Effect of dietary level of protein and fiber on the productive performance and health status of piglets.

To study the interaction between the levels of protein and fiber on the productive performance and health status of piglets, ninety-six 35-d-old piglets (9.11 +/- 0.60 kg of BW) were placed in 32 pens of 3 animals each and allotted to 4 dietary treatments for 21 d. The 4 diets were based on rice, dairy products, and soybean meal in a 2 x 2 factorial arrangement of treatments, with 2 levels of CP (15.4 vs. 19.4%, as-fed basis) and 2 levels of dietary fiber [DF; low fiber (LF) 5.3% NDF and high fiber (HF) 7.15% NDF, as-fed basis]. The HF diet was developed by supplementing the basal diet with 40 g/kg of wheat bran and 20 g/kg of sugar beet pulp. Animal performance was obtained weekly with samples of feces collected for microbiology on the first and the last experimental day and scored from 1 (liquid) to 4 (hard). On the last day, 1 pig from each pen was sampled for blood analyses of the acute-phase protein, major acute-phase protein of pigs (PigMap) and subsequently killed to register the digestive tract weight (including contents) and colon histology. Pigs fed the HF diets had greater ADG (390 vs. 457 g; P < or = 0.001) and large intestine weight (4.4 vs. 5.4% of BW; P < or = 0.05). This coincided with a greater (P < or = 0.05) short-chain fatty acid concentration (especially of acetic and butyric acids), a decrease in Escherichia coli counts (7.77 vs. 6.86 log of cfu/g of feces, P < or = 0.05), and an increase in the ratio of lactobacilli:enterobacteria (0.76 vs. 1.37, P < or = 0.05). However, CP level did not modify the productive performance, but 20% CP increased P < or = 0.05) the relative weight (% of BW) of the small (6.5 vs. 7.7) and large intestine (3.8 vs. 4.3). In the large bowel, the 20% CP diet increased the numbers of goblet cells (4.6 vs. 5.4/100 microm; P < or = 0.05) and reduced the numbers of intraepithelial lymphocytes (1.8 vs. 1.3/100 microm; P < or = 0.05). In relation to health status, increasing DF was dependent of the dietary CP content. Supplementing the 16% CP diet with DF reduced the fecal score and increased the antibiotics interventions, whereas the opposite was the case in the 20% CP diet. Pigs fed the 20% CP diet showed decreased (P < or = 0.05) PigMap concentrations than pigs fed 16% CP diets. As a whole, CP showed major effects on the gastrointestinal weight and gut barrier integrity, whereas DF increased the productive performance and promoted major changes in the microbial colonization and fermentation variables.

Histochemical study of acute and chronic intraperitoneal nicotine effects on several glycolytic and Krebs cycle dehydrogenase activities in the frontoparietal cortex and subcortical nuclei of the rat brain.

The effects of nicotine on the activity of different dehydrogenases in frontoparietal regions and subcortical nuclei of the rat brain have been studied using histochemical methods. Nicotine sulphate was intraperitoneally administered in acute (4 mg/kg/day x 3 days) or chronic (ALZET osmotic pump providing 2 mg/kg/day x 15 days) doses. The enzymes analyzed were glyceraldehyde-3-phosphate, lactate, malate and succinate dehydrogenases (gly3PDH, LDH, MDH, and SDH, respectively). The results demonstrate that chronic as well as acute administration of nicotine produced strong increases in all these enzymatic activities in the superior layers (I, II and III) of the frontoparietal cortex (cingulate, motor and somatosensory regions); but high increases were not seen in the deeper layers of the cortex or in the subcortical nuclei (substantia nigra, caudate-putamen, nucleus accumbens or nucleus basalis magnocellularis). These hyperactivities were produced in brain regions with normally low enzymatic activity (cortex), but not in those with great intensity (subcortical nuclei). The results are in rough agreement with previous reports on nicotine-induced increases in glucose utilization, gly3PDH genic expression and neuronal hyperactivity in the brain cortex; but significant discrepancies between the cortical enzymatic maps and those obtained both in these studies and others on nicotine(N)-receptor localization have been appreciated. The results support the hypothesis that nicotinic cholinergic drugs can have metabolic, long-lasting stimulant effects on cortical neurons at specific points (probably layer III pyramidal cells and structures with alpha7-N-receptors) of the cortical circuits that could be of great interest in improving altered cognitive functions that are present in Alzheimer disease, as well as in other less severe mental disturbances. Mitochondrial hyperfunction should also be evaluated as a possible side-effect (as an oxidative stress inductor) of these kinds of drugs.