Trypsin inhibitors ( TI ) resident in soybeans affects protein utilization. While heat treatment influences residual TI, it simultaneously affects the structure and solubility of the soybean proteins and confounds any response to exogenous proteases. Using purified TI, the effect of exogenous protease to TI can be dissociated from changes in the soybean protein. Thus, the current study was designed to evaluate the growth performance and protein utilization responses of broiler chickens to purified TI and exogenous protease. Soybean meal ( SBM ) was preanalyzed for basal TI (2,996 TIU/g SBM), formulated into nutritionally adequate experimental diets to contain 1,033 TIU/g diet, and purified TI was added at 9,000 TIU/g diet. A total of 320 Cobb-500 broiler chicks were allocated to 4 diets, each with 8 replicate cages and 10 birds per replicate. The experimental diets were arranged as a 2 × 2 factorial with factors being dietary TI (1,033 or 10,033 TIU/g) and exogenous protease (0 or 15,000 PROT/kg). On day 7, 14, and 21 posthatching, protease supplementation improved the BW gain ( P < 0.01) and gain to feed ratio ( P < 0.05) of birds. On day 14 and 21 posthatching, the relative weight of pancreas increased ( P < 0.05) with added TI but was reduced ( P < 0.001) with protease supplementation. Apparent ileal digestibility of all amino acids, except methionine, decreased ( P < 0.001) with added TI but increased ( P < 0.05) with protease supplementation. Jejunal MUC-2 was downregulated ( P < 0.01) and SCL7A-2 was upregulated ( P < 0.05) by protease supplementation. Duodenal trypsin and chymotrypsin activities reduced ( P < 0.05) with added TI but increased (P < 0.01) with protease supplementation. Exogenous protease produced longer villi ( P < 0.05) and deeper crypts ( P < 0.01) in the jejunal tissue. In conclusion, dietary addition of purified TI negatively affects nutrient utilization by broiler chickens. Furthermore, the study showed that the efficacy of the exogenous protease might be independent of dietary TI concentration.

Dietary starch is the major energy source for broiler chickens; therefore, relevant information on its intestinal utilization is important. The present study was designed to evaluate intestinal starch and energy digestibility of broiler chickens fed diets supplemented with α-amylase. A total of 240 day-0 male broiler chicks were randomly assigned to 3 nutritionally adequate corn-soybean–based experimental diets comprising 3 levels of α-amylase supplementation (0, 80, or 160 KNU/kg diet). Each treatment comprised 8 replicate cages of 10 birds each. At day 21 after hatching, digesta was collected from 4 intestinal sites: the anterior jejunum ( AJ ), posterior jejunum ( PJ ), anterior ileum ( AI ), and posterior ileum. Increasing α-amylase supplementation linearly improved ( P < 0.01) overall BW gain and feed efficiency of the birds. There were linear and quadratic ( P < 0.01) responses of increasing α-amylase supplementation on starch and energy digestibility at the PJ and AI. The total tract digestibility of starch increased ( P < 0.05) with increasing α-amylase supplementation. Starch disappearance and digestible energy (kcal/kg) linearly increased ( P < 0.01) with digesta flow from the AJ to PJ as dietary α-amylase supplementation increased. There were linear ( P < 0.01) and quadratic ( P < 0.05) effects of increasing α-amylase supplementation on the villus height in the jejunum. The viscosity of the jejunal digesta decreased ( P < 0.05) with increasing dietary α-amylase supplementation. The results from this study showed the efficacy of exogenous amylase in improving growth performance and starch and energy digestibility in broiler chickens. Furthermore, the digestibility of starch and energy and the impact of the exogenous amylase were higher at the PJ than other intestinal sites.

Background Progressive familial intrahepatic cholestasis (PFIC) type 3 is an autosomal recessive disorder arising from mutations in the ATP-binding cassette subfamily B member 4 (ABCB4) gene. This gene encodes multidrug resistance protein-3 (MDR3) that acts as a hepatocanalicular floppase that transports phosphatidylcholine from the inner to the outer canalicular membrane. In the absence of phosphatidylcholine, the detergent activity of bile salts is amplified and this leads to cholangiopathy, bile duct loss and biliary cirrhosis. Patients usually present in infancy or childhood and often progress to end-stage liver disease before adulthood. Case presentation We report a 32-year-old female who required cadaveric liver transplantation at the age of 17 for cryptogenic cirrhosis. When the patient developed chronic ductopenia in the allograft 15 years later, we hypothesized that the patient’s original disease was due to a deficiency of a biliary transport protein and the ductopenia could be explained by an autoimmune response to neoantigen that was not previously encountered by the immune system. We therefore performed genetic analyses and immunohistochemistry of the native liver, which led to a diagnosis of PFIC3. However, there was no evidence of humoral immune response to the MDR3 and therefore, we assumed that the ductopenia observed in the allograft was likely due to chronic rejection rather than autoimmune disease in the allograft. Conclusions Teenage patients referred for liver transplantation with cryptogenic liver disease should undergo work up for PFIC3. An accurate diagnosis of PFIC 3 is key for optimal management, therapeutic intervention, and avoidance of complications before the onset of end-stage liver disease.

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