High energy diets impair cognition however, the rapidity and time-course of these deficits and the relative contribution of fat and sugar remain unclear. We have previously shown that 1 week of a cafeteria diet with 10 percent sucrose solution (Caf-Sugar), or a regular diet supplemented with 10 percent sucrose (Sugar) can impair hippocampal-dependent place, but not perirhinal-dependent object, recognition memory. These deficits were strongly correlated with markers of hippocampal inflammation, but not neurogenesis, after 1 month of diet (Beilharz et al., 2014).
To determine whether inflammation was present when the deficits first emerged, here we examined a similar cohort after 2 weeks of diet. The Sugar and Caf-Sugar rats again showed selective hippocampal memory deficits. At 2 weeks however, the Sugar rats had higher hippocampal expression of the inflammatory markers TNF-alpha, IL-1beta and SOCS3, compared to Caf-Sugar rats. We found the same pattern in white adipose tissue; Sugar rats had 50-75% higher TNF-alpha and IL-1beta mRNA expression than Caf-Sugar rats. There was no evidence of inflammation in the perirhinal cortex.
These results may be linked to a higher glycaemic response in the Sugar rats. Specifically, while the Sugar rats consumed less total sugar than Caf-Sugar rats, they consumed three times more liquid sugar. Increased liquid sugar may lead to a higher glycaemic response and reduced satiety, which would likely promote further consumption. Indeed, at cull, the Sugar rats tended to have higher blood glucose than the Chow and Caf-Sugar rats. In contrast, the Caf-Sugar rats derived more energy from solid sources of sugar and fat, which would slow gastric transition and produce greater feelings of satiety. Greater fluctuations in blood sugar can promote inflammation - this is consistent with the inflammatory changes we found in both the hippocampus and adipose tissue of Sugar rats.