scholarly journals Polymannuronic acid ameliorated obesity and inflammation associated with a high-fat and high-sucrose diet by modulating the gut microbiome in a murine model

2017 ◽  
Vol 117 (9) ◽  
pp. 1332-1342 ◽  
Author(s):  
Fang Liu ◽  
Xiong Wang ◽  
Hongjie Shi ◽  
Yuming Wang ◽  
Changhu Xue ◽  
...  

AbstractPolymannuronic acid (PM), one of numerous alginates isolated from brown seaweeds, is known to possess antioxidant activities. In this study, we examined its potential role in reducing body weight gain and attenuating inflammation induced by a high-fat and high-sucrose diet (HFD) as well as its effect on modulating the gut microbiome in mice. A 30-d PM treatment significantly reduced the diet-induced body weight gain and blood TAG levels (P<0·05) and improved glucose tolerance in male C57BL/6J mice. PM decreased lipopolysaccharides in blood and ameliorated local inflammation in the colon and the epididymal adipose tissue. Compared with low-fat and low-sucrose diet (LFD), HFD significantly reduced the mean number of species-level operational taxonomic units (OTU) per sample as well as species richness (P<0·05) but did not appear to affect other microbial diversity indices. Moreover, compared with LFD, HFD altered the abundance of approximately 23 % of the OTU detected (log10 linear discriminant analysis (LDA) score>2·0). PM also had a profound impact on the microbial composition in the gut microbiome and resulted in a distinct microbiome structure. For example, PM significantly increased the abundance of a probiotic bacterium, Lactobacillus reuteri (log10 LDA score>2·0). Together, our results suggest that PM may exert its immunoregulatory effects by enhancing proliferation of several species with probiotic activities while repressing the abundance of the microbial taxa that harbor potential pathogens. Our findings should facilitate mechanistic studies on PM as a potential bioactive compound to alleviate obesity and the metabolic syndrome.

Appetite ◽  
2001 ◽  
Vol 37 (3) ◽  
pp. 253-254 ◽  
Author(s):  
S. Goodson ◽  
J.C.G. Halford ◽  
H.C. Jackson ◽  
J.E. Blundell

1997 ◽  
Vol 272 (4) ◽  
pp. R1264-R1270 ◽  
Author(s):  
M. J. Pagliassotti ◽  
T. J. Horton ◽  
E. C. Gayles ◽  
T. A. Koppenhafer ◽  
T. D. Rosenzweig ◽  
...  

To examine the relationship between insulin action and body weight regulation in male rats, the following studies were performed. In study 1, rats (n = 31) were fed a low-fat diet (LFD) for 4 wk, and then glucose kinetics were estimated under basal and hyperinsulinemic conditions using the glucose clamp. After clamps, these same rats were placed on a high-fat diet (HFD) for 5 wk. In study 2, rats (n = 30) were fed an LFD for 3 wk and then a high-sucrose diet for 1 wk to produce selective hepatic insulin resistance. Clamps were then performed, and after clamps, these same rats were placed on an HFD for 5 wk. In study 3, rats (n = 30) were fed an LFD for 1 wk and then a high-sucrose diet for 3 wk to produce widespread insulin resistance. Clamps were then performed, and after clamps, these same rats were placed on an HFD for 5 wk. The rate of glucose appearance (R(a)) during the hyperinsulinemic clamps was the only pre-HFD variable that correlated (r = 0.49, P < 0.01 in study 1; r = 0.51, P < 0.001 in study 2) with weight gain on the HFD. Clamp R(a) also correlated with energy intake on the HFD in study 1 (r = 0.64, P < 0.001) and study 2 (r = 0.59, P < 0.001). Clamp R(a) and energy intake on the HFD accounted for similar portions of the variance in body weight gain on the HFD. Weight gain and fat-pad mass were increased (P < 0.05) in study 2 compared with study 1. In study 3, pre-HFD glucose kinetics were not correlated with energy intake or weight gain on the HFD. Widespread insulin resistance did not significantly reduce the rate of weight gain on the HFD. Thus insulin action on R(a) can influence body weight gain on an HFD. The effects of R(a) on body weight gain appear to be mediated via effects on energy intake. Selective hepatic insulin resistance can increase body weight gain on an HFD, but widespread insulin resistance does not significantly reduce HFD-induced weight gain.


2020 ◽  
pp. 1-15 ◽  
Author(s):  
Caroline M. Daly ◽  
Juhi Saxena ◽  
Jagroop Singh ◽  
Meghan R. Bullard ◽  
Emma O. Bondy ◽  
...  

2020 ◽  
Author(s):  
Fei Huang ◽  
Ruozhi Zhao ◽  
Mi Xia ◽  
Garry Shen

Abstract Background Type 2 Diabetes (T2D) has become one of most common and harmful chronic diseases worldwide. T2D is characterized as insulin resistant and is often associated with unhealthy dietary habits. The present study assessed the effects of freeze-dried Saskatoon berry powder (SBp) and cyanidin-3-glucoside (C3G, an anthocyanin enriched in SBp) on metabolism, inflammatory markers and gut microbiota in high fat-high sucrose diet (HFHS) diet induced insulin resistant mice. Results Male C57 BL/6J mice received control, HFHS, HFHS + SBp (8.0 g/kg body weight/day) or HFHS + C3G (7.2 mg/kg/day, equal amount of C3G in 8.0 g/kg/day SBp) diet for 11 weeks. HFHS diet significantly increased the levels of glucose, cholesterol, triglycerides, insulin resistance and inflammatory mediators in plasma. The results of 16S rRNA gene sequencing demonstrated that HFHS diet increased the ratio of Bacteroidetes/Firmicutes (B/F) phylum bacteria and an elevated abundance of Muriculaceae family bacteria in the feces of mice. SBp or C3G supplementation attenuated HFHS diet-induced disorders in metabolism and inflammatory markers, and increased B/F ratio and Muriculaceae abundance in mouse gut compared to HFHS diet alone. The abundance of Muriculaceae in the gut microbiota negatively correlated with body weight, glucose, lipids, insulin resistance and inflammatory mediators in mice. The results of functional predication analysis suggest that HFHS diet upregulated the genes of gut bacteria involved in inflammation-related cellular processes, and inhibited bacteria involved in metabolism. SBp and C3G partially neutralized the alterations induced by HFHS diet in gut microbiota implicated in metabolism or inflammation. Conclusion The findings of the present study suggest that SBp is a potential prebiotic food mitigating Western diet-induced disorders in metabolism, inflammation and gut dysbiosis, and C3G possibly contributes to the beneficial effects of SBp.


2018 ◽  
Vol 7 (1) ◽  
pp. 159-168 ◽  
Author(s):  
Shane M Regnier ◽  
Andrew G Kirkley ◽  
Daniel Ruiz ◽  
Wakanene Kamau ◽  
Qian Wu ◽  
...  

Emerging evidence implicates environmental endocrine-disrupting chemicals (EDCs) in the pathogenesis of metabolic diseases such as obesity and diabetes; however, the interactions between EDCs and traditional risk factors in disease pathogenesis remain incompletely characterized. The present study interrogates the interaction of the EDC tolylfluanid (TF) and traditional dietary stressors in the promotion of metabolic dysfunction. Eight-week-old male C57BL/6 mice were fed a high-fat, high-sucrose diet (HFHSD) or a high-sucrose diet (HSD), with or without TF supplementation at 100 μg/g, for 12 weeks. Food intake, body weight and visceral adiposity were quantified. Glucose homeostasis was interrogated by intraperitoneal glucose and insulin tolerance tests at 9 and 10 weeks of exposure, respectively. After 12 weeks of dietary exposure, metabolic cage analyses were performed to interrogate nutrient handling and energy expenditure. In the background of an HFHSD, TF promoted glucose intolerance; however, weight gain and insulin sensitivity were unchanged, and visceral adiposity was reduced. In the background of an HSD, TF increased visceral adiposity; however, glucose tolerance and insulin sensitivity were unchanged, while weight gain was reduced. Thus, these analyses reveal that the metabolic perturbations induced by dietary exposure to TF, including the directionality of alterations in body weight gain, visceral adiposity and glucose homeostasis, are influenced by dietary macronutrient composition, suggesting that populations may exhibit distinct metabolic risks based on their unique dietary characteristics.


2015 ◽  
Vol 228 (2) ◽  
pp. 115-125 ◽  
Author(s):  
Tetsuya Kouno ◽  
Nobuteru Akiyama ◽  
Takahito Ito ◽  
Tomohiko Okuda ◽  
Isamu Nanchi ◽  
...  

Ghrelin is an appetite-stimulating hormone secreted from stomach. Since the discovery that acylation of the serine-3 residue by ghrelin O-acyltransferase (GOAT) is essential for exerting its functions, GOAT has been regarded as an therapeutic target for attenuating appetite, and thus for the treatment of obesity and diabetes. However, contrary to the expectations, GOAT-knockout (KO) mice have not shown meaningful body weight reduction, under high-fat diet. Here, in this study, we sought to determine whether GOAT has a role in body weight regulation and glucose metabolism with a focus on dietary sucrose, because macronutrient composition of diet is important for appetite regulation. We found that peripherally administered acylated-ghrelin, but not unacylated one, stimulated sucrose consumption in a two-bottle-drinking test. The role of acylated-ghrelin in sucrose preference was further supported by the finding that GOAT KO mice consumed less sucrose solution compared with WT littermates. Then, we investigated the effect of dietary composition of sucrose on food intake and body weight in GOAT KO and WT mice. As a result, when fed on high-fat diet, food intake and body weight were similar between GOAT KO and WT mice. However, when fed on high-fat, high-sucrose diet, GOAT KO mice showed significantly reduced food intake and marked resistance to obesity, leading to amelioration of glucose metabolism. These results suggest that blockade of acylated-ghrelin production offers therapeutic potential for obesity and metabolic disorders caused by overeating of palatable food.


Obesity ◽  
2014 ◽  
Vol 22 (6) ◽  
pp. 1575-1575 ◽  
Author(s):  
Sara Ramos-Romero ◽  
Eunice Molinar-Toribio ◽  
Livia Gomez ◽  
Jara Perez-Jimenez ◽  
Marta Casado ◽  
...  

Obesity ◽  
2013 ◽  
Vol 22 (4) ◽  
pp. 976-979 ◽  
Author(s):  
Sara Ramos-Romero ◽  
Eunice Molinar-Toribio ◽  
Livia Gómez ◽  
Jara Pérez-Jiménez ◽  
Marta Casado ◽  
...  

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