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document
Differential effects of amino acid and ketoacid on protein metabolism in humans . We examined the effects of insulin , amino acid ( AA ) , and branched-chain ketoacid ( KA ) availability on leucine kinetics in eight healthy volunteers ( age = 22 +/- 2 y , body mass index = 24 +/- 1 kg ) by using the euglycemic insulin clamp and [ 1-14C ] leucine turnover techniques . Four experimental conditions were studied : study I , hyperinsulinemia ; study II , hyperinsulinemia with maintenance of basal plasma AA and branched-chain KA concentrations ; study III , hyperinsulinemia with hyperaminoacidemia and basal plasma branched-chain KA concentrations ; and study IV , hyperinsulinemia plus basal plasma AA concentrations and elevated branched-chain KA levels . Basal endogenous leucine flux ( ELF ) averaged 1.20 +/- 0.05 ( mumol.kg-1.min-1 , mean +/- SE ) ; basal leucine oxidation ( LOX ) was 0.25 +/- 0.01 ; and basal non-oxidative leucine disposal ( NOLD ) was 0.95 +/- 0.04 . ELF significantly decreased in study I ( 0.77 +/- 0.06 mumol.kg-1.min-1 , P < 0.01 versus basal ) . When plasma AA and branched-chain KA were either maintained at their basal levels ( study II ) or increased above baseline values ( studies III and IV ) , ELF declined further ( 0.64 +/- 0.05 , 0.66 +/- 0.02 , and 0.66 +/- 0.03 mumol.kg-1.min-1 , respectively ; all Ps < 0.01 versus basal and P < 0.01 versus study I ) . LOX declined in study I ( 0.12 +/- 0.02 mumol.kg-1.min-1 , P < 0.01 versus basal ) but increased significantly in studies II , III , and IV ( 0.31 +/- 0.04 , 0.37 +/- 0.03 , and 0.40 +/- 0.03 mumol.kg-1.min-1 , respectively , all Ps < 0.01 versus basal , P < 0.05 study IV versus study II , and P < 0.05 study III versus study II ) . NOLD declined in study I ( 0.65 +/- 0.05 mumol/kg.min , P < 0.01 versus basal ) , whereas neither the maintenance of basal plasma AA/branched-chain KA levels ( study II ; 0.89 +/- 0.2 mumol.kg-1.min-1 ) nor the elevation of plasma branched-chain KA concentration ( study IV ; 0.96 +/- 0.1 mumol.kg-1.min-1 ) increased NOLD above baseline level . A stimulation of NOLD was observed only when plasma AA levels were increased ( study III ; 1.23 +/- 0.03 mumol/kg.min , P < 0.01 versus basal ) . In conclusion , the present data do not support the concept of a direct anabolic action of ketoanalogs but do provide additional evidence for the pivotal role of AA availability in the stimulation of whole-body protein synthesis .
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Intervention_Other
euglycemic insulin clamp
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Intervention_Physical
and [ 1-14C ]
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Intervention_Other
leucine turnover
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Intervention_Physical
techniques
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Outcome_Physical
endogenous leucine flux ( ELF )
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Outcome_Physical
leucine oxidation ( LOX )
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Outcome_Physical
non-oxidative leucine disposal ( NOLD )
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Outcome_Physical
ELF
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Outcome_Physical
LOX
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Outcome_Physical
NOLD
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Outcome_Physical
NOLD
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Outcome_Physical
NOLD
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Participant_Condition
healthy volunteers
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Participant_Age
age = 22 +/- 2 y
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Participant_Condition
body mass index = 24 +/- 1 kg