Effects of combined d-fagomine and omega-3 PUFAs on gut microbiota subpopulations and diabetes risk factors in rats fed a high-fat diet

Abstract Food contains bioactive compounds that may prevent changes in gut microbiota associated with Westernized diets. The aim of this study is to explore the possible additive effects of d-fagomine and ω-3 PUFAs (EPA/DHA 1:1) on gut microbiota and related risk factors during early stages in the development of fat-induced pre-diabetes. Male Sprague Dawley (SD) rats were fed a standard diet, or a high-fat (HF) diet supplemented with d-fagomine, EPA/DHA 1:1, a combination of both, or neither, for 24 weeks. The variables measured were fasting glucose and glucose tolerance, plasma insulin, liver inflammation, fecal/cecal gut bacterial subgroups and short-chain fatty acids (SCFAs). The animals supplemented with d-fagomine alone and in combination with ω-3 PUFAs accumulated less fat than those in the non-supplemented HF group and those given only ω-3 PUFAs. The combined supplements attenuated the high-fat-induced incipient insulin resistance (IR), and liver inflammation, while increasing the cecal content, the Bacteroidetes:Firmicutes ratio and the populations of Bifidobacteriales. The functional effects of the combination of d-fagomine and EPA/DHA 1:1 against gut dysbiosis and the very early metabolic alterations induced by a high-fat diet are mainly those of d-fagomine complemented by the anti-inflammatory action of ω-3 PUFAs.

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Effect of Trilobatin from Lithocarpus polystachyus Rehd on Gut Microbiota of Obese Rats Induced by a High-Fat Diet

Nutrients ◽

10.3390/nu13030891 ◽

2021 ◽

Vol 13 (3) ◽

pp. 891

Author(s):

Hailiang Shen ◽

Linhua Huang ◽

Huating Dou ◽

Yali Yang ◽

Houjiu Wu

Keyword(s):

Gut Microbiota ◽

Metabolic Pathways ◽

High Fat Diet ◽

Liver Weight ◽

Short Chain Fatty Acids ◽

Sprague Dawley ◽

High Fat ◽

Independent Manner ◽

Bioactive Component ◽

Obese Rats

Trilobatin was identified as the primary bioactive component in the Lithocarpus polystachyus Rehd (LPR) leaves. This study explored the antiobesity effect of trilobatin from LPR leaves and its influence on gut microbiota in obese rats. Results showed that trilobatin could significantly reduce body and liver weight gain induced by a high-fat diet, and the accumulation of perirenal fat, epididymal fat, and brown fat of SD (Male Sprague–Dawley) obese rats in a dose-independent manner. Short-chain fatty acids (SCFAs) concentrations increased, especially the concentration of butyrate. Trilobatin supplementation could significantly increase the relative abundance of Lactobacillus, Prevotella, CF231, Bacteroides, and Oscillospira, and decrease greatly the abundance of Blautia, Allobaculum, Phascolarctobacterium, and Coprococcus, resulting in an increase of the ratio of Bacteroidetes to Firmicutes (except the genera of Lactobacillus and Oscillospira). The Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway predicted by the Phylogenetic Investigation of Communities by Reconstruction of Unobserved States (PICRUSt) indicated the different relative metabolic pathways after trilobatin supplementation. This study may reveal the contribution of gut microbiota to the antiobesity effect of trilobatin from LPR leaves and predict the potential regulatory mechanism for obesity induced by a high-fat diet.

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Protective effects of a unique combination of nutritionally active ingredients on risk factors and gene expression associated with atherosclerosis in C57BL/6J mice fed a high fat diet

Food & Function ◽

10.1039/d0fo02867c ◽

2021 ◽

Author(s):

Joe W. E. Moss ◽

Jessica O Williams ◽

Wijdan Al-Ahmadi ◽

Victoria O'Morain ◽

Yee-Hung Chan ◽

...

Keyword(s):

Gene Expression ◽

Risk Factors ◽

Cardiovascular Disease ◽

High Fat Diet ◽

Inflammatory Disorder ◽

Protective Effects ◽

Unique Combination ◽

Omega 3 ◽

High Fat ◽

Food Ingredients

Atherosclerosis, an inflammatory disorder of the vasculature and the underlying cause of cardiovascular disease, is responsible for one in three global deaths. Consumption of active food ingredients such as omega-3...

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High fat diet alters gut microbiota but not spatial working memory in early middle-aged Sprague Dawley rats

PLoS ONE ◽

10.1371/journal.pone.0217553 ◽

2019 ◽

Vol 14 (5) ◽

pp. e0217553 ◽

Cited By ~ 9

Author(s):

Nikita Girish Deshpande ◽

Juhi Saxena ◽

Tristan G. Pesaresi ◽

Casey Dylan Carrell ◽

Grayson Breneman Ashby ◽

...

Keyword(s):

Working Memory ◽

Gut Microbiota ◽

High Fat Diet ◽

Spatial Working Memory ◽

Sprague Dawley ◽

High Fat ◽

Middle Aged ◽

Sprague Dawley Rats

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Propensity to high-fat diet-induced obesity in rats is associated with changes in the gut microbiota and gut inflammation

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00098.2010 ◽

2010 ◽

Vol 299 (2) ◽

pp. G440-G448 ◽

Cited By ~ 485

Author(s):

Claire Barbier de La Serre ◽

Collin L. Ellis ◽

Jennifer Lee ◽

Amber L. Hartman ◽

John C. Rutledge ◽

...

Keyword(s):

Gut Microbiota ◽

High Fat Diet ◽

Relative Proportion ◽

Low Grade ◽

Sprague Dawley ◽

High Fat ◽

Intestinal Alkaline Phosphatase ◽

Sprague Dawley Rats ◽

Tlr4 Activation ◽

Fat Diets

Consumption of diets high in fat and calories leads to hyperphagia and obesity, which is associated with chronic “low-grade” systemic inflammation. Ingestion of a high-fat diet alters the gut microbiota, pointing to a possible role in the development of obesity. The present study used Sprague-Dawley rats that, when fed a high-fat diet, exhibit either an obesity-prone (DIO-P) or obesity-resistant (DIO-R) phenotype, to determine whether changes in gut epithelial function and microbiota are diet or obese associated. Food intake and body weight were monitored daily in rats maintained on either low- or high-fat diets. After 8 or 12 wk, tissue was removed to determine adiposity and gut epithelial function and to analyze the gut microbiota using PCR. DIO-P but not DIO-R rats exhibit an increase in toll-like receptor (TLR4) activation associated with ileal inflammation and a decrease in intestinal alkaline phosphatase, a luminal enzyme that detoxifies lipopolysaccharide (LPS). Intestinal permeability and plasma LPS were increased together with phosphorylation of myosin light chain and localization of occludin in the cytoplasm of epithelial cells. Measurement of bacterial 16S rRNA showed a decrease in total bacterial density and an increase in the relative proportion of Bacteroidales and Clostridiales orders in high-fat-fed rats regardless of phenotype; an increase in Enterobacteriales was seen in the microbiota of DIO-P rats only. Consumption of a high-fat diet induces changes in the gut microbiota, but it is the development of inflammation that is associated with the appearance of hyperphagia and an obese phenotype.

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Palmitoleic Acid (N-7) Attenuates the Immunometabolic Disturbances Caused by a High-Fat Diet Independently of PPARα

Mediators of Inflammation ◽

10.1155/2014/582197 ◽

2014 ◽

Vol 2014 ◽

pp. 1-12 ◽

Cited By ~ 26

Author(s):

Camila O. Souza ◽

Alexandre A. S. Teixeira ◽

Edson A. Lima ◽

Helena A. P. Batatinha ◽

Lara M. Gomes ◽

...

Keyword(s):

Insulin Resistance ◽

Oleic Acid ◽

High Fat Diet ◽

Palmitoleic Acid ◽

Serum Levels ◽

Standard Diet ◽

Liver Inflammation ◽

Wild Type ◽

High Fat

Palmitoleic acid (PMA) has anti-inflammatory and antidiabetic activities. Here we tested whether these effects of PMA on glucose homeostasis and liver inflammation, in mice fed with high-fat diet (HFD), are PPAR-αdependent. C57BL6 wild-type (WT) and PPAR-α-knockout (KO) mice fed with a standard diet (SD) or HFD for 12 weeks were treated after the 10th week with oleic acid (OLA, 300 mg/kg of b.w.) or PMA 300 mg/kg of b.w. Steatosis induced by HFD was associated with liver inflammation only in the KO mice, as shown by the increased hepatic levels of IL1-beta, IL-12, and TNF-α; however, the HFD increased the expression of TLR4 and decreased the expression of IL1-Ra in both genotypes. Treatment with palmitoleate markedly attenuated the insulin resistance induced by the HFD, increased glucose uptake and incorporation into muscle in vitro, reduced the serum levels of AST in WT mice, decreased the hepatic levels of IL1-beta and IL-12 in KO mice, reduced the expression of TLR-4 and increased the expression of IL-1Ra in WT mice, and reduced the phosphorylation of NF𝜅B (p65) in the livers of KO mice. We conclude that palmitoleate attenuates diet-induced insulin resistance, liver inflammation, and damage through mechanisms that do not depend on PPAR-α.

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Effects of a Long-Term High-Fat Diet and Switching from a High-Fat to Low-Fat, Standard Diet on Hepatic Fat Accumulation in Sprague-Dawley Rats

Digestive Diseases and Sciences ◽

10.1007/s10620-008-0303-1 ◽

2008 ◽

Vol 53 (12) ◽

pp. 3206-3212 ◽

Cited By ~ 20

Author(s):

Katsuhisa Omagari ◽

Shigeko Kato ◽

Koichi Tsuneyama ◽

Chisato Inohara ◽

Yu Kuroda ◽

...

Keyword(s):

High Fat Diet ◽

Standard Diet ◽

Sprague Dawley ◽

High Fat ◽

Low Fat ◽

Fat Accumulation ◽

Sprague Dawley Rats ◽

Hepatic Fat

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Obesity-Related Metabolome and Gut Microbiota Profiles of Juvenile Göttingen Minipigs—Long-Term Intake of Fructose and Resistant Starch

Metabolites ◽

10.3390/metabo10110456 ◽

2020 ◽

Vol 10 (11) ◽

pp. 456

Author(s):

Mihai V. Curtasu ◽

Valeria Tafintseva ◽

Zachary A. Bendiks ◽

Maria L. Marco ◽

Achim Kohler ◽

...

Keyword(s):

Fatty Acids ◽

Gut Microbiota ◽

Resistant Starch ◽

High Fat Diet ◽

Short Chain Fatty Acids ◽

Short Chain ◽

High Fat ◽

Obesity And Diabetes ◽

Ad Libitum ◽

Chain Fatty Acids

The metabolome and gut microbiota were investigated in a juvenile Göttingen minipig model. This study aimed to explore the metabolic effects of two carbohydrate sources with different degrees of risk in obesity development when associated with a high fat intake. A high-risk (HR) high-fat diet containing 20% fructose was compared to a control lower-risk (LR) high-fat diet where a similar amount of carbohydrate was provided as a mix of digestible and resistant starch from high amylose maize. Both diets were fed ad libitum. Non-targeted metabolomics was used to explore plasma, urine, and feces samples over five months. Plasma and fecal short-chain fatty acids were targeted and quantified. Fecal microbiota was analyzed using genomic sequencing. Data analysis was performed using sparse multi-block partial least squares regression. The LR diet increased concentrations of fecal and plasma total short-chain fatty acids, primarily acetate, and there was a higher relative abundance of microbiota associated with acetate production such as Bacteroidetes and Ruminococcus. A higher proportion of Firmicutes was measured with the HR diet, together with a lower alpha diversity compared to the LR diet. Irrespective of diet, the ad libitum exposure to the high-energy diets was accompanied by well-known biomarkers associated with obesity and diabetes, particularly branched-chain amino acids, keto acids, and other catabolism metabolites.

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Supplementation with Sodium Butyrate Modulates the Composition of the Gut Microbiota and Ameliorates High-Fat Diet-Induced Obesity in Mice

Journal of Nutrition ◽

10.1093/jn/nxy324 ◽

2019 ◽

Vol 149 (5) ◽

pp. 747-754 ◽

Cited By ~ 15

Author(s):

Wanjun Fang ◽

Hongliang Xue ◽

Xu Chen ◽

Ke Chen ◽

Wenhua Ling

Keyword(s):

Gut Microbiota ◽

Chronic Inflammation ◽

Sodium Butyrate ◽

High Fat Diet ◽

Body Weight Gain ◽

Principal Component ◽

Short Chain Fatty Acids ◽

Low Grade ◽

Microbiota Composition ◽

High Fat

ABSTRACT Background Short-chain fatty acids (SCFAs) have been reported to ameliorate obesity. However, the underlying mechanisms require further investigation. Objective The aim of this study was to determine the role of butyrate, an SCFA, in the regulation of obesity, low-grade chronic inflammation, and alterations of microbiota composition in mice. Methods Male C57BL/6J mice, 4–5 wk of age, were divided into 3 groups (n = 8 mice/group): low-fat diet (LFD; 10% energy from fat), high-fat diet (HFD; 45% energy from fat), or high-fat diet plus sodium butyrate (HSB). HSB mice received sodium butyrate at a concentration of 0.1 M in drinking water for 12 wk. Measures of inflammation, obesity, and intestinal integrity were assessed. Serum lipopolysaccharide (LPS) concentrations were measured in the 3 groups. Fecal samples were collected for gut microbiota analysis. Results In HFD mice, body weight gain and hepatic triglyceride (TG), serum interleukin-6 (IL-6), and serum tumor necrosis factor (TNF)-α levels were 1–4 times higher than those in LFD mice (P < 0.05); they were 34–42% lower in HSB mice compared with HFD mice (P < 0.05). The HFD group had 28%–48% lower mRNA expression of both Tjp1 and Ocln in the ileum and colon compared with levels in LFD or HSB mice (P < 0.05), whereas there was no difference in expression levels between LFD and HSB mice. Furthermore, in HSB mice, serum LPS concentration was 53% lower compared with that in HFD mice but still 23% higher than that in LFD mice (P < 0.05). Results from principal component analysis showed that HSB and LFD mice had a similar gut microbiota structure, which was significantly different from that in HFD mice (P < 0.05). Conclusions Sodium butyrate administration beneficially changed HFD-induced gut microbiota composition and improved intestinal barrier, leading to lower serum LPS concentrations. These changes may correspond with improvements in obesity-related lipid accumulation and low-grade chronic inflammation.

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