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[Display omitted] • DHA improves systemic glucose metabolism disorders. • DHA prevents hippocampal neuroinflammation. • DHA attenuates hippocampal oxidative stress. • DHA inhibits hippocampal amyloid formation and Tau phosphorylation. • DHA ameliorates hippocampal insulin resistance. • DHA improves cognitive function. Diminished brain insulin sensitivity is associated with reduced cognitive function. Docosahexaenoic acid (DHA) is known to maintain normal brain function. This study aimed to determine whether DHA impacts hippocampal insulin sensitivity and cognitive function in aged rats fed a high-fat diet (HFD). Eight-month-old female Sprague-Dawley rats were randomly divided into three groups (n = 50 each). Rats in the aged group, HFD group, and DHA treatment group received standard diet (10 kcal% fat), HFD (45 kcal% fat), and DHA-enriched HFD (45 kcal% fat, 1% DHA, W/W) for 10 months, respectively. Four-month-old female rats (n = 40) that received a standard diet served as young controls. Neuroinflammation, oxidative stress, amyloid formation, and tau phosphorylation in the hippocampus, as well as systemic glucose homeostasis and cognitive function, were tested. DHA treatment relieved a block in the insulin signaling pathway and consequently protected aged rats against HFD-induced hippocampal insulin resistance. The beneficial effects were explained by a DHA-induced decrease in systemic glucose homeostasis dysregulation, hippocampal neuroinflammation and oxidative stress. In addition, DHA treatment broke the reciprocal cycle of hippocampal insulin resistance, Aβ burden, and tau hyperphosphorylation. Importantly, treatment of model rats with DHA significantly increased their cognitive capacity, as evidenced by their increased hippocampal-dependent learning and memory, restored neuron morphology, enhanced cholinergic activity, and activated cyclic AMP-response element-binding protein. DHA improves cognitive function by enhancing hippocampal insulin sensitivity. [ABSTRACT FROM AUTHOR]

Abstract High-fat diet (HFD) consumption induces oxidative stress and microbial dysbiosis, the latter of which plays a vital role in the development of metabolic syndrome. We hypothesized that sinapic acid and resveratrol treatment might be a potential strategy to ameliorate the redox state and gut microbiota composition imbalance. In this study, rats were randomised into five groups and fed a high-fat diet supplemented with resveratrol (400 mg/kg), sinapic acid (200 mg/kg) or a combination of both polyphenols. Administration of resveratrol effectively reduced fasting blood glucose levels (p < 0.05) and increased the HDL-c levels (p < 0.05). Reactive oxygen species and malondialdehyde levels were decreased in the colon (p < 0.05), total antioxidant capacity was increased in liver (p < 0.05) by sinapic acid consumption in HFD rats. Moreover, polyphenol supplementation impacted the intestinal microbiome at different taxonomic levels by improving the proportion of butyrate producer Blautia (p < 0.05) and Dorea (p < 0.01) in the Lachaospiraceae family and inhibiting the growth of bacterial species associated with diseases and inflammation such as Bacteroides (p < 0.05) and Desulfovibrionaceaesp (p < 0.01). Spearman correlation analysis showed that some oxidative stress variables were directly correlated with changes in gut microbiota. Our findings demonstrated qualitative differences between the treatments in their abilities to alleviate HFD-induced oxidative stress and modulate the gut microbiota. These findings might be helpful to better understand the effects of bioactive constituents on nutrition for human health. Graphical abstract Unlabelled Image Highlights • Resveratrol and sinapic acid can ameliorate the redox state in HFD rats. • Polyphenols consumption can modulate the gut microbiota without changing the Firmicutes / Bacteroidetes ratio. • The suppression of oxidative stress by two Polyphenols was associated with improved diversity of the gut microbiota. [ABSTRACT FROM AUTHOR]

Brain insulin resistance, induced by neuroinflammation and oxidative stress, contributes to neurodegeneration, that is, processes that are associated with Aβ accumulation and TAU hyperphosphorylation. Here, we tested the effect of chronic administration of melatonin (MLT) on brain insulin resistance and cognition deficits caused by a high‐fat diet (HFD) in aged rats. Results showed that MLT supplementation attenuated peripheral insulin resistance and lowered hippocampal oxidative stress levels. Activated microglia and astrocytes and hippocampal levels of TNF‐α in HFD‐fed rats were reduced by MLT treatment. Melatonin also prevented HFD‐induced increases in beta‐amyloid (Aβ) accumulation and TAU phosphorylation in the hippocampus. In addition, impairments of brain insulin signaling elicited by long‐term HFD were restored by MLT treatment, as confirmed by ex vivo insulin stimulation. Importantly, MLT reversed HFD‐induced cognitive decline as measured by a water maze test, normalized hippocampal LTP and restored CREB activity and BDNF levels as well as cholinergic neuronal activity in the hippocampus. Collectively, these findings indicate that MLT may exhibit substantial protective effects on cognition, via restoration of brain insulin signaling. [ABSTRACT FROM AUTHOR]

• Flaxseed polysaccharide supplementation ameliorated the metabolic syndrome in HFD mice. • Flaxseed polysaccharide supplementation increased the proportion of Akkermansia and Bifidobacterium. • The improvement of lipid metabolism disorder was associated with the modulation of the gut microbiota. Flaxseed (Linum usitatissimum L.) is known as healthy food for its anti-obesity and lipid modulating properties. However, the effects of flaxseed polysaccharide (FSP) on metabolic syndrome (MetS) and gut microbiota are still poorly understood. Here, we investigated the effects of FSP on lipid metabolism and gut microbiota in high-fat-diet-fed mice. FSP effectively reduced the serum fasting glucose, total triglyceride and total cholesterol levels. FSP consumption adipose accumulation impacted the gut microbiome at different taxonomic levels by increasing the proportions of beneficial Akkermansia and Bifidobacterium and decreasing the disease or obesity associated Oscillospira and Odoribacteraceae. These changes were highly correlated with the regulation of expression levels of lipid metabolism involved genes in the liver. The restoration of total SCFAs, especially propionate and butyrate might be an important strategy for mitigating HFD induced metabolic disorders. These findings suggest that FSP may use as a prebiotic for preventing MetS by modulating the gut microbiota. [ABSTRACT FROM AUTHOR]