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The vitamin-E derivative U-83836-E in the low-dose streptozocin- treated mouse: effects on diabetes development
G Papaccio1, G C Baccari, S Frascatore
1Institute of Anatomy, School of Medicine, Second University of Naples, Naples, Italy.
Abstract:
Low-dose streptozocin-treated (LDS) mice were administered an inhibitor of lipid peroxidation, U-83836-E (a derivative of vitamin E), in order to observe its ability to alter the onset of diabetes. Ten or 20 mg/kg body wt. per day of U-83836-E were given to mice for 7 days and they were killed after 21 days. Results revealed that there was a significant increase in glycaemia in treated groups up to day 14 after which no further increase was noticed. Superoxide dismutase (SOD) assay showed that: (1) the LDS treatment significantly reduces SOD activity when compared with untreated controls (P < 0.005); (2) U-83836-E increases SOD levels (when compared with untreated controls); and (3) U-83836-E counteracts LDS treatment, since SOD activity is significantly higher with respect to that found in LDS-controls (P < 0.05), and SOD levels were significantly higher with respect to that found in Group 2 animals (P < 0.05), but significantly lower with respect to those found in groups 3 and 4 (P < 0.005). Moreover, malondialdehyde (MDA), the end-product of lipoperoxidation, was found at much higher levels in LDS controls than in the other groups and the lowest values were found in U-83836-E controls and in normoglycaemic animals treated with both streptozocin and U-83836-E. Morphological observations demonstrated that islet beta cells were of normal appearance in normoglycaemic animals of the treated groups. In conclusion, the in vivo inhibition of lipid peroxidation by this compound produces a limited but significant prevention of the islet beta cell destruction.
Insights
This study investigated how U-83836-E, a vitamin E derivative, affects diabetes onset in mice. The inhibitor of lipid peroxidation showed a limited but significant prevention of islet beta cell destruction in treated animals.
Area of Science:
- Biochemistry
- Endocrinology
- Pharmacology
Background:
- Low-dose streptozocin (LDS) induces diabetes in mice by damaging islet beta cells.
- Lipid peroxidation plays a role in this cellular damage.
- Vitamin E derivatives are known antioxidants.
Purpose of the Study:
- To evaluate the efficacy of U-83836-E, a lipid peroxidation inhibitor, in preventing diabetes onset in LDS-treated mice.
- To assess the impact of U-83836-E on hyperglycemia, superoxide dismutase (SOD) activity, and malondialdehyde (MDA) levels.
Main Methods:
- Mice were treated with low-dose streptozocin (LDS) and administered U-83836-E (10 or 20 mg/kg) for 7 days.
- Blood glucose levels, SOD activity, and MDA levels were measured over 21 days.
- Islet morphology was examined in treated and control groups.
Main Results:
- U-83836-E treatment led to a significant increase in SOD activity compared to LDS controls.
- Malondialdehyde (MDA) levels, a marker of lipid peroxidation, were significantly lower in U-83836-E treated groups.
- Morphological analysis revealed normal islet beta cells in normoglycemic animals receiving U-83836-E.
Conclusions:
- Inhibition of lipid peroxidation by U-83836-E offers a limited but significant protective effect against islet beta cell destruction in a mouse model of diabetes.
- U-83836-E demonstrates potential as a therapeutic agent for preventing or mitigating diabetes progression.
