Next Article in Journal
A Genome-Wide Association Study Identifies the Association between the 12q24 Locus and Black Tea Consumption in Japanese Populations
Previous Article in Journal
Rapid Weight Gain, Infant Feeding Practices, and Subsequent Body Mass Index Trajectories: The CALINA Study
Previous Article in Special Issue
Trends in Beverage Consumption and Related Demographic Factors and Obesity among Korean Children and Adolescents
Open AccessArticle

High-Sugar Diet Disrupts Hypothalamic but Not Cerebral Cortex Redox Homeostasis

1
Department of Physiology, Medical University of Bialystok, 2c Mickiewicza Street, 15-233 Bialystok, Poland
2
Experimental Dentistry Laboratory, Medical University of Bialystok, Sklodowska 24a Street, 15-274 Bialystok, Poland
3
Department of Hygiene, Epidemiology and Ergonomics, Medical University of Bialystok, 15-233 Bialystok, Poland
*
Authors to whom correspondence should be addressed.
Nutrients 2020, 12(10), 3181; https://doi.org/10.3390/nu12103181
Received: 16 September 2020 / Revised: 14 October 2020 / Accepted: 16 October 2020 / Published: 18 October 2020
(This article belongs to the Special Issue Sugary Food Consumption and Its Impact on Health)
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 (n = 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. View Full-Text
Keywords: high-sugar diet; oxidative stress; oxidative damage; cerebral cortex; hypothalamus high-sugar diet; oxidative stress; oxidative damage; cerebral cortex; hypothalamus
Show Figures

Figure 1

MDPI and ACS Style

Żebrowska, E.; Chabowski, A.; Zalewska, A.; Maciejczyk, M. High-Sugar Diet Disrupts Hypothalamic but Not Cerebral Cortex Redox Homeostasis. Nutrients 2020, 12, 3181.

Show more citation formats Show less citations formats
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Search more from Scilit
 
Search
Back to TopTop