No abstract

A 3-mo perdialytic parenteral nutrition (PDPN) regimen was tested in 26 malnourished adults receiving hemodialysis (HD). Subjects were randomly assigned to receive PDPN (n = 12) or not to receive it (n = 14). PDPN was intravenously infused three times a week during HD; each infusion was made up of 1.6 g fat/kg body wt, 0.08 g N/kg body wt, essential and nonessential amino acids, and glycyl-tyrosine. PDPN, together with a PDPN-induced increase in spontaneous eating, increased intakes from 30 +/- 8.4 kcal.kg body wt-1.d-1 (mean +/- SD) and 1 +/- 0.27 g protein.kg body wt-1.d-1 to 39 +/- 8.5 kcal.kg body wt-1.d-1 and 1.25 +/- 0.30 g protein.kg body wt-1.d-1. Compared with control subjects, PDPN patients were characterized by increases in body weight (P less than 0.01), arm-muscle circumference (P less than 0.02), serum transthyretin and albumin concentrations (P less than 0.05), interdialytic creatinine appearance (P less than 0.01), skin-test reactivity (P less than 0.02), plasma leucine (P less than 0.05) without modifications of other amino acids, and plasma apolipoprotein A-I (P less than 0.01) without significant changes in apolipoprotein B, cholesterol, triglyceride, and phospholipid concentrations. Thus, PDPN appeared to be effective and safe with respect to plasma lipids.

The Hitachi L-8500A is a newly available apparatus for amino acid (AA)analysis that allows automatic on-line mixing of the ninhydrin reagent. The within-run precision (human plasma pools at three different concentrations) showed CVs <3.8% except for the lowest concentration of citrulline (4.4%), Tyr (4.5%), and α-aminobutyric acid (7.6%), and for the intermediate concentration of Asp (8.7%). Between-run precision (CV) was <3.1% for 17 AAs and <8.0% for 24 of 25 AAs (CV Asp = 12.0%). For retention times, within-run precision was <0.4% and between-run precision <1.8%. Excellent relations were found between the results from the Hitachi L-8500A and the widely used Beckman 6300 analyzer (0.929≤ r ≤0.999). The detection was still linear at 5 μmol/L except for Pro and hydroxyproline (20 μmol/L). The upper limit was at least 2500 μmol/L for 13 AAs and at least 1000 μmol/L for 27 of 29 AAs (anserine = 500, Val = 600 μmol/L). Values from 100 human plasma samples agreed with previously published data. We conclude that the results obtained with the Hitachi L-8500A are satisfactory when compared with those of other AA analyzers utilizing the same method. Furthermore, the Hitachi L-8500A displays several advantages including programming flexibility, microsample capacity, low noise plotting, ammonia filtering, and manual repacking of the analytical column.

Ornithine alpha-ketoglutarate (OKG) has been useful as an adjuvant of enteral and parenteral nutrition. However, its metabolism and mechanism of action remain unclear although it is known that alpha-ketoglutarate (alpha KG) and ornithine (ORN) follow, in part, common metabolic pathways. Six fasting healthy male subjects underwent three separate oral load tests: (i) they received 10 g of OKG (i.e., 3.6 g of alpha KG and 6.4 g of ORN); (ii) 6.4 g of ORN as ornithine hydrochloride, and (iii) 3.6 g of alpha KG as calcium alpha-ketoglutarate. Blood was drawn 15 times over a five-hour period for measurements of plasma amino acids, alpha KG, insulin, and glucagon. After OKG and ORN administration, plasma ORN peaked at 60-75 min (494 +/- 91 and 541 +/- 85 mumol/L). The increase in plasma alpha KG was very small. OKG, alpha KG, and ORN all increased glutamate concentrations at 60 min (mean: +43%, +68%, +68%, respectively, p less than 0.05 compared to basal values). However, only OKG increased proline and arginine levels at 60 min (mean: +35%, p less than 0.01 and mean: +41%, p less than 0.05). Furthermore, glutamate, proline, and arginine concentrations correlated linearly with ornithine levels at 60 min. Finally, OKG increased insulinemia and glucagonemia (mean: +24% at 15 min, p less than 0.05 and +30% at 60 min, p less than 0.01, respectively). These data provide evidence that the combination of ORN and alpha KG modifies amino acid metabolism in a way which is not observed when they are administered separately. In addition, the OKG-mediated increase in insulin levels probably does not appear to result from a direct action of ORN on pancreatic secretion.