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Published on: December 16, 2021
Gastrointestinal inflammation and the circulating IGF system in humans
I Baricević1, D R Jones, J A Nikolić
1Institute for the Application of Nuclear Energy-INEP, Banatska 31b, Belgrade, Serbia and Montenegro. ivona@inep.co.yu
Patients with gastrointestinal inflammation show an imbalanced insulin-like growth factor (IGF) system. Levels of IGF-I and IGF-II were lower, while binding proteins IGFBP-2 and IGFBP-1 increased, impacting metabolic outcomes.
Area of Science:
- Endocrinology
- Gastroenterology
- Metabolic Research
Background:
- Insulin-like growth factors (IGFs) and their binding proteins (IGFBPs) regulate tissue growth.
- Aberrant IGF system activity is implicated in tumorigenesis.
- Gastrointestinal inflammation may disrupt normal metabolic processes.
Purpose of the Study:
- To investigate the status of the IGF system in adult patients with various gastrointestinal inflammatory conditions.
- To determine circulating concentrations of IGF-I, IGF-II, and their binding proteins (IGFBP-3, IGFBP-2, IGFBP-1).
Main Methods:
- Serum samples from 92 adult patients with gastrointestinal inflammation were analyzed.
- Radioimmunoassay (RIA) was used to measure IGF-I and IGF-II concentrations.
- Immunoblotting characterized IGFBP profiles and proteolytic patterns.
Main Results:
- Significantly lower concentrations of both IGF-I and IGF-II were observed in patients compared to healthy controls (p < 0.001).
- Immunoblotting revealed a ~60% decrease in intact IGFBP-3, with a ~1.7-fold increase in IGFBP-2 and a ~3.5-fold increase in IGFBP-1.
- No significant alterations in IGFBP fragmentation or proteolysis were detected between patients and controls.
Conclusions:
- The insulin-like growth factor system is significantly imbalanced in patients with gastrointestinal inflammation, irrespective of the underlying cause.
- These alterations in the IGF system may contribute to the metabolic consequences of inflammation.
- Understanding these changes could aid in predicting patient recovery efficiency.
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