---
title: "Portal insulin and hepatic GH sensitivity: reframing IGF-1 targets across metabolic disease"
id: "pubmed-42776131"
canonical_url: "https://medichelpline.com/clinical-feed/pubmed-42776131"
content_type: "clinical_feed_article"
specialty: "Pharmacology"
source_name: "PubMed / NCBI"
source_url: "https://pubmed.ncbi.nlm.nih.gov/42776131/"
doi: "10.20945/2359-4292-2026-0115"
published_at: "2026-09-23T00:00:00.000Z"
evidence_level: "Journal Article"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Portal insulin and hepatic GH sensitivity: reframing IGF-1 targets across metabolic disease
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/pubmed-42776131
- **Specialty:** [Pharmacology](https://medichelpline.com/clinical-feed/pharmacology.md)
- **Primary Source:** PubMed / NCBI
- **Source URL:** [Original Journal Publication](https://pubmed.ncbi.nlm.nih.gov/42776131/)
- **DOI:** [10.20945/2359-4292-2026-0115](https://doi.org/10.20945%2F2359-4292-2026-0115)
- **Published At:** 2026-09-23T00:00:00.000Z
- **Evidence Rating:** Journal Article
## Executive GIST (TL;DR)
- Clinical management of growth hormone (GH) deficiency, acromegaly, and diabetes commonly relies on single-analyte targets, chiefly serum **insulin-like growth factor-1 (IGF-1)** and glycated hemoglobin. - The reviewed concept emphasizes that GH does not autonomously determine hepatic IGF-1 production; hepatocyte translation of GH to IGF-1 is gated by the concentration of **insulin** delivered to the liver via the **portal vein**. - Authors propose a unifying variable, **liver sensitivity to GH (LSG)**, defined operationally as portal-insulin–determined hepatic GH receptor availability, which places type 1 and type 2 diabetes, obesity, liver failure, and acromegaly on a continuum. - The molecular basis of insulin-dependent regulation of the GH receptor (GHR) in hepatocytes is developed in the review; details of those molecular mechanisms are discussed in the source. - The review distinguishes the divergent physiological roles of **portal** versus **systemic insulin**, arguing this distinction explains why subcutaneous insulin corrects systemic glycemia in type 1 diabetes but does not restore hepatic GH sensitivity. - Re-appraisal is provided for several clinical issues through the LSG lens: weight gain liability of insulinotropic antidiabetic agents, discordant GH/IGF-1 patterns with **GLP-1 receptor agonists**, prognostic and potential therapeutic roles of **IGF-1** in cirrhosis, and limitations of current acromegaly treatment targets when metabolism is considered. - The stated aim is to offer clinicians a mechanistic—rather than purely biochemical—framework for understanding metabolic behavior across these states. - The abstract does not report numerical data, trial outcomes, or detailed clinical recommendations; those specifics were not provided in the source abstract.
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Affiliations Expand ### Affiliations * 1 Pituitary Center Rotterdam, Department of Medicine, Erasmus University Medical Center, Rotterdam, The Netherlands. * 2 Edison Biotechnology Institute and Heritage College of Osteopathic Medicine, Ohio University, Athens, USA. * 3 Serviço de Endocrinologia e Metabologia do Paraná, Divisão de Endocrinologia, Departamento de Medicina Interna, Universidade Federal do Paraná, Curitiba, PR, Brasil. * PMID: **42776131** * DOI: [ 10.20945/2359-4292-2026-0115 ](https://doi.org/10.20945/2359-4292-2026-0115) Item in Clipboard Review # Beyond insulin-like growth factor-1 (IGF-1) normalization: portal insulin and hepatic growth hormone (GH) sensitivity across metabolic disease Aart J van der Lely et al. Arch Endocrinol Metab. 2026. Show details Display options Display options Format Abstract PubMed PMID Arch Endocrinol Metab Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Arch+Endocrinol+Metab%22%5Bjour%5D&sort=date&sort_order=desc) * [ Search in NLM Catalog ](https://www.ncbi.nlm.nih.gov/nlmcatalog?term=%22Arch+Endocrinol+Metab%22%5BTitle+Abbreviation%5D) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42776131/) . 2026 Sep 23;70(5):e260115. doi: 10.20945/2359-4292-2026-0115. ### Authors [Aart J van der Lely](https://pubmed.ncbi.nlm.nih.gov/?term=van+AJ+der+Lely&cauthor_id=42776131)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42776131/#short-view-affiliation-1 "Pituitary Center Rotterdam, Department of Medicine, Erasmus University Medical Center, Rotterdam, The Netherlands."), [Sebastian J Neggers](https://pubmed.ncbi.nlm.nih.gov/?term=Neggers+SJ&cauthor_id=42776131)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42776131/#short-view-affiliation-1 "Pituitary Center Rotterdam, Department of Medicine, Erasmus University Medical Center, Rotterdam, The Netherlands."), [John J Kopchick](https://pubmed.ncbi.nlm.nih.gov/?term=Kopchick+JJ&cauthor_id=42776131)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42776131/#short-view-affiliation-2 "Edison Biotechnology Institute and Heritage College of Osteopathic Medicine, Ohio University, Athens, USA."), [Cesar L Boguszewski](https://pubmed.ncbi.nlm.nih.gov/?term=Boguszewski+CL&cauthor_id=42776131)[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42776131/#short-view-affiliation-3 "Serviço de Endocrinologia e Metabologia do Paraná, Divisão de Endocrinologia, Departamento de Medicina Interna, Universidade Federal do Paraná, Curitiba, PR, Brasil.") ### Affiliations * 1 Pituitary Center Rotterdam, Department of Medicine, Erasmus University Medical Center, Rotterdam, The Netherlands. * 2 Edison Biotechnology Institute and Heritage College of Osteopathic Medicine, Ohio University, Athens, USA. * 3 Serviço de Endocrinologia e Metabologia do Paraná, Divisão de Endocrinologia, Departamento de Medicina Interna, Universidade Federal do Paraná, Curitiba, PR, Brasil. * PMID: **42776131** * DOI: [ 10.20945/2359-4292-2026-0115 ](https://doi.org/10.20945/2359-4292-2026-0115) Item in Clipboard Cite Display options Display options Format Abstract PubMed PMID ## Abstract Clinical management of growth hormone (GH) deficiency, acromegaly, and diabetes mellitus is dominated by single-analyte targets: serum insulin-like growth factor-1 (IGF-1) in the GH disorders and glycated hemoglobin in diabetes. This reductive framework obscures a central regulatory fact: GH does not autonomously dictate hepatic IGF-1 output. Whether GH is translated into IGF-1 by the hepatocyte is gated by the concentration of insulin reaching the liver through the portal vein. We propose liver sensitivity to GH (LSG), operationally defined as portal-insulin-determined hepatic GH receptor (GHR) availability, as a unifying variable that places type 1 and type 2 diabetes, obesity, liver failure, and acromegaly on a single continuum rather than treating them as separate phenomena. We develop the molecular basis of insulin-dependent GHR regulation, distinguish the divergent roles of portal versus systemic insulin, and argue that this distinction explains why subcutaneous insulin therapy in type 1 diabetes corrects glycemia while leaving the hepatic GH-resistant state intact. We then re-examine the weight-gain liability of insulinotropic antidiabetic agents, the discordant GH/IGF-1 signatures produced by GLP-1 receptor agonists, the prognostic and potentially therapeutic role of IGF-1 in cirrhosis, and the metabolic limitations of current acromegaly treatment targets when viewed through the LSG framework. The aim is to give the treating physician a mechanistic, rather than purely biochemical, account of how metabolism behaves in these states. **Keywords:** GLP-1 receptor agonists; Growth hormone; acromegaly; diabetes mellitus; insulin; insulin-like growth factor-1; liver cirrhosis; portal vein. 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