Skip to content

Study · Non-randomized trial · n = 8 · 2000

7 results

Recombinant human insulin-like growth factor I treatment for 1 week improves metabolic control in type 2 diabetes by ameliorating hepatic and muscle insulin resistance.

Cusi K, DeFronzo R

The Journal of clinical endocrinology and metabolism1 Sept 2000Cited by 49 (Europe PMC)

Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: Publisher copyright. Results still quote short attributed sentences.

Results from this study7

7 results from studies that gave the peptide. 7 results from people.

  1. 01HumanNon-randomized trialEfficacy outcome

    In poorly controlled T2DM, rhIGF-I reduced fasting plasma glucose from baseline.

    In plain wordsIn people with type 2 diabetes, rhIGF-I reduced fasting blood sugar from baseline.

    Outcome
    DecreaseFasting plasma glucose
    Study

    n = 8

    Outcome group
    Glycemic control · Metabolic and weight
    Studied dose
    80 microg/kg twice daily · subcutaneous · 7 daysAs given in this study (human).

    Measurements

    Fasting plasma glucose
    203 mg/dL
    before rhIGF-I (+/- 12)
    Fasting plasma glucose
    134 mg/dL
    during rhIGF-I (+/- 14)
    P value for Fasting plasma glucose
    < 0.01 P
    rhIGF-I versus baseline in poorly controlled T2DM subjects

    Source sentences

    Summary
    rhIGF-I significantly improved fasting (203 +/- 12 vs. 134 +/- 14 mg/dL; P < 0.01)
    1 context sentence
    Summary · context
    To test this hypothesis, we used the euglycemic insulin clamp to measure the response to 7 days of rhIGF-I therapy (80 microg/kg, sc, twice daily) in eight poorly controlled T2DM subjects.
  2. 02HumanNon-randomized trialEfficacy outcome

    In poorly controlled T2DM, rhIGF-I reduced day-long plasma glucose from baseline.

    In plain wordsIn people with type 2 diabetes, rhIGF-I reduced daytime blood sugar from baseline.

    Outcome
    DecreaseDay-long plasma glucose
    Study

    n = 8

    Outcome group
    Glycemic control · Metabolic and weight
    Studied dose
    80 microg/kg twice daily · subcutaneous · 7 daysAs given in this study (human).

    Measurements

    Day-long plasma glucose (0800-1700 h)
    234 mg/dL
    before rhIGF-I (+/- 11)
    Day-long plasma glucose (0800-1700 h)
    153 mg/dL
    during rhIGF-I (+/- 10)
    P value for Day-long plasma glucose (0800-1700 h)
    < 0.01 P
    rhIGF-I versus baseline in poorly controlled T2DM subjects

    Source sentences

    Summary
    rhIGF-I significantly improved fasting (203 +/- 12 vs. 134 +/- 14 mg/dL; P < 0.01) and day-long (0800-1700 h; 234 +/- 11 vs. 153 +/- 10 mg/dL; P < 0.01) plasma glucose levels.
    1 context sentence
    Summary · context
    To test this hypothesis, we used the euglycemic insulin clamp to measure the response to 7 days of rhIGF-I therapy (80 microg/kg, sc, twice daily) in eight poorly controlled T2DM subjects.
  3. 03HumanNon-randomized trialEfficacy outcome

    In poorly controlled T2DM, rhIGF-I reduced basal endogenous glucose production from baseline.

    In plain wordsIn people with type 2 diabetes, rhIGF-I reduced the body's glucose production from baseline.

    Outcome
    DecreaseBasal endogenous glucose production
    Study

    n = 8

    Outcome group
    Glycemic control · Metabolic and weight
    Studied dose
    80 microg/kg twice daily · subcutaneous · 7 daysAs given in this study (human).

    Measurements

    Basal endogenous glucose production
    3.2 mg/kg lean body mass x min
    before rhIGF-I (+/- 0.2)
    Basal endogenous glucose production
    2.7 mg/kg lean body mass x min
    during rhIGF-I (+/- 0.2)
    P value for Basal endogenous glucose production
    < 0.03 P
    rhIGF-I versus baseline in poorly controlled T2DM subjects

    Source sentences

    Summary
    Basal endogenous glucose production decreased from 3.2 +/- 0.2 to 2.7 +/- 0.2 mg/kg lean body mass x min (P < 0.03) despite a concomitant decline in the fasting plasma insulin concentration from 13 +/- 5 to 5 +/- 1 microU/mL (P < 0.01).
    1 context sentence
    Summary · context
    To test this hypothesis, we used the euglycemic insulin clamp to measure the response to 7 days of rhIGF-I therapy (80 microg/kg, sc, twice daily) in eight poorly controlled T2DM subjects.
  4. 04HumanNon-randomized trialEfficacy outcome

    In poorly controlled T2DM, fasting plasma insulin declined during rhIGF-I treatment.

    In plain wordsIn people with type 2 diabetes, fasting insulin fell during rhIGF-I treatment.

    Outcome
    DecreaseFasting plasma insulin
    Study

    n = 8

    Outcome group
    Glycemic control · Metabolic and weight
    Studied dose
    80 microg/kg twice daily · subcutaneous · 7 daysAs given in this study (human).

    Measurements

    Fasting plasma insulin
    13 microU/mL
    before rhIGF-I (+/- 5)
    Fasting plasma insulin
    5 microU/mL
    during rhIGF-I (+/- 1)
    P value for Fasting plasma insulin
    < 0.01 P
    rhIGF-I versus baseline in poorly controlled T2DM subjects

    Source sentences

    Summary
    Basal endogenous glucose production decreased from 3.2 +/- 0.2 to 2.7 +/- 0.2 mg/kg lean body mass x min (P < 0.03) despite a concomitant decline in the fasting plasma insulin concentration from 13 +/- 5 to 5 +/- 1 microU/mL (P < 0.01).
    1 context sentence
    Summary · context
    To test this hypothesis, we used the euglycemic insulin clamp to measure the response to 7 days of rhIGF-I therapy (80 microg/kg, sc, twice daily) in eight poorly controlled T2DM subjects.
  5. 05HumanNon-randomized trialMechanism

    In treated T2DM subjects, decrements in endogenous glucose production correlated with decrements in fasting glucose.

    In plain wordsIn treated people with type 2 diabetes, reduced glucose production was linked to reduced fasting blood sugar.

    Outcome
    Not applicableGlucose production and fasting glucose correlation
    Study

    n = 8

    Outcome group
    Glycemic control · Metabolic and weight
    Studied dose
    80 microg/kg twice daily · subcutaneous · 7 daysAs given in this study (human).

    Measurements

    Correlation between decrement in basal endogenous glucose production and decrement in fasting plasma glucose
    0.78 r
    rhIGF-I-treated T2DM subjects
    P value for Correlation between decrements in basal endogenous glucose production and fasting plasma glucose
    < 0.01 P
    correlation between decrement in basal endogenous glucose production and decrement in fasting plasma glucose in rhIGF-I-treated T2DM subjects

    Source sentences

    Summary
    The decrement in basal endogenous glucose production was closely correlated with the decrement in fasting plasma glucose concentration (r = 0.78; P < 0.01).
    1 context sentence
    Summary · context
    To test this hypothesis, we used the euglycemic insulin clamp to measure the response to 7 days of rhIGF-I therapy (80 microg/kg, sc, twice daily) in eight poorly controlled T2DM subjects.
  6. 06HumanNon-randomized trialEfficacy outcome

    In T2DM subjects, rhIGF-I increased insulin-stimulated glucose disposal by 27% from baseline.

    In plain wordsIn people with type 2 diabetes, rhIGF-I increased insulin-driven glucose removal by 27% from baseline.

    Outcome
    IncreaseInsulin-stimulated glucose disposal
    Study

    n = 8

    Outcome group
    Glycemic control · Metabolic and weight
    Studied dose
    80 microg/kg twice daily · subcutaneous · 7 daysAs given in this study (human).

    Measurements

    Whole body insulin-stimulated glucose disposal
    5.6 mg/kg lean body mass x min
    before rhIGF-I (+/- 0.8)
    Whole body insulin-stimulated glucose disposal
    7.1 mg/kg lean body mass x min
    during rhIGF-I (+/- 0.8)
    Whole body insulin-stimulated glucose disposal increase
    27%
    rhIGF-I versus baseline
    P value for Whole body insulin-stimulated glucose disposal
    < 0.01 P
    rhIGF-I versus baseline in poorly controlled T2DM subjects

    Source sentences

    Summary
    Whole body insulin-stimulated glucose disposal increased by 27% (from 5.6 +/- 0.8 to 7.1 +/- 0.8 mg/kg lean body mass x min; P < 0.01), but remained well below that observed in age- and weight-matched healthy subjects.
    1 context sentence
    Summary · context
    To test this hypothesis, we used the euglycemic insulin clamp to measure the response to 7 days of rhIGF-I therapy (80 microg/kg, sc, twice daily) in eight poorly controlled T2DM subjects.
  7. 07HumanNon-randomized trialEfficacy outcome

    In rhIGF-I-treated T2DM subjects, insulin-stimulated glucose disposal remained below that in matched healthy subjects.

    In plain wordsPeople with type 2 diabetes treated with rhIGF-I still removed less glucose than matched healthy people.

    Outcome
    DecreaseGlucose disposal versus healthy subjects
    Study

    n = 8

    Comparator
    Age- and weight-matched healthy subjects
    Outcome group
    Glycemic control · Metabolic and weight
    Studied dose
    80 microg/kg twice daily · subcutaneous · 7 daysAs given in this study (human).

    Measurements

    Whole body insulin-stimulated glucose disposal
    7.1 mg/kg lean body mass x min
    rhIGF-I-treated T2DM subjects (+/- 0.8)

    Source sentences

    Summary
    Whole body insulin-stimulated glucose disposal increased by 27% (from 5.6 +/- 0.8 to 7.1 +/- 0.8 mg/kg lean body mass x min; P < 0.01), but remained well below that observed in age- and weight-matched healthy subjects.
    1 context sentence
    Summary · context
    To test this hypothesis, we used the euglycemic insulin clamp to measure the response to 7 days of rhIGF-I therapy (80 microg/kg, sc, twice daily) in eight poorly controlled T2DM subjects.

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    14 Oct 2026, 05:02 UTC

    Study results updated

  2. Version 1

    14 Oct 2026, 01:46 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

PepBank is a research reference. Talk to a doctor before you use any peptide.