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Study · Ex vivo tissue · mouse · 2014

5 results

Differential stimulation of insulin secretion by GLP-1 and Kisspeptin-10.

Schwetz TA, Reissaus CA, Piston DW

PloS one17 Nov 2014Cited by 39 (Europe PMC)

PMID25401335 (opens in a new tab)PMCIDPMC4234631 (opens in a new tab)DOI10.1371/journal.pone.0113020 (opens in a new tab)PepBankPUB-25401335
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Summary

β-cells in the pancreatic islet respond to elevated plasma glucose by secreting insulin to maintain glucose homeostasis. In addition to glucose stimulation, insulin secretion is modulated by numerous G-protein coupled receptors (GPCRs). The GPCR ligands Kisspeptin-10 (KP) and glucagon-like peptide-1 (GLP-1) potentiate insulin secretion through Gq and Gs-coupled receptors, respectively. Despite many studies, the signaling mechanisms by which KP and GLP-1 potentiate insulin release are not thoroughly understood. We investigated the downstream signaling pathways of these ligands and their affects on cellular redox potential, intracellular calcium activity ([Ca(2+)]i), and insulin secretion from β-cells within intact murine islets. In contrast to previous studies performed on single β-cells, neither KP nor GLP-1 affect [Ca(2+)]i upon stimulation with glucose. KP significantly increases the cellular redox potential, while no effect is observed with GLP-1, suggesting that KP and GLP-1 potentiate insulin secretion through different mechanisms. Co-treatment with KP and the Gβγ-subunit inhibitor gallein inhibits insulin secretion similar to that observed with gallein alone, while co-treatment with gallein and GLP-1 does not differ from GLP-1 alone. In contrast, co-treatment with the Gβγ activator mSIRK and either KP or GLP-1 stimulates insulin release similar to mSIRK alone. Neither gallein nor mSIRK alter [Ca(2+)]i activity in the presence of KP or GLP-1. These data suggest that KP likely alters insulin secretion through a Gβγ-dependent process that stimulates glucose metabolism without altering Ca(2+) activity, while GLP-1 does so, at least partly, through a Gα-dependent pathway that is independent of both metabolism and Ca(2+).
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study5

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

  1. 01LabEx vivo tissueMechanism

    In intact murine islets, kisspeptin‑10 did not change intracellular calcium activity on stimulation with glucose.

    In plain wordsIn mouse islet cells, kisspeptin‑10 did not change calcium activity when glucose was present.

    Peptide
    Kisspeptin-10
    Outcome
    No significant changeIntracellular calcium activity with glucose
    Study

    mousen: not reported in source

    Intact murine islets
    Outcome group
    Glycemic control · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In contrast to previous studies performed on single β-cells, neither KP nor GLP-1 affect [Ca(2+)]i upon stimulation with glucose.
    1 context sentence
    Summary · context
    We investigated the downstream signaling pathways of these ligands and their affects on cellular redox potential, intracellular calcium activity ([Ca(2+)]i), and insulin secretion from β-cells within intact murine islets.
  2. 02LabEx vivo tissueMechanism

    In intact murine islets, kisspeptin‑10 significantly increased the cellular redox potential.

    In plain wordsIn mouse islet cells, kisspeptin‑10 raised the redox potential of the cells.

    Peptide
    Kisspeptin-10
    Outcome
    IncreaseCellular redox potential
    Study

    mousen: not reported in source

    Intact murine islets
    Outcome group
    Glycemic control · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    KP significantly increases the cellular redox potential
    1 context sentence
    Summary · context
    We investigated the downstream signaling pathways of these ligands and their affects on cellular redox potential, intracellular calcium activity ([Ca(2+)]i), and insulin secretion from β-cells within intact murine islets.
  3. 03LabEx vivo tissueMechanism

    In intact murine islets, kisspeptin‑10 plus the Gbg inhibitor gallein inhibited insulin secretion to the same degree as gallein alone.

    In plain wordsIn mouse islets, adding kisspeptin‑10 to a Gbg blocker did not change insulin release compared with the blocker alone.

    Peptide
    Kisspeptin-10
    Outcome
    No significant changeInsulin secretion with kisspeptin-10 plus gallein
    Study

    mousen: not reported in source

    Intact murine islets
    Comparator
    Gallein alone
    Outcome group
    Glycemic control · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Co-treatment with KP and the Gβγ-subunit inhibitor gallein inhibits insulin secretion similar to that observed with gallein alone
    1 context sentence
    Summary · context
    We investigated the downstream signaling pathways of these ligands and their affects on cellular redox potential, intracellular calcium activity ([Ca(2+)]i), and insulin secretion from β-cells within intact murine islets.
  4. 04LabEx vivo tissueMechanism

    In intact murine islets, kisspeptin‑10 plus the Gbg activator mSIRK stimulated insulin release similar to mSIRK alone.

    In plain wordsIn mouse islets, adding kisspeptin‑10 to a Gbg activator gave insulin release similar to the activator alone.

    Peptide
    Kisspeptin-10
    Outcome
    No significant changeInsulin secretion with kisspeptin-10 plus mSIRK
    Study

    mousen: not reported in source

    Intact murine islets
    Comparator
    mSIRK alone
    Outcome group
    Glycemic control · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    co-treatment with the Gβγ activator mSIRK and either KP or GLP-1 stimulates insulin release similar to mSIRK alone
    1 context sentence
    Summary · context
    We investigated the downstream signaling pathways of these ligands and their affects on cellular redox potential, intracellular calcium activity ([Ca(2+)]i), and insulin secretion from β-cells within intact murine islets.

Studies that did not test the peptide alone1

In this study, Kisspeptin-10 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 Kisspeptin-10.

  1. 05LabNot a test of Kisspeptin-10 aloneEx vivo tissueMechanism

    In intact murine islets, neither gallein nor mSIRK changed intracellular calcium activity in the presence of kisspeptin‑10.

    In plain wordsIn mouse islets, neither a Gbg blocker nor a Gbg activator changed calcium activity when kisspeptin‑10 was present.

    Peptide
    Kisspeptin-10
    Outcome
    No significant changeIntracellular calcium activity with gallein or mSIRK in the presence of kisspeptin-10
    Study

    mousen: not reported in source

    Intact murine islets
    Outcome group
    Glycemic control · Metabolic and weight

    Source sentences

    Summary
    Neither gallein nor mSIRK alter [Ca(2+)]i activity in the presence of KP or GLP-1.
    1 context sentence
    Summary · context
    We investigated the downstream signaling pathways of these ligands and their affects on cellular redox potential, intracellular calcium activity ([Ca(2+)]i), and insulin secretion from β-cells within intact murine islets.

    In this study, Kisspeptin-10 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 Kisspeptin-10.

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

    10 Oct 2026, 09:43 UTC

    Study results updated

  2. Version 1

    9 Oct 2026, 03:04 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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