Protein and energy substrate metabolism in AIDS patients

The objective of this study was to investigate protein and glucose metabolism in ambulatory, asymptomatic acquired immunodeficiency syndrome (AIDS) patients. Nine asymptomatic AIDS patients were compared against 13 controls. We measured whole-body protein synthesis (PSRM), breakdown (PBRM), and the...

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Veröffentlicht in:Metabolism, clinical and experimental clinical and experimental, 1990-08, Vol.39 (8), p.876-881
Hauptverfasser: Stein, T.P., Nutinsky, C., Condoluci, D., Schluter, M.D., Leskiw, M.J.
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Sprache:eng
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Zusammenfassung:The objective of this study was to investigate protein and glucose metabolism in ambulatory, asymptomatic acquired immunodeficiency syndrome (AIDS) patients. Nine asymptomatic AIDS patients were compared against 13 controls. We measured whole-body protein synthesis (PSRM), breakdown (PBRM), and the fractional fibrinogen synthesis rate with 15N glycine, glucose cycling from the difference between the glucose appearance rates as measured with 2-d (Ra 2-d)- and 6,6-d 2 (Ra 6,6-d)-labeled glucose. All of these parameters are increased with hypermetabolism and decreased with undernutrition. In addition, we also determined the plasma aminogram. The principal findings were (1) whole-body protein synthesis and breakdown and the fibrinogen fractional synthesis rate were significantly lower in the AIDS patients; (2) glucose cycling was markedly lower in the AIDS patients, and most of this effect was due to a decrease in Ra 2-d; there was no difference in the endogenous glucose production rate, Ra 6,6d; and (3) the plasma aminogram showed decreased total amino acids and a reduced ratio of essential to nonessential amino acids in the AIDS group. We concluded that the AIDS patients showed a starvation-type response. While the depressed protein synthesis and energy substrate cycling are not likely to be the primary cause of immunodeficiency, they may represent an important facilitating factors contributing to the decreased ability of the patient to respond effectively to opportunistic infections.
ISSN:0026-0495
1532-8600
DOI:10.1016/0026-0495(90)90136-Z