Regulatory Effect of Isomaltodextrin on a High-Fat Diet Mouse Model with LPS-Induced Low-Grade Chronic Inflammation

Abstract

This study aimed to identify the effects of isomaltodextrin (IMD) on sustaining the gut integrity and microbiota composition in a high-fat diet (HFD) with a lipopolysaccharide (LPS)-induced low-grade inflammation mouse model. The homeostasis of the immune response is important to reduce the risk of developing metabolic syndromes. The results of this study showed that pre-treatment of IMD at 5% (w/v) suppressed the concentration of endotoxin and pro-inflammatory mediators TNF-α, MCP-1, and IL-6 while increasing the adiponectin level in the plasma. Subsequently, IMD supplementation maintained the structural integrity and intestinal permeability by upregulating the tight junction protein expressions, leading to reducing D-mannitol concentration in the blood. In addition, dysbiosis was observed in mice induced by HFD plus LPS, suggesting that unhealthy dietary factors elicit metabolic endotoxemia and associated dysbiosis to impair the barrier function. However, IMD supplementation was shown to restore the microbial diversity, promote the growth of Bacteroides-Prevotella, and upregulate the related d-glucarate and d-galactarate degradation pathways, together demonstrating the benefits of IMD as a prebiotic able to promote energy homeostasis. Our results also showed that the blood lipid profile and glucose level in the low-grade inflammation mouse model were modulated by IMD. Moreover, IMD supplementation effectively prevented the metabolic disorder and modulated immune responses in inflamed white adipose tissues by inhibiting the macrophage infiltration and restoring the adiponectin, PPAR-γ, and IRS-1 expression. These findings provide strong evidence for IMD to be a potential prebiotic that acts to sustain a healthy gut microbiota composition and barrier function. By protecting against an unhealthy diet-impaired metabolic balance and maintaining immune homeostasis, IMD may affect the development of metabolic disorders.

Anthocyanin-Rich Butterfly Pea Flower Extract Ameliorating Low-Grade Inflammation in a High-Fat-Diet and Lipopolysaccharide-Induced Mouse Model

“…Diet-induced metabolic endotoxemia directly elicits systemic low-grade chronic inflammation by increasing the release of inflammatory mediators, which has detrimental impacts on overall health . Findings from our previous studies had demonstrated that the intake of HFD with LPS promoted the release of plasma inflammatory cytokines in mice. , Diet-induced metabolic endotoxemia can also disturb tissue immune homeostasis. In the present study, a significant elevation of plasma LPS was detected in HF mice (0.4502 ± 0.04209 EU/mL) over the NC (0.2778 ± 0.01895 EU/mL) (Figure G).…”

“…48 Findings from our previous studies had demonstrated that the intake of HFD with LPS promoted the release of plasma inflammatory cytokines in mice. 46,49 Diet-induced metabolic endotoxemia can also disturb tissue immune homeostasis. In the present study, a significant elevation of plasma LPS was detected in HF mice (0.4502 ± 0.04209 EU/mL) over the NC (0.2778 ± 0.01895 EU/mL) (Figure 2G).…”

Comprehensive analysis of key host gene-microbe networks in the cecum tissues of the obese rabbits induced by a high-fat diet

“…Studies have shown that a large amount of lipids accumulate in the intestine of obese patients, and these adipose tissues can secrete pro-inflammatory factors, such as TNF-α and IL-6 , and anti-inflammatory factor ( Adiponectin ). These pro- and anti-inflammatory factors can affect the intestinal environment and produce different types of secondary metabolites to rebalance the nutritional metabolism of gut microbiota ( Bisanz et al., 2019 ; Liu et al., 2022 ; Bodilly et al., 2023 ). Simultaneously, the different gut microbial metabolites are a major factor regulating the homeostasis of the intestinal environment.…”

Artemether Attenuates Gut Barrier Dysfunction and Intestinal Flora Imbalance in High-Fat and High-Fructose Diet-Fed Mice

“…Food, especially high-fat and high-fructose food, can cause great damage to the intestinal barrier [10]. New shreds of evidence suggest that excess fructose intake may lead to reduced intestinal tight junctions (TJs) and adherens junctions (AJs) expression, expanded intestinal permeability and microbial translocation in the lumen, and elevated lipopolysaccharide (LPS) in the circulatory system [11,12]. LPS is the main component of Gram-negative bacilli's cytoderm, and it has been shown that intestinal microbial disturbances promote the release of LPS, which in turn damages the intestinal barrier and leads to systemic chronic low-severity inflammation in the host [13][14][15].…”