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Growth Hormone Excess Drives Liver Aging via increased Glycation stress
Biorxiv : the Preprint Server for Biology
|January 20, 2025
Summary
High growth hormone (GH) levels cause liver aging and metabolic issues by increasing AGEs. Glycation-lowering compounds reversed these effects, showing therapeutic potential for GH-related conditions.
Area of Science:
- Endocrinology
- Metabolic Regulation
- Molecular Biology
Background:
- Growth hormone (GH) is vital for physiological functions, with dysregulation linked to metabolic disorders.
- The liver is a primary target of GH and plays a key role in metabolic homeostasis.
- Pathological conditions like acromegaly involve elevated GH, impacting liver function.
Purpose of the Study:
- To investigate the impact of high circulating GH on liver metabolism.
- To analyze transcriptomic changes in the liver due to GH overexpression.
- To explore the role of AGEs and potential interventions.
Main Methods:
- Utilized bovine GH overexpressing transgenic (bGH-Tg) mice.
- Conducted comprehensive transcriptomic analysis of hepatic tissues.
- Assessed metabolic parameters and AGE accumulation.
- Evaluated the efficacy of glycation-lowering compounds.
Main Results:
- bGH-Tg mouse livers showed dysregulated fatty acid metabolism and inflammation.
- Transcriptomic profiles indicated accelerated liver aging and cellular senescence.
- Significant accumulation of advanced glycation end products (AGEs) was observed.
- Glycation-lowering compounds reversed insulin resistance and aberrant liver transcriptomes.
Conclusions:
- Chronic GH overexpression leads to liver aging, senescence, and metabolic dysfunction.
- AGE accumulation is a key mediator of GH-induced liver pathology.
- Glycation-lowering agents offer a potential therapeutic strategy for GH-related metabolic disorders.
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