ReviewiScience2025
Ghrelin-GHSR-LEAP2 system in the pathophysiology of type 2 diabetes.
Review in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed.
- Circulating Ghrelin, Nesfatin-1, and Vaspin Levels Across Glycemic Control Categories in Type 2 Diabetes Mellitus: A Cross-Sectional Study.Biomedicines · 2026Article
- LEAP2 Regulates Insulin Secretion from INS-1E Beta Cells and Rat Pancreatic Islets: An In Vitro Study.International journal of molecular sciences · 2026Article
- The Ghrelin-LEAP2 System in Obesity and Diabetes: Pathophysiological Roles and Therapeutic Potential.Current obesity reports · 2026Review
- A Dimer for Dinner: The Impact of GHS-R1a Heterodimerization on Feeding Circuits.Biomolecules · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Ghrelin-GHSR-LEAP2 system plays a multifaceted role in the pathophysiology of type 2 diabetes mellitus (T2DM). Ghrelin, through the activation of its receptor GHS-R1a, contributes to hyperglycemia by suppressing insulin secretion, inducing insulin resistance, and promoting hepatic glucose production. In contrast, LEAP2, an endogenous antagonist and inverse agonist of GHS-R1a, mitigates these effects by enhancing insulin secretion and improving glucose tolerance. Notably, ghrelin also demonstrates protective properties against diabetic complications through anti-inflammatory, antioxidant, and anti-apoptotic mechanisms. This duality highlights the complexity of the therapeutic targeting of the ghrelin-GHSR axis. This review provides an updated overview of the molecular mechanisms and physiological functions of the ghrelin-GHSR-LEAP2 system in T2DM and discusses the therapeutic potential and challenges of modulating this pathway.
Indexed as
Identifiers
What Socratic holds
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.