A major goal of mineral nutrition research is to provide information of feed zinc (Zn) utilization efficiency and gross Zn requirements as affected by changing rearing conditions. This can be achieved only by applying precise experimental models that acknowledge the basic principles of Zn metabolism. This review article summarizes the most important aspects of Zn homeostasis in monogastric species, including molecular aspects of Zn acquisition and excretion. Special emphasis is given to the role of the skeleton as well as the exocrine pancreas for animal Zn metabolism. Finally, we discuss consequences arising from these physiological principles for the experimental design of trials which aim to address questions of Zn requirements and bioavailability.
Animal Feed ; Animal Nutritional Physiological Phenomena ; Animals ; Biological Availability ; Diet ; Genotype ; Homeostasis ; Humans ; Minerals/metabolism* ; Pancreas, Exocrine/metabolism* ; Trace Elements ; Zinc/metabolism*

BACKGROUNDA number of reports based on both animal experiments and clinical investigations have pointed out that total parenteral nutrition (TPN) suppresses the function of the exocrine pancreas. Even though pancreatic hypotrophy and dysfunction resulting from TPN may be explained by several mechanisms, the clinically most important cause is that nutrients in circulation affect pancreatic secretion. The effect of nutrients on the exocrine pancreas is still controversial. The aim of the present study was, therefore, to clarify the influence of intravenous amino acids and hypertonic glucose in TPN solution on the exocrine pancreas.

METHODSThree mixed TPN solutions, consisting of 30% or 50% glucose or of 14% amino acids, were employed. Twenty-four male Sprague-Dawley rats were randomly divided into four groups, six rats in each group, including a control group and one group receiving each of the three TPN solutions. All animals were killed after 10 days of TPN. Body weight, pancreatic content, and enzyme levels in the pancreas were measured.

RESULTSCompared with the control group, pancreatic wet weight was lower in all TPN groups. Glucose significantly decreased the content and concentration of pancreatic protein, but amino acids did not alter the concentration of protein. The level of amylase was lower in all parenterally fed groups, with a greater decrease in the groups treated with amino acids and 30% glucose than with 50% glucose. Trypsin levels in all groups receiving TPN were markedly higher than in the control group.

CONCLUSIONTPN results in atrophy of the pancreas, but trypsin levels increase with TPN treatment. Glucose elevates the amylase level in the pancreas, while amino acids suppress pancreatic amylase. Amino acids used as a source of protein maintain normal pancreatic protein levels.

Amino Acids ; administration & dosage ; Amylases ; analysis ; Animals ; Body Water ; metabolism ; Body Weight ; Glucose ; administration & dosage ; Infusions, Intravenous ; Male ; Organ Size ; Pancreas, Exocrine ; metabolism ; Parenteral Nutrition, Total ; Proteins ; analysis ; Rats ; Rats, Sprague-Dawley ; Trypsin ; analysis

OBJECTIVETo evaluate the effect of intrajejunal nutrition on uptake of amino acid and enzyme-protein synthesis in pancreatic acinar cell and subcellular fractionation and zymogen granules in dogs with acute pancreatitis.

METHODSFifteen dogs were induced acute pancreatitis by retrograde injection of 5% sodium-taurocholate into the pancreatic duct. Radioactive tracing and electron microscope were used to evaluate the change of amino acid uptake, enzyme-protein synthesis in acinar cell, subcellular fractionation, the quantitative analysis of mean zymogen granule number and mean zymogen granule area after injection L-(3)H-phenylalanine 30, 60, 120 1nd 180 min on the 7(th) day.

RESULTSThe radioactivity of L-(3)H phenylalanine uptake by pancreatic acinar cells and incorporations of L-(3)H phenylalanine into newly synthesized enzyme-protein peaked at 60 min. In enteral nutrition (EN) group it was higher that that in parenteral nutrition (PN) group (P < 0.05), and then gradually declined. The radioactivity peaked at 60 min in zymogen granule, lysosomal-mitochondria and microsomal subcellular fractionation. The latter two decreased, bat there was no significant difference (P > 0.05). The change of the mean number and mean area of zymogen granules were not significant different between the EN group and PN group (P > 0.05).

CONCLUSIONEN or PN do not stimulate pancreatic acinar uptake amino acid and enzyme-protein synthesis in acinar cell and subcellular fractionation.

Acute Disease ; Amino Acids ; metabolism ; Animals ; Disease Models, Animal ; Dogs ; Enteral Nutrition ; Enzyme Precursors ; biosynthesis ; Female ; Male ; Pancreas, Exocrine ; metabolism ; Pancreatitis ; pathology ; physiopathology ; therapy ; Parenteral Nutrition ; Random Allocation ; Treatment Outcome

OBJECTIVETo investigate the effect of resveratrol on the apoptosis of pancreatic acinar cells in rats with severe acute pancreatitis (SAP) and explore the mechanism of such effect.

METHODSD rats with 3.5% sodium taurocholate-induced SAP were treated with resveratrol, and the serum amylase was detected with automatic biochemistry analyzer. The apoptosis of the pancreatic acinar cells in the rats was detected by TUNEL assay, and the expression of Fas and FasL genes was determined by RT-PCR and Western blotting. The pathological changes of the pancreas were observed under optical microscope.

RESULTSCompared with SAP group, the resveratrol-treated rats showed obviously decreased serum amylase and scores for pancreatic histopathological lesions. Resveratrol treatment significantly increased the apoptotic indices of pancreatic acinar cells and the levels of FasL mRNA and protein in rats with SAP.

CONCLUSIONResveratrol produces important therapeutic effect on SAP in rats by inducing pancreatic acinar cell apoptosis possibly as a result of up-regulated FasL gene expression.

Animals ; Apoptosis ; drug effects ; Fas Ligand Protein ; drug effects ; genetics ; metabolism ; Male ; Pancreas, Exocrine ; pathology ; Pancreatitis, Acute Necrotizing ; chemically induced ; drug therapy ; pathology ; RNA, Messenger ; genetics ; metabolism ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Stilbenes ; therapeutic use ; Taurocholic Acid ; Up-Regulation

Whether M3 cholinergic receptor signal transduction pathway is involved in regulation of the activation of NF-kappaB and the expression of chemokine MOB-1, MCP-lgenes in pancreatic acinar cells was investigated. Rat pancreatic acinar cells were isolated, cultured and treated with carbachol, atropine and PDTC in vitro. The MOB-1 and MCP-1 mRNA expression was detected by using RT-PCR. The activation of NF-kappaB was monitored by using electrophoretic mobility shift assay. The results showed that as compared with control group, M3 cholinergic receptor agonist (10(-3) mol/L, 10(-4) mol/L carbachol) could induce a concentration-dependent and time-dependent increase in the expression of MOB-1, MCP-1 mRNA in pancreatic acinar cells. After treatment with 10(-3) mol/L carbachol for 2 h, the expression of MOB-1, MCP-1 mRNA was strongest. The activity of NF-kappaB in pancreatic acinar cells was significantly increased (P<0.01) after treated with M3 cholinergic receptor agonist (10(-3) mol/L carbachol) in vitro for 30 min. Either M3 cholinergic receptor antagonist (10(-5) mol/L atropine) or NF-kappaB inhibitor (10(-2) mol/L PDTC) could obviously inhibit the activation of NF-kappaB and the chemokine MOB-1, MCP-1 mRNA expression induced by carbachol (P<0.05). This inhibitory effect was significantly increased by atropine plus PDTC (P<0.01). The results of these studies indicated that M3 cholinergic receptor signal transduction pathway was likely involved in regulation of the expression of chemokine MOB-1 and MCP-lgenes in pancreatic acinar cells in vitro through the activation of NF-kappaB.
Adaptor Proteins, Signal Transducing ; Carbachol ; pharmacology ; Carrier Proteins ; biosynthesis ; genetics ; Chemokine CCL2 ; biosynthesis ; genetics ; Chemokines ; biosynthesis ; genetics ; Humans ; NF-kappa B ; biosynthesis ; genetics ; Pancreas, Exocrine ; metabolism ; Pancreatitis ; etiology ; RNA, Messenger ; biosynthesis ; genetics ; Receptor, Muscarinic M3 ; agonists ; physiology ; Signal Transduction