High-Sugar Diet Disrupts Hypothalamic but Not Cerebral Cortex Redox Homeostasis
Despite several reports on the relationship between metabolic and neurodegenerative diseases, the effect of a high-sugar diet (HSD) on brain function is still unknown. Given the crucial role of oxidative stress in the pathogenesis of these disorders, this study was the first to compare the effect of...
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MDPI AG
2020-10-01
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| Series: | Nutrients |
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| Online Access: | https://www.mdpi.com/2072-6643/12/10/3181 |
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| author | Ewa Żebrowska Adrian Chabowski Anna Zalewska Mateusz Maciejczyk |
| author_facet | Ewa Żebrowska Adrian Chabowski Anna Zalewska Mateusz Maciejczyk |
| author_sort | Ewa Żebrowska |
| collection | DOAJ |
| description | Despite several reports on the relationship between metabolic and neurodegenerative diseases, the effect of a high-sugar diet (HSD) on brain function is still unknown. Given the crucial role of oxidative stress in the pathogenesis of these disorders, this study was the first to compare the effect of an HSD on the activity of prooxidative enzymes, enzymatic and non-enzymatic antioxidants, and protein oxidative damage in the brain structures regulating energy metabolism (hypothalamus) and cognitive functions (cerebral cortex). Male Wistar rats were randomly divided into two groups (<i>n</i> = 10)—control diet (CD) and high-sugar diet (HSD)—for 8 weeks. We showed a decrease in glutathione peroxidase and superoxide dismutase activity and an increase in catalase activity in the hypothalamus of HSD rats compared to controls. The activity of xanthine oxidase and NADPH oxidase and the contents of oxidation (protein carbonyls), glycoxidation (dityrosine, kynurenine and N-formylkynurenine) and protein glycation products (advanced glycation end products and Amadori products) were significantly higher only in the hypothalamus of the study group. The HSD was also responsible for the disruption of antioxidant systems and oxidative damage to blood proteins, but we did not show any correlation between systemic redox homeostasis and the brain levels. In summary, HSD is responsible for disorders of enzymatic antioxidant defenses only at the central (plasma/serum) and hypothalamic levels but does not affect the cerebral cortex. The hypothalamus is much more sensitive to oxidative damage caused by an HSD than the cerebral cortex. |
| first_indexed | 2024-03-10T15:32:56Z |
| format | Article |
| id | doaj.art-ddd8cf5b4d3040ab866db3e9562b8585 |
| institution | Directory Open Access Journal |
| issn | 2072-6643 |
| language | English |
| last_indexed | 2024-03-10T15:32:56Z |
| publishDate | 2020-10-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Nutrients |
| spelling | doaj.art-ddd8cf5b4d3040ab866db3e9562b85852023-11-20T17:32:57ZengMDPI AGNutrients2072-66432020-10-011210318110.3390/nu12103181High-Sugar Diet Disrupts Hypothalamic but Not Cerebral Cortex Redox HomeostasisEwa Żebrowska0Adrian Chabowski1Anna Zalewska2Mateusz Maciejczyk3Department of Physiology, Medical University of Bialystok, 2c Mickiewicza Street, 15-233 Bialystok, PolandDepartment of Physiology, Medical University of Bialystok, 2c Mickiewicza Street, 15-233 Bialystok, PolandExperimental Dentistry Laboratory, Medical University of Bialystok, Sklodowska 24a Street, 15-274 Bialystok, PolandDepartment of Hygiene, Epidemiology and Ergonomics, Medical University of Bialystok, 15-233 Bialystok, PolandDespite several reports on the relationship between metabolic and neurodegenerative diseases, the effect of a high-sugar diet (HSD) on brain function is still unknown. Given the crucial role of oxidative stress in the pathogenesis of these disorders, this study was the first to compare the effect of an HSD on the activity of prooxidative enzymes, enzymatic and non-enzymatic antioxidants, and protein oxidative damage in the brain structures regulating energy metabolism (hypothalamus) and cognitive functions (cerebral cortex). Male Wistar rats were randomly divided into two groups (<i>n</i> = 10)—control diet (CD) and high-sugar diet (HSD)—for 8 weeks. We showed a decrease in glutathione peroxidase and superoxide dismutase activity and an increase in catalase activity in the hypothalamus of HSD rats compared to controls. The activity of xanthine oxidase and NADPH oxidase and the contents of oxidation (protein carbonyls), glycoxidation (dityrosine, kynurenine and N-formylkynurenine) and protein glycation products (advanced glycation end products and Amadori products) were significantly higher only in the hypothalamus of the study group. The HSD was also responsible for the disruption of antioxidant systems and oxidative damage to blood proteins, but we did not show any correlation between systemic redox homeostasis and the brain levels. In summary, HSD is responsible for disorders of enzymatic antioxidant defenses only at the central (plasma/serum) and hypothalamic levels but does not affect the cerebral cortex. The hypothalamus is much more sensitive to oxidative damage caused by an HSD than the cerebral cortex.https://www.mdpi.com/2072-6643/12/10/3181high-sugar dietoxidative stressoxidative damagecerebral cortexhypothalamus |
| spellingShingle | Ewa Żebrowska Adrian Chabowski Anna Zalewska Mateusz Maciejczyk High-Sugar Diet Disrupts Hypothalamic but Not Cerebral Cortex Redox Homeostasis Nutrients high-sugar diet oxidative stress oxidative damage cerebral cortex hypothalamus |
| title | High-Sugar Diet Disrupts Hypothalamic but Not Cerebral Cortex Redox Homeostasis |
| title_full | High-Sugar Diet Disrupts Hypothalamic but Not Cerebral Cortex Redox Homeostasis |
| title_fullStr | High-Sugar Diet Disrupts Hypothalamic but Not Cerebral Cortex Redox Homeostasis |
| title_full_unstemmed | High-Sugar Diet Disrupts Hypothalamic but Not Cerebral Cortex Redox Homeostasis |
| title_short | High-Sugar Diet Disrupts Hypothalamic but Not Cerebral Cortex Redox Homeostasis |
| title_sort | high sugar diet disrupts hypothalamic but not cerebral cortex redox homeostasis |
| topic | high-sugar diet oxidative stress oxidative damage cerebral cortex hypothalamus |
| url | https://www.mdpi.com/2072-6643/12/10/3181 |
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