Subclinical zinc deficiency impairs pancreatic digestive enzyme activity and digestive capacity of weaned piglets

This study investigated the effects of short-term subclinical Zn deficiency on exocrine pancreatic activity and changes in digestive capacity. A total of forty-eight weaned piglets were fed ad libitum a basal diet (maize and soyabean meal) with adequate Zn supply (88mg Zn/kg diet) during a 2-week acclimatisation phase. Animals were then assigned to eight dietary treatment groups (n 6) according to a complete randomised block design considering litter, live weight and sex. All pigs were fed restrictively (450 g diet/d) the basal diet but with varying ZnSO4 center dot 7H(2)O additions, resulting in 28.1, 33.6, 38.8, 42.7, 47.5, 58.2, 67.8 and 88.0 mg Zn/kg diet for a total experimental period of 8 d. Pancreatic Zn concentrations and pancreatic activities of trypsin, chymotrypsin, carboxypeptidase A and B, elastase and a-amylase exhibited a broken-line response to stepwise reduction in dietary Zn by declining beneath thresholds of 39.0, 58.0, 58.0, 41.2, 47.5, 57.7 and 58.0 mg Zn/kg diet, respectively. Furthermore, carboxypeptidase B and a-amylase activities were significantly lower in samples with reduced pancreatic Zn contents. Coefficients of faecal digestibility of DM, crude protein, total lipids and crude ash responded similarly to pancreatic enzyme activities by declining below dietary thresholds of 54.7, 45.0, 46.9 and 58.2 mg Zn/kg diet, respectively. In conclusion, (1) subclinical Zn deficiency impaired pancreatic exocrine enzymes, (2) this response was connected to pancreatic Zn metabolism and (3) the decline in catalytic activity impaired faecal digestibility already after 1 week of insufficient alimentary Zn supply and very early before clinical deficiency symptoms arise.