ArticlePloS one2014
Differential stimulation of insulin secretion by GLP-1 and Kisspeptin-10.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.
- GLP-1 receptor agonists and pancreatic beta cell apoptosis in diabetes mellitus: a systematic review and meta-analysis of preclinical studies.Frontiers in clinical diabetes and healthcare · 2025Pooled it
- The effects of kisspeptin on β-cell function, serum metabolites and appetite in humans.Diabetes, obesity & metabolism · 2018Trial
- Enzymatic Stability and Comparative Effects of Kisspeptin-14, Kisspeptin-13 and Kisspeptin-10 on Beta-Cell Function, Glucose Homeostasis and Appetite Regulation.Metabolites · 2026Article
- Kisspeptin Restores Placental mTOR Signaling and Improves Glucose Homeostasis Mediators Disrupted by Maternal Hypothyroidism in Rats.Acta physiologica (Oxford, England) · 2026Article
- Kisspeptin and neurokinin B: roles in reproductive health.Physiological reviews · 2025Review
- Polycystic Ovary Syndrome and Eating Disorders-A Literature Review.Journal of clinical medicine · 2024Review
- Biasing GMolecular pharmacology · 2024Article
- Kisspeptin a potential therapeutic target in treatment of both metabolic and reproductive dysfunction.Journal of diabetes · 2024Review
- Kisspeptin upregulates β-cell serotonin production during pregnancy.The Journal of endocrinology · 2024Article
- The Emerging Therapeutic Potential of Kisspeptin and Neurokinin B.Endocrine reviews · 2024Review
- Kisspeptin Suppresses Inflammasome-NLRP3 Activation and Pyroptosis Caused by Hypothyroidism at the Maternal-Fetal Interface of Rats.International journal of molecular sciences · 2023Article
- The Role of Kisspeptin in the Pathogenesis of Pregnancy Complications: A Narrative Review.International journal of molecular sciences · 2022Review
- Metabolic actions of kisspeptin signaling: Effects on body weight, energy expenditure, and feeding.Pharmacology & therapeutics · 2022Review
- Kisspeptin in the Prediction of Pregnancy Complications.Frontiers in endocrinology · 2022Review
- Kisspeptin treatment improves fetal-placental development and blocks placental oxidative damage caused by maternal hypothyroidism in an experimental rat model.Frontiers in endocrinology · 2022Article
- Metabolic effects of prolactin and the role of dopamine agonists: A review.Frontiers in endocrinology · 2022Review
- Effects of empagliflozin on the expression of kisspeptin gene and reproductive system function in streptozotocin-induced diabetic male rats.Frontiers in endocrinology · 2022Article
- Functions of galanin, spexin and kisspeptin in metabolism, mood and behaviour.Nature reviews. Endocrinology · 2021Review
- Intraperitoneal Treatment of Kisspeptin Suppresses Appetite and Energy Expenditure and Alters Gastrointestinal Hormones in Mice.Digestive diseases and sciences · 2020Article
- Activation of Protein Kinase A (PKA) signaling mitigates congenital hyperinsulinism associated hypoglycemia in the Sur1-/- mouse model.PloS one · 2020Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
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+).
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.