The effects of subclinical Zn deficiency on depletion and redistribution of body Zn were studied in weaned piglets. Forty-eight weaned piglets (German-Large-White×Land-Race×Piétrain; 50 % female, 50 % male-castrated; body weight 8·5 (sd 0·27) kg) were fed restrictively (450 g/d) a basal maize–soyabean meal-based diet supplemented with varying amounts of ZnSO4.7H2O (analysed dietary Zn: 28·1, 33·6, 38·8, 42·7, 47·5, 58·2, 67·8, 88·0 mg/kg diet) for an experimental period of 8 d. Analyses comprised Zn concentrations in soft tissues. Statistical analyses included regression models and k-means cluster analysis. Jejunum and kidney Zn correlated positively with dietary Zn (P<0·05). Other Zn pools responded in a non-linear fashion by declining (colon, epidermis, spleen) or increasing (mesenteric lymph follicles, thymus, skeletal muscle) below 63·6, 48·0, 47·5, 68·0, 43·0 and 53·1 mg Zn/kg diet, respectively (P<0·01). Above these thresholds, Zn concentrations in epidermis, mesenteric lymph follicles and skeletal muscle plateaued (P<0·0001), whereas they exhibited a decrease in colon and thymus (P<0·01) as well as a numerical increase in spleen. Clustering by dietary Zn concentration indicated clusters of varying Zn supply status and pathophysiological status. Clustering by biological matrices revealed a discrimination between storage, transport and excretion media as well as soft tissues. Taken together, novel response patterns indicated compensation reactions in tissues that are essential for the acute survival of growing animals (heart, skeletal muscle, immune tissues). Furthermore, this is to our knowledge the first study that mapped the gross Zn requirement by clustering tissue Zn concentrations between treatment groups.

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 (88 mg 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 ZnSO4.7H2O 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 α-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 α-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.