TDK conference 2017

Mounting evidence supports the negative impact of a western diet (WD) rich in saturated fats and refined carbohydrates on metabolic systems and on cognitive function. Previous studies had shown that high consumption of high fructose corn syrup – a common sweetener of processed foods known as HFCS-55 - and sucrose (dietary sugar - a dimer containing 1 fructose and 1 glucose) results in neuroinflammation and decreased hippocampal neurogenesis, which leads to disrupted spatial memory. Diminishing the intense hippocampal neurogenesis during adolescence supposedly has long-lasting effects on memory and learning, and could later facilitate the development of diseases.

Neuroinflammation and impaired spatial learning were observed after high sugar intake in adolescent rats and mice. Decreased hippocampal neurogenesis was noted in mice but not rats. Our study aimed to fill this gap.

18 adolescent male rats (postnatal day 21) were randomly divided into 2 groups. During the 6 weeks of the expreiment they were given free access to either water or 23% sucrose solution and standard rat chow. To investigate neurogenesis, 2 weeks into the study the animals recieved intraperitoneal 5-bromo-2′-deoxyuridine injection. The sugar-fed group chose to eat less and less solid food while drinking more and more of the sucrose solution. Their weight gain did not exceed that of the control group. 4 weeks later the rats were perfused transcardially. The brains were removed and stored in sucrose solution until analysis. After sectioning we performed immunhistochemistry on the 40 µm thick sections and mounted them on slides. We then visualised the results using confocal laser scanning microscopy. Quantification took place in the gyrus dentatus of the hippocampus.

There was a significant increase in the overall number of Brdu+ cells in the dentate gyrus of the sucrfose-fed group. The total number of newborn neurons (Brdu/Neun+ cells) did not differ in the two groups. However, we found significantly more non-neuron newborn cells in the sucrose-fed group, and if we accept the number of these cells as a rough estimate of newborn glia cells, the possibility of gliosis emerges. Gliosis is a hallmark of neuronal damage. It is known from previous studies that a high-fat diet activates astrocyte cells and supposedly induces microglial accumulation in the hypothalamus. It would be important to repeat our study and expand it with glia markers in the light of our present findings.