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Muscle protein synthesis and breakdown and amino acid transport were measured in 7 healthy young (30 +/- 2 yr) and 8 healthy elderly (71 +/- 2 yr) volunteers in the postabsorptive state and during the oral administration of an amino acid mixture with L-[ring-(2)H(5)]phenylalanine infusion, femoral artery and vein catheterization, and muscle biopsies. Phenylalanine first-pass splanchnic extraction was measured by adding L-[ring-(13)C(6)]phenylalanine to the mixture. In the postabsorptive state, no differences in muscle amino acid kinetics were detected between young and elderly volunteers. Phenylalanine first-pass splanchnic extraction was significantly higher in the elderly (P < 0. 003) during ingestion of amino acids, but the delivery to the leg increased to the same extent in both groups. Phenylalanine transport into the muscle, muscle protein synthesis, and net balance increased significantly (P < 0.01) and similarly in both the young and the elderly. We conclude that, despite an increased splanchnic first-pass extraction, muscle protein anabolism can be stimulated by oral amino acids in the elderly as well as in the young.

The effects of combined hyperglycemia-hyperinsulinemia on whole body, splanchnic, and leg fatty acid metabolism were determined in five volunteers. Catheters were placed in a femoral artery and vein and a hepatic vein. U-13C-labeled fatty acids were infused, once in the basal state and, on a different occasion, during infusion of dextrose (clamp; arterial glucose 8.8 +/- 0.5 mmol/l). Lipids and heparin were infused together with the dextrose to maintain plasma fatty acid concentrations at basal levels. Fatty acid availability in plasma and fatty acid uptake across the splanchnic region and the leg were similar during the basal and clamp experiments. Dextrose infusion decreased fatty acid oxidation by 51.8% (whole body), 47.4% (splanchnic), and 64.3% (leg). Similarly, the percent fatty acid uptake oxidized decreased at the whole body level (53 to 29%), across the splanchnic region (30 to 13%), and in the leg (48 to 22%) during the clamp. We conclude that, in healthy men, combined hyperglycemia-hyperinsulinemia inhibits fatty acid oxidation to a similar extent at the whole body level, across the leg, and across the splanchnic region, even when fatty acid availability is constant.

The effect of hyperglycemia ( approximately 8 mmol/l) on splanchnic fatty acid oxidation and triacylglycerol (TG) secretion rates was investigated in five healthy men. U-13C-labeled fatty acids were infused to estimate fatty acid kinetics and oxidation across the splanchnic region, and in vivo labeled very low density lipoprotein (VLDL)-TG was infused to estimate TG secretion rate. Plasma fatty acid carbon enrichment and concentration were maintained constant by infusion of lipids and heparin in the hyperglycemia experiments. Fatty acid uptake by the splanchnic region was 1.4 +/- 0.2 and 2.2 +/- 0.9 micromol. kg-1. min-1 in the basal and clamp experiments, respectively, whereas fatty acid oxidation decreased from 0.4 +/- 0. 04 to 0.2 +/- 0.05 micromol. kg-1. min-1 (P < 0.05). Hepatic TG secretion increased from 0.35 +/- 0.07 micromol. kg-1. min-1 in the basal state to 0.53 +/- 0.11 micromol. kg-1. min-1 after 15 h of hyperglycemia (P < 0.05). Similarly, plasma VLDL-TG concentration increased from 0.28 +/- 0.06 to 0.43 +/- 0.05 mmol/l during the clamp (P < 0.05). In summary, hyperglycemia attenuates fatty acid oxidation in the splanchnic region in human volunteers, even when fatty acid availability is constant. This adaptation results in a significant increase in the VLDL-TG secretion rate and concentration in plasma.