No abstract

This study was conducted to determine the effect of zinc level and source on growth performance, tissue Zn concentrations, intracellular distribution of Zn, and immune response in weanling pigs. Ninety-six 3-wk-old crossbred weanling pigs (BW = 6.45 +/- 0.17 kg) were assigned to one of six dietary treatments (four pigs per pen, four replicates per treatment) based on weight and litter origin. Treatments consisted of the following: 1) a corn-soybean meal-whey diet (1.2% lysine) with a basal level of 80 ppm of supplemental Zn from ZnSO4 (control; contained 104 ppm total Zn); 2) control + 80 ppm added Zn from ZnSO4; 3) control + 80 ppm added Zn from Zn methionine (ZnMet); 4) control + 80 ppm added Zn from Zn lysine (ZnLys); 5) control + 40 ppm added Zn from ZnMet and 40 ppm added Zn from ZnLys (ZnML); and 6) control + 160 ppm added Zn from ZnSO4. Zinc supplementation of the control diet had no effect on ADG or ADFI. Gain efficiency was less (P < 0.05) for pigs fed 80 ppm of Zn from ZnSO4 than for control pigs and pigs fed 160 ppm of Zn from ZnSO4. Organ weights, Zn concentration, and intracellular distribution of Zn in the liver, pancreas, and spleen were not affected (P = 0.12) by Zn level or source. Skin thickness response to phytohemagglutinin (PHA) was not affected (P = 0.53) by dietary treatment. Lymphocyte proliferation in response to PHA was greater (P < 0.05) in pigs fed ZnLys than in pigs fed the control diet or the ZnML diet; however, when pokeweed mitogen was used, lymphocyte proliferation was greatest (P < 0.05) in pigs fed the ZnMet diet than pigs fed the control, ZnLys, ZnML, or 160 ppm ZnSO4 diets. Antibody response to sheep red blood cells was not affected by dietary treatments. Supplementation of 80 ppm of Zn from ZnSO4 or ZnMet and 160 ppm of Zn from ZnSO4 decreased (P < 0.05) the antibody response to ovalbumin on d 7 compared with control pigs, but not on d 14. Phagocytic capability of peritoneal exudate cells was increased (P < 0.05) when 160 ppm of Zn from ZnSO4 was supplemented to the diet. The number of red blood cells ingested per phagocytic cell was increased (P < 0.05) in pigs fed the diet supplemented with a combination of ZnMet and ZnLys and the diet with 160 ppm of Zn from ZnSO4. Results suggest that the level of Zn recommended by NRC for weanling pigs was sufficient for optimal growth performance and immune responses, although macrophage function may be enhanced at greater levels of Zn. Source of Zn did not alter these measurements.

Some products of the sorbitol metabolic pathway of glucose were extracted from peripheral nerves and spinal cords of rats, identified, and measured. Within a few days after a diabetic state was induced with streptozotocin, glucose, sorbitol, and fructose in nerve and cord had risen sharply as blood glucose increased. These levels were partially controlled when the blood sugar was restricted by insulin, but they increased rapidly when the insulin was withheld. Withdrawal of treatment resulted in a much greater rise of the fructose in the nervous system in animals that had been diabetic for six weeks before institution of treatment with insulin than in animals treated from induction. When phen-formin was used as a controlling agent in place of insulin, accumulation of glucose and fructose in the nervous system was enhanced, whereas fructose was found to decrease when tolbutamide was used. Earlier workers have shown that the sorbitol pathway seems to be associated with the Schwann cell and that dysfunction of this cell leads to segmental demyelination. We find that accumulation in nerves of the products of the sorbitol pathway may be minimized when blood sugar is controlled; since we have evidence that in human beings with diabetes good control improves the state of myelination of already damaged nerves, it is postulated that herein lies the mechanism whereby control of diabetes is likely to lead to a reduction in the incidence of nerve damage.

Two cases of lactic acidosis are described in which the time sequence of events made it certain that phenformin was the precipitating cause. In one patient the condition arose because of self administration of an overdose; in the other, phenformin had been administered to a patient on maintenance dialysis. After recovery, and in the absence of phenformin therapy the second patient was able to clear an intravenous lactate load at a rate similar to that observed in other patients on Chronic dialysis.-A review of the literature re-emphasizes the possible danger of phenformin in the presence of diminished renal or hepatic function, which should be shown to be normal before starting the drug and assessed periodically during therapy.