FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2892282705> ?p ?o ?g. }

• W2892282705 endingPage "4692" @default.
• W2892282705 startingPage "4681" @default.
• W2892282705 abstract "Key points It has been suggested that leucine is primarily responsible for the increase in muscle protein synthesis after protein ingestion because leucine uniquely activates the mTOR‐p70S6K signalling cascade. We compared the effects of ingesting protein or an amount of leucine equal to that in the protein during a hyperinsulinaemic‐euglycaemic clamp (to eliminate potential confounding as a result of differences in the insulinogenic effect of protein and leucine ingestion) on muscle anabolic signalling and protein turnover in 28 women. We found that protein, but not leucine, ingestion increased muscle p‐mTOR Ser2448 and p‐p70S6K Thr389 , although only protein, and not leucine, ingestion decreased muscle p‐eIF2α Ser51 and increased muscle protein synthesis. Abstract It has been suggested that leucine is primarily responsible for the increase in muscle protein synthesis (MPS) after protein ingestion because leucine uniquely activates the mTOR‐p70S6K signalling cascade. We tested this hypothesis by measuring muscle p‐mTOR Ser2448 , p‐p70S6K Thr389 and p‐eIF2α Ser51 , as well as protein turnover (by stable isotope labelled amino acid tracer infusion in conjunction with leg arteriovenous blood and muscle tissue sampling), in 28 women who consumed either 0.45 g protein kg −1 fat‐free mass (containing 0.0513 g leucine kg −1 fat‐free mass) or a control drink ( n = 14) or 0.0513 g leucine kg −1 fat‐free mass or a control drink ( n = 14) during a hyperinsulinaemic‐euglycaemic clamp procedure (HECP). Compared to basal conditions, the HECP alone (without protein or leucine ingestion) suppressed muscle protein breakdown by ∼20% and increased p‐mTOR Ser2448 and p‐p70S6K Thr389 by >50% (all P < 0.05) but had no effect on p‐eIF2α Ser51 and MPS. Both protein and leucine ingestion further increased p‐mTOR Ser2448 and p‐p70S6K Thr389 , although only protein, and not leucine, ingestion decreased (by ∼35%) p‐eIF2α Ser51 and increased (by ∼100%) MPS (all P < 0.05). Accordingly, leg net protein balance changed from negative (loss) during basal conditions to equilibrium during the HECP alone and the HECP with concomitant leucine ingestion and to positive (gain) during the HECP with concomitant protein ingestion. These results provide new insights into the regulation of MPS by demonstrating that leucine and mTOR signalling alone are not responsible for the muscle anabolic effect of protein ingestion during physiological hyperinsulinaemia, most probably because they fail to signal to eIF2α to initiate translation and/or additional amino acids are needed to sustain translation." @default.
• W2892282705 created "2018-09-27" @default.
• W2892282705 creator A5013729922 @default.
• W2892282705 creator A5021042114 @default.
• W2892282705 creator A5028110237 @default.
• W2892282705 creator A5035073613 @default.
• W2892282705 creator A5042024378 @default.
• W2892282705 creator A5072000963 @default.
• W2892282705 creator A5074264255 @default.
• W2892282705 creator A5077263580 @default.
• W2892282705 creator A5087586661 @default.
• W2892282705 date "2018-08-29" @default.
• W2892282705 modified "2023-10-11" @default.
• W2892282705 title "The muscle anabolic effect of protein ingestion during a hyperinsulinaemic euglycaemic clamp in middle‐aged women is not caused by leucine alone" @default.
• W2892282705 cites W14752674 @default.
• W2892282705 cites W154549817 @default.
• W2892282705 cites W1772573417 @default.
• W2892282705 cites W1907574285 @default.
• W2892282705 cites W1925594358 @default.
• W2892282705 cites W1967545335 @default.
• W2892282705 cites W1972023001 @default.
• W2892282705 cites W1973854729 @default.
• W2892282705 cites W1984225039 @default.
• W2892282705 cites W2019584487 @default.
• W2892282705 cites W2024393219 @default.
• W2892282705 cites W2029296519 @default.
• W2892282705 cites W2046956654 @default.
• W2892282705 cites W2054411296 @default.
• W2892282705 cites W2058799138 @default.
• W2892282705 cites W2070254527 @default.
• W2892282705 cites W2079758889 @default.
• W2892282705 cites W2092033643 @default.
• W2892282705 cites W2097835018 @default.
• W2892282705 cites W2107671204 @default.
• W2892282705 cites W2111020389 @default.
• W2892282705 cites W2119448420 @default.
• W2892282705 cites W2121168414 @default.
• W2892282705 cites W2122074109 @default.
• W2892282705 cites W2125928541 @default.
• W2892282705 cites W2126031921 @default.
• W2892282705 cites W2126265811 @default.
• W2892282705 cites W2128583851 @default.
• W2892282705 cites W2146458354 @default.
• W2892282705 cites W2148932398 @default.
• W2892282705 cites W2152053288 @default.
• W2892282705 cites W2164925388 @default.
• W2892282705 cites W2165232899 @default.
• W2892282705 cites W2165360725 @default.
• W2892282705 cites W2166966082 @default.
• W2892282705 cites W2167013734 @default.
• W2892282705 cites W2167335342 @default.
• W2892282705 cites W2168854627 @default.
• W2892282705 cites W2285680126 @default.
• W2892282705 cites W2497214543 @default.
• W2892282705 cites W2551962319 @default.
• W2892282705 cites W2746114113 @default.
• W2892282705 cites W2783860417 @default.
• W2892282705 cites W2794300809 @default.
• W2892282705 doi "https://doi.org/10.1113/jp276504" @default.
• W2892282705 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6166086" @default.
• W2892282705 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30054913" @default.
• W2892282705 hasPublicationYear "2018" @default.
• W2892282705 type Work @default.
• W2892282705 sameAs 2892282705 @default.
• W2892282705 citedByCount "10" @default.
• W2892282705 countsByYear W28922827052020 @default.
• W2892282705 countsByYear W28922827052021 @default.
• W2892282705 countsByYear W28922827052022 @default.
• W2892282705 crossrefType "journal-article" @default.
• W2892282705 hasAuthorship W2892282705A5013729922 @default.
• W2892282705 hasAuthorship W2892282705A5021042114 @default.
• W2892282705 hasAuthorship W2892282705A5028110237 @default.
• W2892282705 hasAuthorship W2892282705A5035073613 @default.
• W2892282705 hasAuthorship W2892282705A5042024378 @default.
• W2892282705 hasAuthorship W2892282705A5072000963 @default.
• W2892282705 hasAuthorship W2892282705A5074264255 @default.
• W2892282705 hasAuthorship W2892282705A5077263580 @default.
• W2892282705 hasAuthorship W2892282705A5087586661 @default.
• W2892282705 hasBestOaLocation W28922827051 @default.
• W2892282705 hasConcept C1008401 @default.
• W2892282705 hasConcept C126322002 @default.
• W2892282705 hasConcept C134018914 @default.
• W2892282705 hasConcept C185592680 @default.
• W2892282705 hasConcept C193230392 @default.
• W2892282705 hasConcept C195580219 @default.
• W2892282705 hasConcept C2776580952 @default.
• W2892282705 hasConcept C2779572773 @default.
• W2892282705 hasConcept C2779959927 @default.
• W2892282705 hasConcept C3675279 @default.
• W2892282705 hasConcept C515207424 @default.
• W2892282705 hasConcept C55493867 @default.
• W2892282705 hasConcept C62231903 @default.
• W2892282705 hasConcept C71924100 @default.
• W2892282705 hasConcept C86803240 @default.
• W2892282705 hasConceptScore W2892282705C1008401 @default.
• W2892282705 hasConceptScore W2892282705C126322002 @default.
• W2892282705 hasConceptScore W2892282705C134018914 @default.
• W2892282705 hasConceptScore W2892282705C185592680 @default.

• next