Effect of a High-Fat Diet on the Small-Intestinal Environment and Mucosal Integrity in the Gut-Liver Axis (original) (raw)
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International Journal of Molecular Sciences, 2018
Development of non-alcoholic fatty liver disease (NAFLD) is linked to obesity, adipose tissue inflammation, and gut dysfunction, all of which depend on diet. So far, studies have mainly focused on diet-related fecal microbiota changes, but other compartments may be more informative on host health. We present a first systematic analysis of microbiota changes in the ileum and colon using multiple diets and investigating both fecal and mucosal samples. Ldlr−/−.Leiden mice received one of three different energy-dense (ED)-diets (n = 15/group) for 15 weeks. All of the ED diets induced obesity and metabolic risk factors, altered short-chain fatty acids (SCFA), and increased gut permeability and NAFLD to various extents. ED diets reduced the diversity of high-abundant bacteria and increased the diversity of low-abundant bacteria in all of the gut compartments. The ED groups showed highly variable, partially overlapping microbiota compositions that differed significantly from chow. Correlat...
Journal of Nutrition, 2013
High-fat (HF) diets can produce obesity and have been linked to the development of nonalcoholic fatty liver disease and changes in the gut microbiome. To test the hypothesis that HF feeding increases certain predominant hind gut bacteria and development of steatohepatitis, C57BL/6 mice were fed an HF (45% energy) or low-fat (LF) (10% energy) diet for 10 wk. At the end of the feeding period, body weights in the HF group were 34% greater than those in the LF group (P < 0.05). These changes were associated with dramatic increases in lipid droplet number and size, inflammatory cell infiltration, and inducible nitric oxide (NO) synthase protein concentration in the livers of mice fed the HF diet. Consistent with the fatty liver phenotype, plasma leptin and tumor necrosis factor-a concentrations were also elevated in mice fed the HF diet, indicative of chronic inflammation. Eight of 12 pairs of polymerase chain reaction (PCR) primers for bacterial species that typically predominate hind gut microbial ecology generated specific PCR products from the fecal DNA samples. The amount of DNA from Lactobacillus gasseri and/or Lactobacillus taiwanensis in the HF group was 6900-fold greater than that in the LF group. Many of these bacteria are bile acid resistant and are capable of bile acid deconjugation. Because bile acids are regulators of hepatic lipid metabolism, the marked increase of gut L. gasseri and/or L. taiwanensis species bacteria with HF feeding may play a role in development of steatohepatitis in this model.
Lipids, 2019
Energy-dense foods can alter gut microbial diversity. However, the physiological effects of dietinduced microbial changes on the development of nonalcoholic fatty liver disease (NAFLD) remain debatable. We hypothesized that high-fat intake for 6 weeks would promote intestinal dysbiosis by increasing grampositive bacteria, inducing the intestinal production of proinflammatory cytokines and subsequent hepatic lipid infiltration in young male rats. Six-week old male Sprague-Dawley rats were divided into two groups and fed either a standard rodent chow or a 60% high-fat diet (HFD) for 6 weeks. Chromogenic endotoxin quantification assays indicate an increase in lipopolysaccharide concentration in the plasma of HFD rats (p = 0.032). Additionally, Western blot analyses of the cecum showed significantly greater protein expression of the transcription factor, nuclear factor kappa B (NF-kB), (p = 0.037) and the proinflammatory cytokine, interleukin-1β (IL-1β), (p = 0.042) in rats fed HFD. Linear discriminate analysis of effect size (LEfSe) showed greater abundance of Firmicutes and Actinobacteria in the samples collected from the cecum of HFD rats compared to chow. Consistent with the development of steatosis, the Oil-RedO stained area was increased in liver sections from HFD rats. Hepatic triacylglycerol concentrations (p < 0.001) and plasma alanine aminotransferase (p < 0.001) were significantly increased in HFD-fed animals compared to chow. These findings show that a short duration of high-fat consumption can have profound deleterious effects on gastrointestinal health and the inflammatory state of these young male Sprague-Dawley rats. Keywords Gut microbiome Á High-fat diet Á Inflammation Á Intestinal dysbiosis Á Steatosis Lipids (2019).
American journal of physiology. Gastrointestinal and liver physiology, 2015
A causal relationship between the pathophysiological changes in the gut epithelium, altered gut microbiota with the onset of obesity have been suggested, but not defined. The aim of this study was to determine the temporal relationship between impaired intestinal barrier function and microbial dysbiosis in the small and large intestine in rodent high-fat (HF) diet-induced obesity. Rats were fed HF diet (45% fat) or normal chow (C, 10% fat) for 1, 3 or 6 weeks; food intake, body weight and adiposity were measured. Barrier function ex vivo, using FITC-labelled dextran (4,000 kDa, FD-4) and horseradish peroxidase (HRP) probes in Ussing chambers, gene expression, and gut microbial communities were assessed. After one week, there was an immediate but reversible increase in paracellular permeability, decrease in IL10 expression, and decrease in abundance of genera within the class Clostridia in the ileum. In the large intestine, HRP flux and abundance of genera within the order Bacteroida...
Nutrients
Several studies have observed that gut microbiota can play a critical role in nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) development. The gut microbiota is influenced by different environmental factors, which include diet. The aim of the present review is to summarize the information provided in the literature concerning the impact of changes in gut microbiota on the effects which dietary fat has on liver steatosis in rodent models. Most studies in which high-fat feeding has induced steatosis have reported reduced microbiota diversity, regardless of the percentage of energy provided by fat. At the phylum level, an increase in Firmicutes and a reduction in Bacteroidetes is commonly found, although widely diverging results have been described at class, order, family, and genus levels, likely due to differences in experimental design. Unfortunately, this fact makes it difficult to reach clear conclusions concerning the specific microbiota patterns ...
Intestinal Dysbiosis and Non-Alcoholic Fatty Liver Disease
Human Microbiome
Non-alcoholic fatty liver disease (NAFLD) affects 20–30% of the population, with an increased prevalence in industrialized regions. Some patients with NAFLD develop an inflammatory condition termed non-alcoholic steatohepatitis (NASH) that is characterized by hepatocellular injury, innate immune cell-mediated inflammation, and progressive liver fibrosis. In clinical practice, abdominal imaging, which reveals hepatic steatosis, is sufficient for NAFLD diagnosis if other diseases have been rejected. However, a liver biopsy is needed to differentiate NASH from simple steatosis. Therapeutic strategies used to treat obesity and metabolic syndrome improve NAFLD, but there is no specific treatment effective for NASH. The gut microbiota (GM) is composed of millions of microorganisms. Changes in the GM have a significant impact on host health. Intestinal dysbiosis is an imbalance in the GM that can induce increased permeability of the epithelial barrier, with migration of GM-derived mediator...
Intestinal Microbiome Shifts, Dysbiosis, Inflammation, and Non-alcoholic Fatty Liver Disease
Frontiers in microbiology, 2018
Adverse fluctuations in the distribution of the intestinal microbiome cohort has been associated with the onset of intra- and extra-intestinal inflammatory conditions, like the metabolic syndrome (MetS) and it's hepatic manifestation, non-alcoholic fatty liver disease (NAFLD). The intestinal microbial community of obese compared to lean subjects has been shown to undergo configurational shifts in various genera, including but not limited to increased abundances of , and and decreased levels of , and genera. At the phylum level, decreased and increased have been reported. The intestinal microbiota therefore presents an important target for designing novel therapeutic modalities that target extra-intestinal inflammatory disorders, such as NAFLD. This review hypothesizes that disruption of the intestinal-mucosal macrophage interface is a key factor in intestinal-liver axis disturbances. Intestinal immune responses implicated in the manifestation, maintenance and progression of NAFL...
Gut Microbiota: The Missing Link in Obesity Induced Nonalcoholic Liver Disease
Background and objective: Recent research has elucidated a close association between intestinal microbiota, obesity, insulin resistance and nonalcoholic hepatic injury. Various studies have also indicated an increase in hepatic marker enzymes in obesity. Hence, this study aims to evaluate the association of gut microbiota with obesity, insulin resistance and hepatic marker enzymes. Material and Method: This case-control study was conducted during March 2015 to October 2016 At S.C.B Medical College, Cuttack, Odisha. The study included 186 subjects (86 irritable bowel syndrome patients as per the Rome III criteria and hundred matched controls). Plasma fasting glucose, serum lipid profile, hepatic marker enzymes were analysed by commercial kits adapted to automated clinical chemistry analyser and serum fasting insulin was estimated by kits adapted to Lisa Scan. Observation: Compared to controls the Irritable bowel syndrome patients had significantly higher Body mass index (20.9± 5.6 vs 30.1±0.22), Waist-hip ratio (0.9 ± 0.11 vs 1.02 ± 0.06), lipid profile, hepatic marker enzymes and insulin resistance. Conclusion: IBS patients were obese, and exhibited dyslipidemia, insulin resistance, elevated hepatic enzymes suggesting development of NAFLD.