The gut microbiota is directly influenced by dietary components, and it plays critical roles in chronic diseases. Excessive consumption of trans-fatty acids (TFA) is associated with obesity induced by alterations in gut microbiota, but the links between obesity and gut microbiota remain unclear. Therefore, studies examining the impact of TFA on intestinal microflora are essential. In our study, we performed 16S ribosomal RNA gene sequencing on faecal samples from Sprague–Dawley rats fed a basal diet (control (CON) group), high-fat (HF) diet (diet-induced obesity (DIO) group) or TFA diets (1 % TFA group and 8 % TFA group) for 8 weeks to investigate the effects of TFA/HF diets on obesity and gut microbiota composition. We found that the TFA/HF diets significantly induced obesity and changes in blood and brain physiological parameters of the rats. The relative abundance of the phyla Firmicutes and Bacteroidetes was inversely altered in the three test groups compared with the CON group. Proteobacteria increased slightly in the DIO, 1 % TFA and 8 % TFA groups. The genus Bacteroides increased in the DIO and 1 % TFA groups, but Muribaculaceae decreased in all experimental groups compared with the CON group. Moreover, significant differences were observed among clusters of orthologous group functional categories of the four dietary groups. Our observations suggested that the TFA/HF diets induced obesity and dysfunction of gut microbiota. Gut dysbiosis might mediate the obesity effects of TFA/HF diets.

Previous studies have demonstrated that 27‐hydroxycholesterol (27‐OHC), a cholesterol metabolite, was involved in the inflammatory process of Alzheimer's disease (AD). The present study aimed to investigate the 27‐OHC‐induced inflammatory damage to neurons and astrocytes and the underlying mechanism(s) accounting for this damage. Human neuroblastoma cells (SH‐SY5Y cells) and rat glioma cells (C6 cells) were treated with vehicle or 27‐OHC (5, 10, or 20 μM) for 24 hr. The levels of secreted interleukin‐1β (IL‐1β), interleukin‐10 (IL‐10), tumor necrosis factor alpha (TNF‐α), and inducible nitric oxide synthase (iNOS) were determined by using an enzyme‐linked immunosorbent assay (ELISA). Immunofluorescence staining was used to determine the cellular expression of toll‐like receptor 4 (TLR4) and transforming growth factor‐β (TGF‐β). The mRNA and protein expression levels of nuclear factor‐κB p65 (NF‐κB p65), nuclear factor‐κB p50 (NF‐κB p50) and cyclooxygenase‐2 (COX‐2) in both SH‐SY5Y and C6 cells were also detected by real‐time PCR and Western blot, respectively. The results of this study showed that 27‐OHC treatment increased secretion of TNF‐α and iNOS and decreased secretion of IL‐10, upregulated expression of TGF‐β, NF‐κB p65 and p50, and downregulated expression of COX‐2 in SH‐SY5Y cells. In C6 cells, treatment with 27‐OHC resulted in decreased secretion of IL‐1β, IL‐10, TNF‐α, and iNOS, and increased expression of TLR4 and TGF‐β. These results suggest that 27‐OHC may cause inflammatory damage to neurons by activating the TGF‐β/NF‐κB signaling pathway and to astrocytes by activating the TLR4/TGF‐β signaling, which results in the subsequent release of inflammatory cytokines.

Obesity increases the risk of cognitive impairment and dementia, and the gut microbiota can affect brain cognitive function and obesity through a variety of pathways such as the gut-brain axis. This study aimed to discover how fatty acid affect cognitive function by regulating intestinal flora in obesity. Obese subjects were recruited for cognitive function assessment, and participants were divided into obese group with cognitive impairment (MCI, n = 49) and obese cognitively normal group (Non_MCI, n = 55). In the erythrocyte membrane, the proportion of polyunsaturated fatty acids (PUFA), linoleic acid (C18:2 n-6) and arachidonic acid (C20:4 n-6) and n-6/n-3 ratio was higher in the MCI group than in the Non_MCI group. However, the α-linolenic acid (C18:3 n-3) percentage of the erythrocyte membrane was lower in the MCI group. We found that Coriobacteriales_Incertae_Sedis was positively correlated with erythrocyte membrane C20:4 n-6 and n-6 PUFA and negatively correlated with cognitive scores in obese patients. In addition, several of the functional pathways we predicted were significantly different in the MCI and Non_MCI groups. Higher levels of n-6/n-3 polyunsaturated fatty acids ratio in the erythrocyte membranes may influence the inflammatory response in the organism causing obesity induced cognitive damage. Moreover, high levels of n-6/n-3 polyunsaturated fatty acids ratio may also affect the intestinal flora of obese patients, which in turn may affect the cognitive function of obese patients.

(2019). The association of blood non-esterified fatty acid, saturated fatty acids, and polyunsaturated fatty acids levels with mild cognitive impairment in Chinese population aged 35–64 years: a cross-sectional study. Nutritional Neuroscience. Ahead of Print.