Evidence map›Paper›PMID 41045492›Full record

ArticleAging2025

Growth hormone excess drives liver aging via increased glycation stress.

Parminder Singh, Anil Gautam, Marissa N Trujillo, Praveen Singh, Lizbeth Enriquez Najera, James J Galligan, Lisa Hensley, Pankaj Kapahi, Andrzej Bartke

Abstract read
In one paragraph

Article in Aging, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Protective Effects of Nongxiang-TypeFood science & nutrition · 2026
    Article
  2. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors.

Parminder SinghBuck Institute for Research on Aging, CA 94945, USA.
Anil GautamDepartment of Internal Medicine, Southern Illinois University School of Medicine, Springfield, IL 62702, USA.
Marissa N TrujilloDepartment of Pharmacology and Toxicology, College of Pharmacy, University of Arizona, Tucson, AZ 85721, USA.
Praveen SinghBuck Institute for Research on Aging, CA 94945, USA.
Lizbeth Enriquez NajeraBuck Institute for Research on Aging, CA 94945, USA.
James J GalliganDepartment of Pharmacology and Toxicology, College of Pharmacy, University of Arizona, Tucson, AZ 85721, USA.
Lisa HensleyDepartment of Internal Medicine, Southern Illinois University School of Medicine, Springfield, IL 62702, USA.
Pankaj KapahiBuck Institute for Research on Aging, CA 94945, USA.
Andrzej BartkeDepartment of Internal Medicine, Southern Illinois University School of Medicine, Springfield, IL 62702, USA.

Funding

Advanced glycation endproducts (AGEs) as metabolic by-products that mediate neurodegeneration.R01AG061165 · NIA · BUCK INSTITUTE FOR RESEARCH ON AGING · PI KAPAHI, PANKAJ · 2019 to 2023
$3.3M
Methylglyoxal drives astrocyte senescence to mediate neurodegeneration in Alzheimer's diseaseR01AG068288 · NIA · BUCK INSTITUTE FOR RESEARCH ON AGING · PI KAPAHI, PANKAJ · 2020 to 2024
$2.6M
Molecular Mechanisms of Lifespan Extension by Dietary Restriction in DrosophilaR01AG038688 · NIA · BUCK INSTITUTE FOR RESEARCH ON AGING · PI KAPAHI, PANKAJ · 2011 to 2015
$2.3M
NIA NIH HHS R01 AG038688NIA NIH HHS R01 AG061165NIA NIH HHS R01 AG068288
6 · The paper itself

Abstract

Growth hormone (GH) plays a crucial role in various physiological functions, with its secretion tightly regulated by complex endocrine mechanisms. Pathological conditions such as acromegaly or pituitary tumors result in elevated circulating GH levels, which have been implicated in a spectrum of metabolic disorders, potentially by regulating liver metabolism. In this study, we focused on the liver, a key organ in metabolic regulation and a primary target of GH, to investigate the impact of high circulating GH on liver metabolism. We used bovine GH overexpressing transgenic (bGH-Tg) mice to conduct a comprehensive transcriptomic analysis of hepatic tissues. The bGH-Tg mouse livers exhibit dysregulated fatty acid metabolism and heightened inflammatory responses. Notably, the transcriptomic profile of young bGH-Tg mouse livers resembled that of aged livers and displayed markers of increased cellular senescence. Furthermore, these mice exhibited a significant accumulation of advanced glycation end products (AGEs). Intervention with glycation-lowering compounds effectively reversed the insulin resistance and aberrant transcriptomic signatures in the liver that are associated with elevated GH levels. These findings underscore the potential therapeutic value of glycation-lowering agents in mitigating the deleterious effects of chronic GH overexpression.

Indexed as

AgingGlycation End Products, AdvancedGrowth HormoneLiverAnimalsCattleCellular SenescenceInsulin ResistanceMaleMiceMice, TransgenicTranscriptomeGlycation End Products, AdvancedGrowth Hormonegrowth hormone, bovineagingglycation stressGly-Lowgrowth hormone

Identifiers

PMID41045492
PMCPMC12606965

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 OpenQuestion graph.