Steviol glycosides affect trace element status in diabetic rat
Type
Journal article
Language
English
Date issued
2025
Author
Faculty
Wydział Nauk o Żywności i Żywieniu
Journal
Acta Scientiarum Polonorum, Technologia Alimentaria
ISSN
1644-0730
Volume
24
Number
2
Pages from-to
189-202
Abstract (EN)
Background. Steviol glycosides (stevioside and rebaudioside A) have been reported to have lipid and glu¬cose regulatory potential. The published literature presents conflicting results regarding the impact of hyper¬glycemia on Fe, Zn, and Cu levels, and almost no data exist on whether supplementary steviol glycosides can affect the status of trace elements in diabetes. This study aimed to evaluate the effect of hyperglycemia and dietary steviol glycoside supplementation on Fe, Zn, and Cu levels and the ratios of these elements in the liver and kidneys of diabetic rats.
Material and methods. The experiment was conducted on 70 male Wistar rats, of which 60 were fed a high-fat diet for 8 weeks, followed by intraperitoneal streptozotocin injection to induce type 2 diabetes, while 10 healthy controls were fed the AIN-93M diet. Thereafter, the diabetic rats were allocated to the following six high-fat diet-fed experimental groups: untreated, supplemented with metformin, or supplemented with stevioside or rebaudioside A (0.5 or 2.5%) for 5 weeks. After the experiment, internal organs were harvested for mineral analyses. The Fe, Zn, and Cu content in tissues were determined using the Atomic Absorption Spectroscopy (AAS) method.
Results. Hyperglycemia was found to significantly elevate the liver Zn/Cu ratio and decrease the kidney Fe level, as well as the kidney Fe/Zn and Zn/Cu ratios, in diabetic non-supplemented rats. In the supplemented groups, steviol glycosides tended to normalize the kidney Zn/Cu ratio, while high doses of steviol glycosides tended to normalize the kidney Fe concentration. Higher doses of steviol normalized the liver Zn/Cu ratio, and higher doses of rebaudioside A normalized the kidney Fe/Zn ratio. The type of glycoside affected the kidney Zn level and the Fe/Zn ratio in diabetic rats.
Conclusion. Hyperglycemia affected Fe, Zn, and Cu balance in diabetic rats, while steviol glycosides showed potential to normalize mineral levels depending on dosage and type. Future research should explore the underlying mechanisms and long-term effects of steviol glycoside supplementation on trace element homeo¬stasis in diabetes.
Material and methods. The experiment was conducted on 70 male Wistar rats, of which 60 were fed a high-fat diet for 8 weeks, followed by intraperitoneal streptozotocin injection to induce type 2 diabetes, while 10 healthy controls were fed the AIN-93M diet. Thereafter, the diabetic rats were allocated to the following six high-fat diet-fed experimental groups: untreated, supplemented with metformin, or supplemented with stevioside or rebaudioside A (0.5 or 2.5%) for 5 weeks. After the experiment, internal organs were harvested for mineral analyses. The Fe, Zn, and Cu content in tissues were determined using the Atomic Absorption Spectroscopy (AAS) method.
Results. Hyperglycemia was found to significantly elevate the liver Zn/Cu ratio and decrease the kidney Fe level, as well as the kidney Fe/Zn and Zn/Cu ratios, in diabetic non-supplemented rats. In the supplemented groups, steviol glycosides tended to normalize the kidney Zn/Cu ratio, while high doses of steviol glycosides tended to normalize the kidney Fe concentration. Higher doses of steviol normalized the liver Zn/Cu ratio, and higher doses of rebaudioside A normalized the kidney Fe/Zn ratio. The type of glycoside affected the kidney Zn level and the Fe/Zn ratio in diabetic rats.
Conclusion. Hyperglycemia affected Fe, Zn, and Cu balance in diabetic rats, while steviol glycosides showed potential to normalize mineral levels depending on dosage and type. Future research should explore the underlying mechanisms and long-term effects of steviol glycoside supplementation on trace element homeo¬stasis in diabetes.
Keywords (EN)
License
CC-BY - Attribution
Open access date
March 17, 2025