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Study · Animal study (in vivo) · rat and mouse · 2020

11 results

Glucagon stimulates gluconeogenesis by INSP3R1-mediated hepatic lipolysis.

Perry RJ, Zhang D, Guerra MT, Brill AL, Goedeke L, Nasiri AR, Rabin-Court A, Wang Y, Peng L, Dufour S, Zhang Y, Zhang XM and 8 more

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Butrico GM, Toussaint K, Nozaki Y, Cline GW, Petersen KF, Nathanson MH, Ehrlich BE, Shulman GI

Nature4 Mar 2020Cited by 174 (Europe PMC)

PMID32132708 (opens in a new tab)PMCIDPMC7101062 (opens in a new tab)DOI10.1038/s41586-020-2074-6 (opens in a new tab)PepBankPUB-32132708
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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 study11

9 results from studies that gave the peptide. No result from this study comes from people.

  1. 01AnimalAnimal study (in vivo)Mechanism

    In the animal study, glucagon stimulated hepatic gluconeogenesis through INSP3R1-mediated mechanisms.

    In plain wordsIn animals, glucagon increased glucose production in the liver.

    Peptide
    Glucagon
    Outcome
    IncreaseHepatic gluconeogenesis
    Study

    n: not reported in source

    Outcome group
    Glycemic control · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Here we show that glucagon stimulates hepatic gluconeogenesis by increasing the activity of hepatic adipose triglyceride lipase, intrahepatic lipolysis, hepatic acetyl-CoA content and pyruvate carboxylase flux
  2. 02AnimalAnimal study (in vivo)Mechanism

    In the animal study, glucagon increased hepatic adipose triglyceride lipase activity.

    In plain wordsIn animals, glucagon increased the activity of a liver enzyme that breaks down fat.

    Peptide
    Glucagon
    Outcome
    IncreaseHepatic adipose triglyceride lipase activity
    Study

    n: not reported in source

    Outcome group
    Receptor activity and mechanism · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Here we show that glucagon stimulates hepatic gluconeogenesis by increasing the activity of hepatic adipose triglyceride lipase, intrahepatic lipolysis, hepatic acetyl-CoA content and pyruvate carboxylase flux
  3. 03AnimalAnimal study (in vivo)Mechanism

    In the animal study, glucagon increased intrahepatic lipolysis.

    In plain wordsIn animals, glucagon increased fat breakdown in the liver.

    Peptide
    Glucagon
    Outcome
    IncreaseIntrahepatic lipolysis
    Study

    n: not reported in source

    Outcome group
    Lipids · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Here we show that glucagon stimulates hepatic gluconeogenesis by increasing the activity of hepatic adipose triglyceride lipase, intrahepatic lipolysis, hepatic acetyl-CoA content and pyruvate carboxylase flux
  4. 04AnimalAnimal study (in vivo)Mechanism

    In the animal study, glucagon increased hepatic acetyl-CoA content.

    In plain wordsIn animals, glucagon increased acetyl-CoA in the liver.

    Peptide
    Glucagon
    Outcome
    IncreaseHepatic acetyl-CoA content
    Study

    n: not reported in source

    Outcome group
    Receptor activity and mechanism · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Here we show that glucagon stimulates hepatic gluconeogenesis by increasing the activity of hepatic adipose triglyceride lipase, intrahepatic lipolysis, hepatic acetyl-CoA content and pyruvate carboxylase flux
  5. 05AnimalAnimal study (in vivo)Mechanism

    In the animal study, glucagon increased pyruvate carboxylase flux.

    In plain wordsIn animals, glucagon increased activity through the pyruvate carboxylase pathway.

    Peptide
    Glucagon
    Outcome
    IncreasePyruvate carboxylase flux
    Study

    n: not reported in source

    Outcome group
    Receptor activity and mechanism · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Here we show that glucagon stimulates hepatic gluconeogenesis by increasing the activity of hepatic adipose triglyceride lipase, intrahepatic lipolysis, hepatic acetyl-CoA content and pyruvate carboxylase flux
  6. 06AnimalAnimal study (in vivo)Mechanism

    In rats and mice, chronic physiological increases in glucagon increased mitochondrial fat oxidation in the liver.

    In plain wordsIn rats and mice, chronic glucagon treatment increased fat oxidation in liver mitochondria.

    Peptide
    Glucagon
    Outcome
    IncreaseMitochondrial fat oxidation
    Study

    rats and micen: not reported in source

    diet-induced hepatic steatosis and insulin resistance
    Outcome group
    Mitochondrial function · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In rats and mice, chronic physiological increases in plasma glucagon concentrations increased mitochondrial oxidation of fat in the liver and reversed diet-induced hepatic steatosis and insulin resistance.
  7. 07AnimalAnimal study (in vivo)Efficacy outcome

    In rats and mice, chronic physiological increases in glucagon reversed diet-induced hepatic steatosis.

    In plain wordsIn rats and mice, chronic glucagon treatment reversed diet-induced liver fat accumulation.

    Peptide
    Glucagon
    Outcome
    DecreaseHepatic steatosis
    Study

    rats and micen: not reported in source

    diet-induced hepatic steatosis and insulin resistance
    Outcome group
    Liver fat and liver function · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In rats and mice, chronic physiological increases in plasma glucagon concentrations increased mitochondrial oxidation of fat in the liver and reversed diet-induced hepatic steatosis and insulin resistance.
  8. 08AnimalAnimal study (in vivo)Efficacy outcome

    In rats and mice, chronic physiological increases in glucagon reversed diet-induced insulin resistance.

    In plain wordsIn rats and mice, chronic glucagon treatment reversed diet-induced insulin resistance.

    Peptide
    Glucagon
    Outcome
    DecreaseInsulin resistance
    Study

    rats and micen: not reported in source

    diet-induced hepatic steatosis and insulin resistance
    Outcome group
    Glycemic control · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In rats and mice, chronic physiological increases in plasma glucagon concentrations increased mitochondrial oxidation of fat in the liver and reversed diet-induced hepatic steatosis and insulin resistance.
  9. 09AnimalAnimal study (in vivo)Mechanism

    In the animal study, glucagon increased mitochondrial fat oxidation through INSP3R1 stimulation.

    In plain wordsIn animals, glucagon increased mitochondrial fat oxidation through INSP3R1 stimulation.

    Peptide
    Glucagon
    Outcome
    IncreaseINSP3R1-mediated mitochondrial fat oxidation
    Study

    n: not reported in source

    Outcome group
    Mitochondrial function · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    while also increasing mitochondrial fat oxidation-all of which are mediated by stimulation of the inositol triphosphate receptor 1 (INSP3R1).

Studies that did not test the peptide alone2

In this study, Glucagon was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking Glucagon.

  1. 10AnimalNot a test of Glucagon aloneAnimal study (in vivo)Mechanism

    In Insp3r1-knockout mice, chronic glucagon treatment no longer reversed hepatic steatosis.

    In plain wordsIn mice without Insp3r1, chronic glucagon treatment did not reverse liver fat accumulation.

    Peptide
    Glucagon
    Outcome
    Direction not reportedHepatic steatosis response
    Study

    micen: not reported in source

    Insp3r1-knockout mice
    Outcome group
    Liver fat and liver function · Liver

    Source sentences

    Summary
    However, these effects of chronic glucagon treatment-reversing hepatic steatosis and glucose intolerance-were abrogated in Insp3r1 (also known as Itpr1)-knockout mice.

    In this study, Glucagon was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Glucagon.

  2. 11AnimalNot a test of Glucagon aloneAnimal study (in vivo)Mechanism

    In Insp3r1-knockout mice, chronic glucagon treatment no longer reversed glucose intolerance.

    In plain wordsIn mice without Insp3r1, chronic glucagon treatment did not reverse glucose intolerance.

    Peptide
    Glucagon
    Outcome
    Direction not reportedGlucose intolerance response
    Study

    micen: not reported in source

    Insp3r1-knockout mice
    Outcome group
    Glycemic control · Liver

    Source sentences

    Summary
    However, these effects of chronic glucagon treatment-reversing hepatic steatosis and glucose intolerance-were abrogated in Insp3r1 (also known as Itpr1)-knockout mice.

    In this study, Glucagon was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Glucagon.

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

    28 Oct 2026, 02:03 UTC

    Study results updated

  2. Version 1

    27 Oct 2026, 16:35 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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