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Effect of cortisol on liver, gluconeogenesis
  1. #1
    Susan Guest

    Default Effect of cortisol on liver, gluconeogenesis

    x-no-archive: yes

    Am J Physiol Endocrinol Metab 258: E569-E575, 1990;
    0193-1849/90 $5.00

    AJP - Endocrinology and Metabolism, Vol 258, Issue 4 E569-E575,
    Copyright © 1990 by American Physiological Society

    ARTICLES

    Glucagon-cortisol interactions on glucose turnover and lactate
    gluconeogenesis in normal humans

    L. Lecavalier, G. Bolli and J. Gerich
    Department of Medicine, University of Pittsburgh School of Medicine,
    Pennsylvania 15261.

    To determine the mechanism for cortisol enhancement of
    glucagon-stimulated overall hepatic glucose output (OHGO), we employed
    the glucose-insulin clamp technique with infusions of [6-3H]glucose and
    [U-14C]lactate and measured OHGO, glucose utilization, and the turnover
    and incorporation of lactate in plasma glucose in normal volunteers
    under four experimental conditions: 1) normoglucagonemia (approximately
    150 pg/ml)- normocortisolemia (approximately 14 micrograms/dl); 2)
    isolated hyperglucagonemia (approximately 550 pg/ml); 3) isolated
    hypercortisolemia (approximately 32 micrograms/dl); and 4) combined
    hyperglucagonemia-hypercortisolemia. Isolated hyperglucagonemia caused
    initial increases in OHGO and lactate gluconeogenesis, which were
    maximal at 1 h (23.9 +/- 1 and 2.7 +/- 0.4 mumol.kg-1.min-1,
    respectively) but remained significantly above values in control
    experiments through 5 h (10.3 +/- 0.7 vs. 8.2 +/- 1.1, P less than 0.03;
    2.2 +/- 0.4 vs. 1.2 +/- 0.3, mumol.kg-1.min-1, P less than 0.04,
    respectively). Hypercortisolemia has no effect on OHGO but increased
    lactate gluconeogenesis after 3 h. Superimposition of hypercortisolemia
    on hyperglucagonemia did not further increase OHGO (11.1 +/- 0.7 vs.
    10.3 +/- 0.7 mumol.kg-1.min-1, P = NS) but augmented lactate
    gluconeogenesis additively (isolated hyperglucagonemia = 0.96, isolated
    hypercortisolemia = 0.98; combined = 2.02 mumol.kg-1.min-1). Neither
    glucagon nor cortisol affected lactate turnover or glucose utilization.
    We conclude that glucagon has a persistent effect on OHGO largely
    accounted for by increased gluconeogenesis.

    Cortisol augments glucagon-stimulated gluconeogenesis in an additive
    manner best explained by changes in gluconeogenic enzymes rather than in
    substrate availability.
    ************************************************** ***********************
    Finally, the fact that cortisol increased gluconeogenesis without
    affecting glucose utilization suggests that the liver is more sensitive
    to the diabetogenic effects of cortisol than are peripheral tissues.
    ************************************************** ************************

  2. #2
    Susan Guest

    Default Re: Effect of cortisol on liver, gluconeogenesis

    x-no-archive: yes

    Am J Physiol Endocrinol Metab 286: E102-E110, 2004. First published
    September 9, 2003; doi:10.1152/ajpendo.00566.2002

    Impaired basal glucose effectiveness but unaltered fasting glucose
    release and gluconeogenesis during short-term hypercortisolemia in
    healthy subjects

    Michael F. Nielsen,1,3 Andrea Caumo,4 Visvanathan Chandramouli,6 William
    C. Schumann,6 Claudio Cobelli,5 Bernard R. Landau,6 Hendrik Vilstrup,2
    Robert A. Rizza,7 and Ole Schmitz1
    1Department of Endocrinology, Aarhus Kommunehospital and Department of
    Clinical Pharmacology, University of Aarhus, 2Department of Medicine V,
    Aarhus University Hospital, and 3Department of Surgical Gastroenterology
    L, Aarhus Kommunehospital, DK-8000 Aarhus, Denmark; 4Metabolism and
    Nutrition Unit, San Raffaele Scientific Institute, 20132 Milan, and
    5Department of Electronics and Informatics University of Padova, 35128
    Padua, Italy; 6Department of Medicine, Case Western Reserve University
    School of Medicine, Cleveland, Ohio 44106; and 7Endocrine Research Unit,
    Mayo Clinic, Rochester, Minnesota 55905

    Submitted 23 December 2002 ; accepted in final form 8 September 2003

    Excess cortisol has been demonstrated to impair hepatic and extrahepatic
    insulin action. To determine whether glucose effectiveness and, in terms
    of endogenous glucose release (EGR), gluconeogenesis, also are altered
    by hypercortisolemia, eight healthy subjects were studied after
    overnight infusion with hydrocortisone or saline. Glucose effectiveness
    was assessed by a combined somatostatin and insulin infusion protocol to
    maintain insulin concentration at basal level in the presence of
    prandial glucose infusions. Despite elevated insulin concentrations (P <
    0.05), hypercortisolemia resulted in higher glucose (P < 0.05) and free
    fatty acid concentrations (P < 0.05). Furthermore, basal insulin
    concentrations were higher during hydrocortisone than during saline
    infusion (P < 0.01), indicating the presence of steroid-induced insulin
    resistance. Postabsorptive glucose production (P = 0.64) and the
    fractional contribution of gluconeogenesis to EGR (P = 0.33) did not
    differ on the two study days. During the prandial glucose infusion, the
    integrated glycemic response above baseline was higher in the presence
    of hydrocortisone than during saline infusion (P < 0.05), implying a
    decrease in net glucose effectiveness (4.42 ± 0.52 vs. 6.65 ± 0.83
    ml·kg-1·min-1; P < 0.05). To determine whether this defect is
    attributable to an impaired ability of glucose to suppress glucose
    production, to stimulate its own uptake, or both, glucose turnover and
    "hot" (labeled) indexes of glucose effectiveness (GE) were calculated.
    Hepatic GE was lower during cortisol than during saline infusion (2.39 ±
    0.24 vs. 3.82 ± 0.51 ml·kg-1·min-1; P < 0.05), indicating a defect in
    the ability of glucose to restrain its own production. In addition, in
    the presence of excess cortisol, glucose disappearance was inappropriate
    for the prevailing glucose concentration, implying a decrease in glucose
    clearance (P < 0.05). The decrease in glucose clearance was confirmed by
    the higher increment in [3-3H]glucose during hydrocortisone than during
    saline infusion (P < 0.05), despite the administration of identical
    tracer infusion rates. In conclusion, short-term hypercortisolemia in
    healthy individuals with normal -cell function decreases insulin action
    but does not alter rates of EGR and gluconeogenesis. In addition,
    cortisol impairs the ability of glucose to suppress its own production,
    which due to accumulation of glucose in the glucose space results in
    impaired peripheral glucose clearance. These results suggest that
    cortisol excess impairs glucose tolerance by decreasing both insulin
    action and glucose effectiveness.

    insulin action




    On 8/22/2010 12:57 PM, Susan wrote:
    > x-no-archive: yes
    >
    > Am J Physiol Endocrinol Metab 258: E569-E575, 1990;
    > 0193-1849/90 $5.00
    >
    > AJP - Endocrinology and Metabolism, Vol 258, Issue 4 E569-E575,
    > Copyright © 1990 by American Physiological Society
    >
    > ARTICLES
    >
    > Glucagon-cortisol interactions on glucose turnover and lactate
    > gluconeogenesis in normal humans
    >
    > L. Lecavalier, G. Bolli and J. Gerich
    > Department of Medicine, University of Pittsburgh School of Medicine,
    > Pennsylvania 15261.
    >
    > To determine the mechanism for cortisol enhancement of
    > glucagon-stimulated overall hepatic glucose output (OHGO), we employed
    > the glucose-insulin clamp technique with infusions of [6-3H]glucose and
    > [U-14C]lactate and measured OHGO, glucose utilization, and the turnover
    > and incorporation of lactate in plasma glucose in normal volunteers
    > under four experimental conditions: 1) normoglucagonemia (approximately
    > 150 pg/ml)- normocortisolemia (approximately 14 micrograms/dl); 2)
    > isolated hyperglucagonemia (approximately 550 pg/ml); 3) isolated
    > hypercortisolemia (approximately 32 micrograms/dl); and 4) combined
    > hyperglucagonemia-hypercortisolemia. Isolated hyperglucagonemia caused
    > initial increases in OHGO and lactate gluconeogenesis, which were
    > maximal at 1 h (23.9 +/- 1 and 2.7 +/- 0.4 mumol.kg-1.min-1,
    > respectively) but remained significantly above values in control
    > experiments through 5 h (10.3 +/- 0.7 vs. 8.2 +/- 1.1, P less than 0.03;
    > 2.2 +/- 0.4 vs. 1.2 +/- 0.3, mumol.kg-1.min-1, P less than 0.04,
    > respectively). Hypercortisolemia has no effect on OHGO but increased
    > lactate gluconeogenesis after 3 h. Superimposition of hypercortisolemia
    > on hyperglucagonemia did not further increase OHGO (11.1 +/- 0.7 vs.
    > 10.3 +/- 0.7 mumol.kg-1.min-1, P = NS) but augmented lactate
    > gluconeogenesis additively (isolated hyperglucagonemia = 0.96, isolated
    > hypercortisolemia = 0.98; combined = 2.02 mumol.kg-1.min-1). Neither
    > glucagon nor cortisol affected lactate turnover or glucose utilization.
    > We conclude that glucagon has a persistent effect on OHGO largely
    > accounted for by increased gluconeogenesis.
    >
    > Cortisol augments glucagon-stimulated gluconeogenesis in an additive
    > manner best explained by changes in gluconeogenic enzymes rather than in
    > substrate availability.
    > ************************************************** ***********************
    > Finally, the fact that cortisol increased gluconeogenesis without
    > affecting glucose utilization suggests that the liver is more sensitive
    > to the diabetogenic effects of cortisol than are peripheral tissues.
    > ************************************************** ************************



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