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Metabolism

One Week’s Treatment With the Long-Acting Glucagon-Like Peptide 1 Derivative Liraglutide (NN2211) Markedly Improves 24-h Glycemia and α- and β-Cell Function and Reduces Endogenous Glucose Release in Patients with Type 2 Diabetes

  1. Kristine B. Degn1,
  2. Claus B. Juhl1,
  3. Jeppe Sturis2,
  4. Grethe Jakobsen2,
  5. Birgitte Brock1,
  6. Visvanathan Chandramouli3,
  7. Joergen Rungby1,
  8. Bernard R. Landau3 and
  9. Ole Schmitz1
  1. 1Department of Endocrinology (M & C), University Hospital of Aarhus, and Department of Clinical Pharmacology, University of Aarhus, Aarhus, Denmark
  2. 2Novo Nordisk A/S, Bagsværd, Denmark
  3. 3Case Western Reserve University School of Medicine, Cleveland, Ohio
  1. Address correspondencereprint requests to Ole Schmitz, MD, Department of Medicine M (Endocrinology & Diabetes), University Hospital of Aarhus, AKH, Nørrebrogade 42-44 DK-8000 Aarhus C, Denmark. E-mail: ole.schmitz{at}iekf.au.dk
Diabetes 2004 May; 53(5): 1187-1194. https://doi.org/10.2337/diabetes.53.5.1187
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  • FIG. 1.
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    FIG. 1.

    Flow sheet illustrating the procedures on study day 9. See text for details.

  • FIG. 2.
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    FIG. 2.

    Twenty-four-hour profiles of plasma glucose (A), serum FFAs (B), serum insulin (C), and plasma glucagon (D) (means ± SEM), day 8. ○, placebo; •, liraglutide; □, meals. (Statistical details are listed in Table 1.)

  • FIG. 3.
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    FIG. 3.

    Fasting EGR, GNG, and GLY, day 9. Data are means ± SEM. □, placebo; ▪, liraglutide; *P < 0.05, liraglutide vs. placebo.

  • FIG. 4.
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    FIG. 4.

    Plasma glucose (A) and serum insulin (B) concentrations during an intravenous glucose bolus, hyperglycemic clamp, and arginine stimultion test, day 9. ○, placebo; •, liraglutide, ▿, glucose bolus (25 g); ⊡, arginine bolus (5 g). Plasma glucagon (C) is depicted from 1105. Steady state of hyperglycemic clamp was in the interval 1045–1115. The insert in the middle panel is a blow-up of the first-phase insulin response. Data are means ± SEM. (Statistical details are listed in Table 2.)

  • FIG. 5.
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    FIG. 5.

    Concentration profiles of liraglutide. Dosing time was 0730. Gray lines indicate individual concentration profiles; black line indicates mean ± SEM.

Tables

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  • TABLE 1

    Twenty-four-hour profiles and fasting values

    LiraglutidePlaceboP
    Fasting values
     Plasma glucose (mmol/l)8.06 ± 0.529.39 ± 0.760.078
     Plasma glucose day 9 (mmol/l)7.56 ± 0.429.20 ± 0.780.025
     FFA (mmol/l)0.52 ± 0.030.51 ± 0.030.536
     Insulin (pmol/l)95.6 ± 15.187.2 ± 17.90.513
     ISR (nmol/h)17.7 ± 2.016.1 ± 2.10.206
     Proinsulin/insulin ratio0.17 ± 0.040.27 ± 0.050.009
     Glucagon (pg/ml)92.8 ± 7.294.5 ± 5.60.586
    24-h total AUCs
     Plasma glucose (mmol · l−1 · h)187.5 ± 14.0232.3 ± 21.90.014
     FFA (mmol · l−1 · h)8.54 ± 0.518.65 ± 0.680.876
     Insulin (pmol · l−1 · h)3,854 ± 5814,154 ± 8810.375
     ISR (nmol)566.1 ± 55.1561.6 ± 72.60.982
     Glucagon (pg · ml−1 · h)2,179 ± 1182,371 ± 1350.037
    Postprandial total AUCs
     Plasma glucose 8–12 h (mmol · l−1 · h)38.66 ± 3.5247.51 ± 3.950.010
     Plasma glucose 12–16 h (mmol · l−1 · h)32.52 ± 2.9241.89 ± 4.540.017
     Plasma glucose 18–22 h (mmol · l−1 · h)33.76 ± 2.5041.10 ± 3.940.016
     Insulin 8–12 h (pmol · l−1 · h)999 ± 1731,056 ± 2530.512
     Insulin 12–16 h (pmol · l−1 · h)723 ± 107808 ± 1620.312
     Insulin 18–22 h (pmol · l−1 · h)1,017 ± 1601,117 ± 2210.392
     Proinsulin/insulin ratio 8–12 h0.12 ± 0.030.19 ± 0.040.008
     Glucagon 8–12 h (pg · ml−1 · h)383.0 ± 22.8413.4 ± 25.60.080
     Glucagon 12–16 h (pg · ml−1 · h)362.6 ± 18.6374.2 ± 19.50.384
     Glucagon 18–22 h (pg · ml−1 · h)397.3 ± 23.9470.1 ± 35.20.009
    • Data are means ± SEM. Twenty-four-hour AUCs were calculated from samples obtained from 0800 to 0800. Fasting values were calculated from samples taken at 0730 and 0800 on days 8 and 9.

  • TABLE 2

    Islet cell function tests, insulin sensitivity, and disposition index

    LiraglutidePlaceboP
    Intravenous glucose tolerance test
     Insulin total AUC 9.15–9.32 h (pmol · l−1 · h)55.45 ± 9.9334.26 ± 6.40.008
     Maximal insulin concentration 9.15–9.32 h (pmol/l)262.6 ± 47.5166.5 ± 32.40.007
    Hyperglycemic clamp, steady state
     Insulin concentration (pmol/l)929.6 ± 262.9271.9 ± 53.30.015
     Proinsulin/insulin ratio0.09 ± 0.020.18 ± 0.030.001
     Glucagon concentration (pg/ml)55.5 ± 3.766.7 ± 3.50.005
     GIR/average serum insulin (arbitrary units)0.13 ± 0.030.15 ± 0.040.392
    Arginine stimulation test
     Insulin total AUC 11.15–11.45 h (pmol · l−1 · h)799.6 ± 190307.2 ± 65.50.004
     Maximal insulin concentration (pmol/l)2,539 ± 5231,518 ± 2960.005
     Glucagon total AUC 11.15–11.45 h (pg · l−1 · h)40.7 ± 2.548.7 ± 3.00.012
     Maximal glucagon concentration (pg/ml)162.0 ± 13.7193.4 ± 140.034
    HOMA analysis
     β-Cell function (% of normal)59.95 ± 8.8446.07 ± 9.860.010
     Insulin resistance (fold normal)4.09 ± 0.844.74 ± 1.150.373
    Disposition index (pmol/l*HOMA-R)80.4 ± 1441.9 ± 50.008
    • Data are means ± SEM. GIR, glucose infusion rate.

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One Week’s Treatment With the Long-Acting Glucagon-Like Peptide 1 Derivative Liraglutide (NN2211) Markedly Improves 24-h Glycemia and α- and β-Cell Function and Reduces Endogenous Glucose Release in Patients with Type 2 Diabetes
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One Week’s Treatment With the Long-Acting Glucagon-Like Peptide 1 Derivative Liraglutide (NN2211) Markedly Improves 24-h Glycemia and α- and β-Cell Function and Reduces Endogenous Glucose Release in Patients with Type 2 Diabetes
Kristine B. Degn, Claus B. Juhl, Jeppe Sturis, Grethe Jakobsen, Birgitte Brock, Visvanathan Chandramouli, Joergen Rungby, Bernard R. Landau, Ole Schmitz
Diabetes May 2004, 53 (5) 1187-1194; DOI: 10.2337/diabetes.53.5.1187

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One Week’s Treatment With the Long-Acting Glucagon-Like Peptide 1 Derivative Liraglutide (NN2211) Markedly Improves 24-h Glycemia and α- and β-Cell Function and Reduces Endogenous Glucose Release in Patients with Type 2 Diabetes
Kristine B. Degn, Claus B. Juhl, Jeppe Sturis, Grethe Jakobsen, Birgitte Brock, Visvanathan Chandramouli, Joergen Rungby, Bernard R. Landau, Ole Schmitz
Diabetes May 2004, 53 (5) 1187-1194; DOI: 10.2337/diabetes.53.5.1187
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