serum total protein, and albumin concentrations of pigs among the dietary treatments. Compared with the high protein + high NE diet, pigs fed low protein + high NE and low protein + low NE diets had lower N intake, urine N, and total N excretion in each phase. At the end of the experiment, pigs fed the low protein + high NE and low protein + low NE diets had lower blood urea nitrogen, serum NH3-N concentrations, faecal pH value, faecal NH3-N concentration, and faecal Escherichia coli count than those fed the high protein + high NE diet. However, there was no significant difference in all of the above indexes between low protein + high NE and low protein + low NE diets. Decreasing the dietary protein content by 3.5 percentage units has no adverse effects on growth performance and nutrient digestibility of pigs while significantly reduces N excretion and faecal Escherichia coli count. Moreover, further decreasing dietary NE level in the low-protein diet by 0.35-0.5 MJ/kg does not affect growth performance, nutrient digestibility, N excretion, blood profiles, and faecal Escherichia coli count of pigs.(AU)

Effect of CRABP2 on the proliferation and odontoblastic differentiation of hDPSCs.

Cellular retinoic acid-binding protein 2 (CRABP2) has been detected in several organs during embryonic development. Recent studies have demonstrated that CRABP2 plays important roles in the retinoic acid, ß-catenin and Notch signaling pathways, as well as in the interaction between epithelial and mesenchymal cells, which are important for human dental pulp stem cells (hDPSCs) and tooth development. In the present study, the expression of CRABP2 during mouse molar development and the role of CRABP2 in hDPSC odontoblastic differentiation were evaluated. CRABP2 was gradually decreased during the development of the first maxillary molar, which exhibited the same trend as the expression of CRABP2 during the odontoblastic induction of hDPSCs. CRABP2 knockdown inhibited the proliferative ability of hDPSCs, while it enhanced odontoblastic differentiation via promoting mineralization nodule formation and upregulating the activity of alkaline phosphatase and the expression of mineralization-related genes. The present study uncovered a novel function of CRABP2 in hDPSCs. Our data suggest that CRABP2 may act as a regulator during the proliferation and differentiation of hDPSCs.

Effect of CRABP2 on the proliferation and odontoblastic differentiation of hDPSCs

Abstract: Cellular retinoic acid-binding protein 2 (CRABP2) has been detected in several organs during embryonic development. Recent studies have demonstrated that CRABP2 plays important roles in the retinoic acid, β-catenin and Notch signaling pathways, as well as in the interaction between epithelial and mesenchymal cells, which are important for human dental pulp stem cells (hDPSCs) and tooth development. In the present study, the expression of CRABP2 during mouse molar development and the role of CRABP2 in hDPSC odontoblastic differentiation were evaluated. CRABP2 was gradually decreased during the development of the first maxillary molar, which exhibited the same trend as the expression of CRABP2 during the odontoblastic induction of hDPSCs. CRABP2 knockdown inhibited the proliferative ability of hDPSCs, while it enhanced odontoblastic differentiation via promoting mineralization nodule formation and upregulating the activity of alkaline phosphatase and the expression of mineralization-related genes. The present study uncovered a novel function of CRABP2 in hDPSCs. Our data suggest that CRABP2 may act as a regulator during the proliferation and differentiation of hDPSCs.