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Titolo:
Leucine suppresses acid-induced protein wasting in L6 rat muscle cells
Autore:
Bevington, A; Brown, J; Walls, J;
Indirizzi:
Leicester Gen Hosp, Dept Nephrol, Leicester LE5 4PW, Leics, England Leicester Gen Hosp Leicester Leics England LE5 4PW E5 4PW, Leics, England
Titolo Testata:
EUROPEAN JOURNAL OF CLINICAL INVESTIGATION
fascicolo: 6, volume: 31, anno: 2001,
pagine: 497 - 503
SICI:
0014-2972(200106)31:6<497:LSAPWI>2.0.ZU;2-V
Fonte:
ISI
Lingua:
ENG
Soggetto:
SKELETAL-MUSCLE; DIALYSIS PATIENTS; MESSENGER-RNAS; DEGRADATION; METABOLISM; NUTRITION; INHIBITION; MYOBLASTS; TRANSPORT; MECHANISM;
Keywords:
branched-chain amino acids; metabolic acidosis; metabolic alkalosis; proteolysis; skeletal muscle; uraemia;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
28
Recensione:
Indirizzi per estratti:
Indirizzo: Bevington, A Leicester Gen Hosp, Dept Nephrol, Gwendolen Rd, Leicester LE54PW, Leics, England Leicester Gen Hosp Gwendolen Rd Leicester Leics England LE5 4PW
Citazione:
A. Bevington et al., "Leucine suppresses acid-induced protein wasting in L6 rat muscle cells", EUR J CL IN, 31(6), 2001, pp. 497-503

Abstract

Background Metabolic acidosis induces protein wasting in skeletal muscle cells, accompanied by decreased glycolysis and compensatory increased consumption of other metabolic fuels, implying that protein wasting arises from fuel starvation and might be rectified by fuel supplements. Design To test this hypothesis, total protein and protein degradation (release of C-14-phenylalanine) were measured in L6 skeletal muscle cells cultured in Eagle's Minimum Essential Medium at pH 7.1-7.5 for 3 days with metabolic inhibitors or metabolic fuel supplements. Results Inducing metabolic fuel starvation with inhibitors (1 mmol L-1 2-deoxyglucose or 0.1 mmol L-1 KCN [potassium cyanide]) failed to stimulate protein degradation or net protein wasting under nonacidaemic conditions (pH 7.5). Conversely metabolic fuel supplements (1 mmol L-1 octanoate, pyruvateor alanine) failed to increase the protein content of the cultures at any pH tested, in spite of significant consumption of the fuels by the cells. Only leucine (1-3 mmol L-1) increased protein content and suppressed proteindegradation in opposition to the catabolic effect of acidaemia (pH 7.1). Conclusion Leucine exerts a beneficial anabolic effect on cultured skeletal muscle cells in the face of metabolic acidaemia. The failure of other metabolic fuels to do this, and of the metabolic inhibitors to exert a catabolic effect, suggests that leucine acts as a specific modulator of protein turnover and not as a nonspecific source of carbon for oxidation as a fuel.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/03/20 alle ore 00:54:42