Abstract
BackgroundChronic high-fat diet (HFD) consumption caused not only obese-insulin resistance, but also cognitive decline and microglial hyperactivity. Modified gut microbiota by prebiotics and probiotics improved obese-insulin resistance. However, the effects of prebiotics, probiotics, and synbiotics on cognition and microglial activity in an obese-insulin resistant condition have not yet been investigated. We aimed to evaluate the effect of prebiotic (Xyloolidosaccharide), probiotic (Lactobacillus paracasei HII01), or synbiotics in male obese-insulin resistant rats induced by a HFD.MethodsMale Wistar rats were fed with either a normal diet or a HFD for 12 weeks. At week 13, the rats in each dietary group were randomly divided into four subgroups including vehicle group, prebiotics group, probiotics group, and synbiotics group. Rats received their assigned intervention for an additional 12 weeks. At the end of experimental protocol, the cognitive functioning of each rat was investigated; blood and brain samples were collected to determine metabolic parameters and investigate brain pathology.ResultsWe found that chronic HFD consumption leads to gut and systemic inflammation and impaired peripheral insulin sensitivity, which were improved by all treatments. Prebiotics, probiotics, or synbiotics also improved hippocampal plasticity and attenuated brain mitochondrial dysfunction in HFD-fed rats. Interestingly, hippocampal oxidative stress and apoptosis were significantly decreased in HFD-fed rats with all therapies, which also decreased microglial activation, leading to restored cognitive function.ConclusionsThese findings suggest that consumption of prebiotics, probiotics, and synbiotics restored cognition in obese-insulin resistant subjects through gut-brain axis, leading to improved hippocampal plasticity, brain mitochondrial function, and decreased microglial activation.
Highlights
Chronic high-fat diet (HFD) consumption caused obese-insulin resistance, and cognitive decline and microglial hyperactivity
At week 13, the rats in each dietary group were randomly divided into four subgroups including normal diet (ND)- and HFD-fed rats oral feeding with phosphate buffer saline (PBS) as the vehicle group (NDV and HFV); ND- and HFD-fed rats oral feeding with prebiotics (10% XOS in PBS, 1 ml/day; NDPE and HFPE); ND- and HFD-fed rats oral feeding with probiotics (1 × 108 cfu of L. paracasei HII01, 1 ml/day; NDPO and HFPO), and ND- and HFD-fed rats oral feeding with 2 ml of synbiotics (a 1:1 mixture of 10% XOS and 108 cfu L. paracasei HII01; NDC and HFC)
Long-term HFD consumption induced gut dysbiosis and systemic inflammation, which was attenuated by prebiotic XOS, probiotic L. paracasei HIIO1, or synbiotics Pro-inflammatory cytokine interleukin (IL)-1 and Interleukin 6 (IL-6) mRNA expression levels were significantly increased in the colon of rats fed with a HFD compared to rats fed with a ND, whereas the immunosuppressive cytokine IL-10 mRNA level was not altered (Fig. 2a–c)
Summary
Chronic high-fat diet (HFD) consumption caused obese-insulin resistance, and cognitive decline and microglial hyperactivity. We aimed to evaluate the effect of prebiotic (Xyloolidosaccharide), probiotic (Lactobacillus paracasei HII01), or synbiotics in male obese-insulin resistant rats induced by a HFD. Growing evidence from our group have clearly demonstrated that obesity in rats, induced by long-term high-fat diet (HFD) consumption, caused peripheral insulin resistance, and brain insulin resistance, dyslipidemia, and increased oxidative stress [3]. Chronic HFD-fed rats have been shown to have the hippocampal synaptic dysfunction as indicated by the impairment of long-term potentiation (LTP) and dendritic spine loss, leading to cognitive decline [4,5,6]. Cumulative evidence showed that the modulation of gut microbiota by prebiotics and probiotics could be effective therapeutic strategies to improve obesity and insulin resistance [20]. A previous study demonstrated that 108 colony-forming unit (cfu) of the Lactobacillus paracasei HII01 could survive in the acidic environment of the gastrointestinal tract and in the presence of gastric enzymes, bile salts, and considered as a safe dose [28]
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