---
title: "Gut–pancreatic peptide therapies in metabolic disease: from GLP-1 mono-agonists to multi-agonist s"
id: "pubmed-42307179"
canonical_url: "https://medichelpline.com/clinical-feed/pubmed-42307179"
content_type: "clinical_feed_article"
specialty: "Pharmacology"
source_name: "PubMed / NCBI"
source_url: "https://pubmed.ncbi.nlm.nih.gov/42307179/"
doi: "10.1042/BSR20250114"
published_at: "2026-08-19T00:00:00.000Z"
evidence_level: "Journal Article"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Gut–pancreatic peptide therapies in metabolic disease: from GLP-1 mono-agonists to multi-agonist s
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/pubmed-42307179
- **Specialty:** [Pharmacology](https://medichelpline.com/clinical-feed/pharmacology.md)
- **Primary Source:** PubMed / NCBI
- **Source URL:** [Original Journal Publication](https://pubmed.ncbi.nlm.nih.gov/42307179/)
- **DOI:** [10.1042/BSR20250114](https://doi.org/10.1042%2FBSR20250114)
- **Published At:** 2026-08-19T00:00:00.000Z
- **Evidence Rating:** Journal Article
## Executive GIST (TL;DR)
- The global burden of interrelated metabolic disorders — **type 2 diabetes (T2D)**, **obesity**, and metabolic dysfunction-associated steatotic liver disease — is driving rapid evolution in pharmacotherapy. - Traditional diabetes treatments (insulin, metformin) are being supplemented by gut-peptide analogue therapies that offer broader metabolic benefits. - **GLP-1 receptor agonists** have transformed T2D and obesity management and spurred interest in other gut–pancreatic peptides. - Additional peptides of interest include **glucose-dependent insulinotropic polypeptide (GIP)**, **glucagon**, **amylin**, and **peptide YY (PYY)**, each with distinct physiological actions and therapeutic potential. - Dual and triple incretin agonists (GLP-1/GIP; GLP-1/GIP/glucagon) aim to recruit complementary signalling pathways (cAMP/PKA, PI3K/AKT, AMPK, PLC/Ca2+) to enhance insulin secretion, weight loss, insulin sensitivity, adipose nutrient partitioning, hepatic lipid handling, and energy expenditure. - Mechanistic rationale for multi-agonism includes broadened receptor signalling, reduced receptor internalisation, biased signalling, and additive effects on gut–brain–liver axes controlling satiety, gastric emptying, and hepatic metabolism. - **Amylin** and **PYY** act via gut–brain circuits to reduce appetite and modify postprandial metabolism and are being explored as adjuncts or components of multi-peptide therapeutics. - The review summarizes mechanisms of action, therapeutic efficacy, known limitations, and development status of peptide-based non-insulin therapies, and outlines emerging avenues and future potential in treating T2D, obesity, and associated liver disease.
## Clinical Analysis & Structured Key Points
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more resources ](https://pubmed.ncbi.nlm.nih.gov/42307179/#linkout) Title & authors Abstract Conflict of interest statement Figures Similar articles References Publication types MeSH terms Substances Related information LinkOut - more resources Review Biosci Rep Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Biosci+Rep%22%5Bjour%5D&sort=date&sort_order=desc) * [ Search in NLM Catalog ](https://www.ncbi.nlm.nih.gov/nlmcatalog?term=%22Biosci+Rep%22%5BTitle+Abbreviation%5D) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42307179/) . 2026 Aug 19;46(8):BSR20250114. doi: 10.1042/BSR20250114. # The evolving therapeutic landscape of gut-pancreatic peptide signalling in metabolic disorders: from mono- to multi-agonist therapies [Mohan Patil](https://pubmed.ncbi.nlm.nih.gov/?term=Patil+M&cauthor_id=42307179)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42307179/#full-view-affiliation-1 "Molecular Endocrinology and Pharmacology, Harry Perkins Institute of Medical Research and Centre for Medical Research, The University of Western Australia, Nedlands, WA, Australia.")[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42307179/#full-view-affiliation-2 "School of Biomedical Sciences, The University of Western Australia, Nedlands, WA, Australia."), [Federico Piccinini](https://pubmed.ncbi.nlm.nih.gov/?term=Piccinini+F&cauthor_id=42307179)[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42307179/#full-view-affiliation-3 "Department of Medicine and Surgery, University of Parma, Parma 43125, Italy."), [Elizabeth K M Johnstone](https://pubmed.ncbi.nlm.nih.gov/?term=Johnstone+EKM&cauthor_id=42307179)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42307179/#full-view-affiliation-1 "Molecular Endocrinology and Pharmacology, Harry Perkins Institute of Medical Research and Centre for Medical Research, The University of Western Australia, Nedlands, WA, Australia.")[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42307179/#full-view-affiliation-2 "School of Biomedical Sciences, The University of Western Australia, Nedlands, WA, Australia."), [Ilaria Casari](https://pubmed.ncbi.nlm.nih.gov/?term=Casari+I&cauthor_id=42307179)[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42307179/#full-view-affiliation-3 "Department of Medicine and Surgery, University of Parma, Parma 43125, Italy."), [Marco Falasca](https://pubmed.ncbi.nlm.nih.gov/?term=Falasca+M&cauthor_id=42307179)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42307179/#full-view-affiliation-1 "Molecular Endocrinology and Pharmacology, Harry Perkins Institute of Medical Research and Centre for Medical Research, The University of Western Australia, Nedlands, WA, Australia.")[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42307179/#full-view-affiliation-2 "School of Biomedical Sciences, The University of Western Australia, Nedlands, WA, Australia.")[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42307179/#full-view-affiliation-3 "Department of Medicine and Surgery, University of Parma, Parma 43125, Italy.")[ 4 ](https://pubmed.ncbi.nlm.nih.gov/42307179/#full-view-affiliation-4 "Lipovexa SRL, Via Giuseppe Mangionello, 12, 73024 Maglie \(LE\), Italy.") Affiliations Expand ### Affiliations * 1 Molecular Endocrinology and Pharmacology, Harry Perkins Institute of Medical Research and Centre for Medical Research, The University of Western Australia, Nedlands, WA, Australia. * 2 School of Biomedical Sciences, The University of Western Australia, Nedlands, WA, Australia. * 3 Department of Medicine and Surgery, University of Parma, Parma 43125, Italy. * 4 Lipovexa SRL, Via Giuseppe Mangionello, 12, 73024 Maglie (LE), Italy. * PMID: **42307179** * PMCID: [ PMC13376848 ](https://pmc.ncbi.nlm.nih.gov/articles/PMC13376848/) * DOI: [ 10.1042/BSR20250114 ](https://doi.org/10.1042/bsr20250114) Item in Clipboard Review # The evolving therapeutic landscape of gut-pancreatic peptide signalling in metabolic disorders: from mono- to multi-agonist therapies Mohan Patil et al. Biosci Rep. 2026. Show details Display options Display options Format Abstract PubMed PMID Biosci Rep Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Biosci+Rep%22%5Bjour%5D&sort=date&sort_order=desc) * [ Search in NLM Catalog ](https://www.ncbi.nlm.nih.gov/nlmcatalog?term=%22Biosci+Rep%22%5BTitle+Abbreviation%5D) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42307179/) . 2026 Aug 19;46(8):BSR20250114. doi: 10.1042/BSR20250114. ### Authors [Mohan Patil](https://pubmed.ncbi.nlm.nih.gov/?term=Patil+M&cauthor_id=42307179)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42307179/#short-view-affiliation-1 "Molecular Endocrinology and Pharmacology, Harry Perkins Institute of Medical Research and Centre for Medical Research, The University of Western Australia, Nedlands, WA, Australia.")[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42307179/#short-view-affiliation-2 "School of Biomedical Sciences, The University of Western Australia, Nedlands, WA, Australia."), [Federico Piccinini](https://pubmed.ncbi.nlm.nih.gov/?term=Piccinini+F&cauthor_id=42307179)[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42307179/#short-view-affiliation-3 "Department of Medicine and Surgery, University of Parma, Parma 43125, Italy."), [Elizabeth K M Johnstone](https://pubmed.ncbi.nlm.nih.gov/?term=Johnstone+EKM&cauthor_id=42307179)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42307179/#short-view-affiliation-1 "Molecular Endocrinology and Pharmacology, Harry Perkins Institute of Medical Research and Centre for Medical Research, The University of Western Australia, Nedlands, WA, Australia.")[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42307179/#short-view-affiliation-2 "School of Biomedical Sciences, The University of Western Australia, Nedlands, WA, Australia."), [Ilaria Casari](https://pubmed.ncbi.nlm.nih.gov/?term=Casari+I&cauthor_id=42307179)[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42307179/#short-view-affiliation-3 "Department of Medicine and Surgery, University of Parma, Parma 43125, Italy."), [Marco Falasca](https://pubmed.ncbi.nlm.nih.gov/?term=Falasca+M&cauthor_id=42307179)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42307179/#short-view-affiliation-1 "Molecular Endocrinology and Pharmacology, Harry Perkins Institute of Medical Research and Centre for Medical Research, The University of Western Australia, Nedlands, WA, Australia.")[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42307179/#short-view-affiliation-2 "School of Biomedical Sciences, The University of Western Australia, Nedlands, WA, Australia.")[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42307179/#short-view-affiliation-3 "Department of Medicine and Surgery, University of Parma, Parma 43125, Italy.")[ 4 ](https://pubmed.ncbi.nlm.nih.gov/42307179/#short-view-affiliation-4 "Lipovexa SRL, Via Giuseppe Mangionello, 12, 73024 Maglie \(LE\), Italy.") ### Affiliations * 1 Molecular Endocrinology and Pharmacology, Harry Perkins Institute of Medical Research and Centre for Medical Research, The University of Western Australia, Nedlands, WA, Australia. * 2 School of Biomedical Sciences, The University of Western Australia, Nedlands, WA, Australia. * 3 Department of Medicine and Surgery, University of Parma, Parma 43125, Italy. * 4 Lipovexa SRL, Via Giuseppe Mangionello, 12, 73024 Maglie (LE), Italy. * PMID: **42307179** * PMCID: [ PMC13376848 ](https://pmc.ncbi.nlm.nih.gov/articles/PMC13376848/) * DOI: [ 10.1042/BSR20250114 ](https://doi.org/10.1042/bsr20250114) Item in Clipboard Full text links Cite Display options Display options Format Abstract PubMed PMID ## Abstract The pharmacotherapeutic landscape for the clinical management of type-2 diabetes (T2D), obesity, metabolic dysfunction-associated steatotic liver disease, and steatohepatitis is evolving swiftly in response to the escalating global prevalence and incidence of these interrelated metabolic disorders. Although insulin and metformin formulations have long constituted the foundation of diabetes care, a paradigm shift in T2D management has been observed with the advent of novel pharmacotherapies. Gut peptide analogues are at the forefront of this transformation. The emergence of glucagon-like peptide-1 (GLP-1) receptor agonists represents a watershed moment, fundamentally reshaping the therapeutic landscape for both T2D and obesity due to multifaceted metabolic benefits. The clinical success of GLP-1-based therapies has stimulated pharmaceutical interest in other metabolic peptides. Gut-pancreatic peptides such as glucose-dependent insulinotropic polypeptide, glucagon, amylin, and peptide YY are of particular interest due to their distinct pharmacological benefits and therapeutic promise in metabolic disorders. The present review aims to provide a comprehensive and current overview of non-insulin gut-pancreatic peptide signalling-based therapies that are either clinically approved or under clinical investigation, with a focus on the emerging therapeutic convergence between T2D, obesity, and associated liver disease. The review critically narrates their mechanisms of action, therapeutic efficacy, limitations, current development status, and positioning in the treatment landscape. Furthermore, the review delineates the emerging avenues in the development of novel peptide-based pharmacotherapies, offering insights into their future potential and acquainting the reader with developments in non-insulin gut-pancreatic peptide signalling-based therapies for metabolic disorders. **Keywords:** glucagon-like peptide-1; non alcoholic fatty liver disease; obesity; type 2 diabetes. © 2026 The Author(s). [PubMed Disclaimer](https://pubmed.ncbi.nlm.nih.gov/disclaimer/) ## Conflict of interest statement M.F. is a member of LIPOVEXA S.r.l., a spin-off company focused on developing innovative treatments for diabetes, obesity, and liver health. The other authors declare no conflicts of interest. ## Figures [ ![Figure 1](https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71c9/13376848/3a4b227dc68f/bsr-46-bsr20250114-g1.gif) ](https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71c9/13376848/82f0bfa908fc/bsr-46-bsr20250114-g1.jpg) ** Figure 1. Metabolic Peptides of Pharmaceutical Interest… ** ** Figure 1. Metabolic Peptides of Pharmaceutical Interest in Metabolic Disorders: Origin, Structure, and Physiological Actions ** **Figure 1. Metabolic Peptides of Pharmaceutical Interest in Metabolic Disorders: Origin, Structure, and Physiological Actions** Metabolic peptides of growing pharmaceutical interest in metabolic disorders: origin, structure, and actions. Figure created with BioRender.com. [ ![Figure 2](https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71c9/13376848/f4b4aa5060dc/bsr-46-bsr20250114-g2.gif) ](https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71c9/13376848/2c807cbc4ab5/bsr-46-bsr20250114-g2.jpg) ** Figure 2. Schematic overview of the signalling… ** ** Figure 2. Schematic overview of the signalling architecture and metabolic consequences of mono-, dual-, and… ** **Figure 2. Schematic overview of the signalling architecture and metabolic consequences of mono-, dual-, and triple-incretin agonist therapies** (**A**) GLP-1 mono-agonism predominantly activates G protein alpha-s (Gαs) signalling, increasing cAMP and engaging protein kinase A (PKA), exchange protein directly activated by cAMP (EPAC), phosphoinositide 3-kinase/protein kinase B (PI3K/AKT), and AMP-activated protein kinase (AMPK) pathways. These downstream signals enhance glucose-stimulated insulin secretion (GSIS), suppress glucagon secretion, promote satiety through hypothalamic neuropeptide Y/agouti-related peptide (NPY/AgRP) and pro-opiomelanocortin/cocaine-and amphetamine-regulated transcript (POMC/CART) neuronal circuits, delay gastric emptying, and indirectly improve hepatic glucose and lipid homeostasis. (**B**) Dual GLP-1/GIP agonism broadens incretin signalling by adding GIP-mediated Gαs-cAMP-PKA/EPAC, PI3K/AKT, and AMPK inputs, while reducing β-arrestin recruitment and receptor internalisation, consistent with biased GLP-1 receptor signalling. This expanded signalling network may augment β-cell insulinotropic activity, improve insulin sensitivity, and promote adipose nutrient partitioning and lipid storage with reduced ectopic fat deposition, thereby conferring greater metabolic efficacy than GLP-1 mono-agonism alone. (**C**) Triple GLP-1/GIP/glucagon agonism further extends the signalling repertoire through glucagon receptor (GCGR)-mediated Gαs and Gαq pathways, engaging AC/cAMP and phospholipase C (PLC)/inositol 1,4,5-trisphosphate (IP3)/intracellular calcium (Ca+2) signalling. These additional inputs provide direct hepatic actions that increase amino acid catabolism, hepatic glucose production, lipid mobilisation, and fatty acid oxidation and may increase energy expenditure. In parallel, triple agonism may potentiate insulin secretion and strengthen gut–brain–liver satiety signalling and delayed gastric emptying. Collectively, the progressive recruitment of complementary metabolic pathways provides a mechanistic basis for the broader and potentially additive benefits of dual and triple agonism on glycaemic control, weight loss, and MASH. Figure created with BioRender.com. [ ![Figure 3](https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71c9/13376848/bfdeea7e3eed/bsr-46-bsr20250114-g3.gif) ](https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71c9/13376848/94d3f155683b/bsr-46-bsr20250114-g3.jpg) ** Figure 3. Mechanisms of Amylin and PYY… ** ** Figure 3. Mechanisms of Amylin and PYY Action in Gut–Brain Circuits Controlling Appetite and Postprandial… ** **Figure 3. Mechanisms of Amylin and PYY Action in Gut–Brain Circuits Controlling Appetite and Postprandial Metabolism** Mechanistic overview of (**A**) amylin and (**B**) PYY sig
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