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Updated: Jul 17, 2026

A Murine Pancreatic Islet Cell-based Screening for Diabetogenic Environmental Chemicals
Published on: June 25, 2018
Pancreatic B-cell function is altered by oxidative stress induced by acute hyperglycaemia
Y Miyazaki1, H Kawano, T Yoshida
1Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kumamoto University, Honjo, Kumamoto City, Japan.
Acute hyperglycemia after glucose intake impairs pancreatic beta-cell function, indicated by declining thioredoxin levels. This suggests postprandial hyperglycemia contributes to diabetes development.
Area of Science:
- Endocrinology
- Metabolic Health
- Oxidative Stress Research
Background:
- Type 2 diabetes development involves a phase of impaired glucose tolerance (IGT).
- Pancreatic beta-cell function declines during glucose intolerance.
- Postprandial hyperglycemia is common in IGT when fasting glucose is normal.
Purpose of the Study:
- To investigate changes in pancreatic beta-cell function during acute hyperglycemia induced by oral glucose loading.
- To assess the relationship between hyperglycemia, cellular redox state, and oxidative stress markers.
Main Methods:
- A 75-g oral glucose tolerance test (OGTT) was administered to 45 subjects (NGT, IGT, Type 2 diabetes).
- Pancreatic beta-cell function was assessed using the insulinogenic index (I.I.).
- Serum thioredoxin (redox marker) and 8-hydroxy-2'-deoxyguanosine (8-OHdG, oxidative stress marker) were measured.
Main Results:
- Thioredoxin levels significantly decreased post-glucose loading.
- 8-OHdG concentrations peaked at 30 minutes and then declined.
- The insulinogenic index correlated positively with changes in thioredoxin levels.
Conclusions:
- Acute hyperglycemia following oral glucose intake impairs pancreatic beta-cell function.
- Decreasing thioredoxin levels suggest altered cellular redox state due to hyperglycemia.
- Repeated postprandial hyperglycemia may be a significant factor in diabetes mellitus progression.
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