There is much public debate around the detrimental impact of sugar, particularly in the form of sweetened beverages, to overall health. We investigated the impact of chronic sucrose post-weaning on hippocampal genes related to plasticity, neurogenesis, stress responses and mitochondrial biogenesis. Female rats were provided with chow and 30% sucrose (in addition to water) to drink from weaning, and hippocampus was collected at 13 weeks. Control rats drank water. Sucrose intake was associated with marked reductions in expression of genes related to neurogenesis (Reln, Neurod1, Gsk3a) and mitochondrial biogenesis (Pgc-1α, Nrf-1). Expression of markers related to the stress response (GR, Homer 1) were also downregulated. Thus chronic sucrose consumption impacted an array of genes that govern development, and emotional and other brain functions.
We have shown in rats that both high fat, and high sugar, diets can impair hippocampal dependent behaviours, even after short-term exposure. Similar deficits are seen in young men exposed to poor diet for less than one week. Potential mechanisms underlying the cognitive deficits include neuroinflammation, changes in brain neurotrophic factors, and diet-related changes in gut microbiota. Even intermittent exposure to an energy-dense, western diet can shift the biota towards that seen in obese rats, with reduced microbial diversity. We compared the effects of added fat plus sugar, or added liquid sugar only, on behavior and hippocampal gene expression after 2 weeks of diet. When animals drank liquid sugar (10%) for 2 weeks, we observed increased expression of hippocampal proinflammatory cytokines, along with memory deficits (place recognition). Cytokine mRNA expression correlated with blood glucose concentrations. Other work has shown that greater sucrose consumption leads to distinct microbiota profiles, in the absence of weight differences. Examining key underlying processes is an essential step to enable testing of novel interventions in humans to combat diet-related cognitive deficits.