Dietary saturated fat and monounsaturated fat have reversible effects on brain function and the secretion of pro-inflammatory cytokines in young women.

BACKGROUND: Previous literature suggests that a higher ratio of palmitic acid (PA)/oleic acid (OA) in the diet induces inflammation, which may result in deficient brain insulin signaling, and, secondarily, impaired physical activity, sleep efficiency, and cognitive functioning. OBJECTIVE: We hypothesized that lowering the typical dietary PA/OA would affect the activation of relevant brain networks during a working memory task and would also lower secretion of pro-inflammatory cytokines. DESIGN: In 12 female subjects participating in a randomized, cross-over trial comparing 3-week high PA diet (HPA) and low PA and a high OA diet (HOA), we evaluated functional magnetic resonance imaging (fMRI) using an N-back test of working memory, cytokine secretion by lipopolysaccharide (LPS)-stimulated peripheral blood mononuclear cells (PBMC), and plasma cytokine concentrations. RESULTS: Brain activation during the HPA diet compared to the HOA diet was increased in regions of the basal ganglia including the caudate and putamen (p<0.005). In addition, compared to the HOA diet, during the HPA diet, the plasma concentrations of IL-6 (p=0.04) and IL-1ß (p=0.05) were higher, and there was a higher secretion of IL-18 (p=0.015) and a trend for higher IL-1ß secretion (p=0.066) from LPS-stimulated PBMCs. CONCLUSIONS: The HPA diet resulted in increased brain activation in the basal ganglia compared to the HOA diet as well as increased secretion of pro-inflammatory cytokines. These data provide evidence that short-term (2week) diet interventions impact brain network activation during a working memory task and that these effects are reversible since the order of the study diets was randomized. These data are consistent with the hypothesis that lowering the dietary PA content via substitution with OA also could affect cognition.

Dietary interventions for metabolic syndrome: role of modifying dietary fats.

In humans, insulin sensitivity is relatively impaired by diets that are low in oleic acid (OA), a cis monounsaturated fatty acid (MUFA), or rich in trans MUFA or palmitic acid (PA), a saturated fatty acid (FA). Emerging evidence exists that PA, in contrast to OA, causes insulin resistance via stimulation of inflammatory signaling and production of cytosolic lipid compounds (diacylglycerol and ceramide), leading one to presume that dietary or pharmacologic maneuvers that facilitate transport of FA into the mitochondria would be beneficial. However, in some models, insulin resistance is caused by excessive FA transport into the mitochondria, coupled with deficient electron transport and possibly increased reactive oxygen species formation; PA may impair electron transport via effects on gene expression. A research challenge is to determine whether feeding humans diets with markedly different contents of PA and OA would alter insulin sensitivity and/or critical biochemical mechanisms impacting muscle insulin signaling.