Acute alcohol administration inhibits the refeeding response after starvation in rat skeletal muscle

A A Sneddon, M Koll, M C Wallace, J Jones, J P Miell, P J Garlick, V R Preedy

    Research output: Contribution to journalArticle

    17 Citations (Scopus)

    Abstract

    This study determined whether an acute alcohol dose could inhibit the refeeding response in starved muscle. Rats starved for 24 h were pretreated with alcohol or saline before refeeding by intragastric or intravenous infusion of enteral diet ( ENT), total parenteral nutrition (TPN), or saline. Refeeding by TPN or ENT stimulated increases in the fractional rate of protein synthesis (k(s)) in skeletal muscle. Alcohol prevented the increase in ks when refeeding occurred intragastrically (TPN or ENT) (P < 0.001) but not intravenously (TPN). Upon intragastric refeeding, alcohol inhibited the increase in both eukaryotic initiation factor 4E-binding protein-1 (4E-BP1) and p70 S6 kinase (p70(S6K)) phosphorylation in plantaris but caused only partial inhibition in soleus muscle (ENT only). When rats were refed intravenously, alcohol had no effect on the increased 4E-BP1 or p70(S6K) phosphorylation in either muscle. Plasma insulin levels were augmented by alcohol. Alcohol-related changes in plasma amino acid concentrations were similar irrespective of the route of feeding, whereas IGF-I levels showed differential changes. This is the first study to demonstrate that acute alcohol ingestion impedes the starved-to-fed response in skeletal muscle.

    Original languageEnglish
    Pages (from-to)874-882
    Number of pages9
    JournalAmerican Journal of Physiology: Endocrinology and Metabolism
    Volume284
    DOIs
    Publication statusPublished - 2003

    Keywords

    • fasting
    • myopathy
    • protein synthesis
    • ethanol
    • feeding
    • GROWTH-FACTOR-I
    • PROTEIN-SYNTHESIS
    • CHRONIC ETHANOL
    • AMINO-ACIDS
    • INSULIN
    • METABOLISM
    • MYOPATHY
    • EIF4E
    • PHOSPHORYLATION
    • MALNUTRITION

    Cite this

    Acute alcohol administration inhibits the refeeding response after starvation in rat skeletal muscle. / Sneddon, A A ; Koll, M ; Wallace, M C ; Jones, J ; Miell, J P ; Garlick, P J ; Preedy, V R .

    In: American Journal of Physiology: Endocrinology and Metabolism, Vol. 284, 2003, p. 874-882.

    Research output: Contribution to journalArticle

    Sneddon, A A ; Koll, M ; Wallace, M C ; Jones, J ; Miell, J P ; Garlick, P J ; Preedy, V R . / Acute alcohol administration inhibits the refeeding response after starvation in rat skeletal muscle. In: American Journal of Physiology: Endocrinology and Metabolism. 2003 ; Vol. 284. pp. 874-882.
    @article{8119fa2c91e54efa99ffdddf11e6ab55,
    title = "Acute alcohol administration inhibits the refeeding response after starvation in rat skeletal muscle",
    abstract = "This study determined whether an acute alcohol dose could inhibit the refeeding response in starved muscle. Rats starved for 24 h were pretreated with alcohol or saline before refeeding by intragastric or intravenous infusion of enteral diet ( ENT), total parenteral nutrition (TPN), or saline. Refeeding by TPN or ENT stimulated increases in the fractional rate of protein synthesis (k(s)) in skeletal muscle. Alcohol prevented the increase in ks when refeeding occurred intragastrically (TPN or ENT) (P < 0.001) but not intravenously (TPN). Upon intragastric refeeding, alcohol inhibited the increase in both eukaryotic initiation factor 4E-binding protein-1 (4E-BP1) and p70 S6 kinase (p70(S6K)) phosphorylation in plantaris but caused only partial inhibition in soleus muscle (ENT only). When rats were refed intravenously, alcohol had no effect on the increased 4E-BP1 or p70(S6K) phosphorylation in either muscle. Plasma insulin levels were augmented by alcohol. Alcohol-related changes in plasma amino acid concentrations were similar irrespective of the route of feeding, whereas IGF-I levels showed differential changes. This is the first study to demonstrate that acute alcohol ingestion impedes the starved-to-fed response in skeletal muscle.",
    keywords = "fasting, myopathy, protein synthesis, ethanol, feeding, GROWTH-FACTOR-I, PROTEIN-SYNTHESIS, CHRONIC ETHANOL, AMINO-ACIDS, INSULIN, METABOLISM, MYOPATHY, EIF4E, PHOSPHORYLATION, MALNUTRITION",
    author = "Sneddon, {A A} and M Koll and Wallace, {M C} and J Jones and Miell, {J P} and Garlick, {P J} and Preedy, {V R}",
    year = "2003",
    doi = "10.1152/ajpendo.00209.2002",
    language = "English",
    volume = "284",
    pages = "874--882",
    journal = "American Journal of Physiology: Endocrinology and Metabolism",
    issn = "0193-1849",
    publisher = "American Physiological Society",

    }

    TY - JOUR

    T1 - Acute alcohol administration inhibits the refeeding response after starvation in rat skeletal muscle

    AU - Sneddon, A A

    AU - Koll, M

    AU - Wallace, M C

    AU - Jones, J

    AU - Miell, J P

    AU - Garlick, P J

    AU - Preedy, V R

    PY - 2003

    Y1 - 2003

    N2 - This study determined whether an acute alcohol dose could inhibit the refeeding response in starved muscle. Rats starved for 24 h were pretreated with alcohol or saline before refeeding by intragastric or intravenous infusion of enteral diet ( ENT), total parenteral nutrition (TPN), or saline. Refeeding by TPN or ENT stimulated increases in the fractional rate of protein synthesis (k(s)) in skeletal muscle. Alcohol prevented the increase in ks when refeeding occurred intragastrically (TPN or ENT) (P < 0.001) but not intravenously (TPN). Upon intragastric refeeding, alcohol inhibited the increase in both eukaryotic initiation factor 4E-binding protein-1 (4E-BP1) and p70 S6 kinase (p70(S6K)) phosphorylation in plantaris but caused only partial inhibition in soleus muscle (ENT only). When rats were refed intravenously, alcohol had no effect on the increased 4E-BP1 or p70(S6K) phosphorylation in either muscle. Plasma insulin levels were augmented by alcohol. Alcohol-related changes in plasma amino acid concentrations were similar irrespective of the route of feeding, whereas IGF-I levels showed differential changes. This is the first study to demonstrate that acute alcohol ingestion impedes the starved-to-fed response in skeletal muscle.

    AB - This study determined whether an acute alcohol dose could inhibit the refeeding response in starved muscle. Rats starved for 24 h were pretreated with alcohol or saline before refeeding by intragastric or intravenous infusion of enteral diet ( ENT), total parenteral nutrition (TPN), or saline. Refeeding by TPN or ENT stimulated increases in the fractional rate of protein synthesis (k(s)) in skeletal muscle. Alcohol prevented the increase in ks when refeeding occurred intragastrically (TPN or ENT) (P < 0.001) but not intravenously (TPN). Upon intragastric refeeding, alcohol inhibited the increase in both eukaryotic initiation factor 4E-binding protein-1 (4E-BP1) and p70 S6 kinase (p70(S6K)) phosphorylation in plantaris but caused only partial inhibition in soleus muscle (ENT only). When rats were refed intravenously, alcohol had no effect on the increased 4E-BP1 or p70(S6K) phosphorylation in either muscle. Plasma insulin levels were augmented by alcohol. Alcohol-related changes in plasma amino acid concentrations were similar irrespective of the route of feeding, whereas IGF-I levels showed differential changes. This is the first study to demonstrate that acute alcohol ingestion impedes the starved-to-fed response in skeletal muscle.

    KW - fasting

    KW - myopathy

    KW - protein synthesis

    KW - ethanol

    KW - feeding

    KW - GROWTH-FACTOR-I

    KW - PROTEIN-SYNTHESIS

    KW - CHRONIC ETHANOL

    KW - AMINO-ACIDS

    KW - INSULIN

    KW - METABOLISM

    KW - MYOPATHY

    KW - EIF4E

    KW - PHOSPHORYLATION

    KW - MALNUTRITION

    U2 - 10.1152/ajpendo.00209.2002

    DO - 10.1152/ajpendo.00209.2002

    M3 - Article

    VL - 284

    SP - 874

    EP - 882

    JO - American Journal of Physiology: Endocrinology and Metabolism

    JF - American Journal of Physiology: Endocrinology and Metabolism

    SN - 0193-1849

    ER -