scholarly journals Effect of stevia on the gut microbiota and glucose tolerance in a murine model of diet-induced obesity

2020 ◽  
Vol 96 (6) ◽  
Author(s):  
Sarah L Becker ◽  
Edna Chiang ◽  
Anna Plantinga ◽  
Hannah V Carey ◽  
Garret Suen ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Gut Microbiota ◽  
Glucose Intolerance ◽  
High Fat Diet ◽  
High Fat ◽  
Low Fat ◽  
Treatment Groups ◽  
Low Fat Diet ◽  
Taxonomic Groups ◽  
Induced Changes

ABSTRACT Artificial sweeteners have been shown to induce glucose intolerance by altering the gut microbiota; however, little is known about the effect of stevia. Here, we investigate whether stevia supplementation induces glucose intolerance by altering the gut microbiota in mice, hypothesizing that stevia would correct high fat diet-induced glucose intolerance and alter the gut microbiota. Mice were split into four treatment groups: low fat, high fat, high fat + saccharin and high fat + stevia. After 10 weeks of treatment, mice consuming a high fat diet (60% kcal from fat) developed glucose intolerance and gained more weight than mice consuming a low fat diet. Stevia supplementation did not impact body weight or glucose intolerance. Differences in species richness and relative abundances of several phyla were observed in low fat groups compared to high fat, stevia and saccharin. We identified two operational taxonomic groups that contributed to differences in beta-diversity between the stevia and saccharin groups: Lactococcus and Akkermansia in females and Lactococcus in males. Our results demonstrate that stevia does not rescue high fat diet-induced changes in glucose tolerance or the microbiota, and that stevia results in similar alterations to the gut microbiota as saccharin when administered in concordance with a high fat diet.

scholarly journals Effect of a long-term high-protein diet on survival, obesity development, and gut microbiota in mice

2016 ◽  
Vol 310 (11) ◽  
pp. E886-E899 ◽  
Author(s):  
Pia Kiilerich ◽  
Lene Secher Myrmel ◽  
Even Fjære ◽  
Qin Hao ◽  
Floor Hugenholtz ◽  
...  
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Gut Microbiota ◽  
Dietary Fat ◽  
High Fat Diet ◽  
High Fat ◽  
Low Fat ◽  
Low Fat Diet ◽  
Low Protein

Female C57BL/6J mice were fed a regular low-fat diet or high-fat diets combined with either high or low protein-to-sucrose ratios during their entire lifespan to examine the long-term effects on obesity development, gut microbiota, and survival. Intake of a high-fat diet with a low protein/sucrose ratio precipitated obesity and reduced survival relative to mice fed a low-fat diet. By contrast, intake of a high-fat diet with a high protein/sucrose ratio attenuated lifelong weight gain and adipose tissue expansion, and survival was not significantly altered relative to low-fat-fed mice. Our findings support the notion that reduced survival in response to high-fat/high-sucrose feeding is linked to obesity development. Digital gene expression analyses, further validated by qPCR, demonstrated that the protein/sucrose ratio modulated global gene expression over time in liver and adipose tissue, affecting pathways related to metabolism and inflammation. Analysis of fecal bacterial DNA using the Mouse Intestinal Tract Chip revealed significant changes in the composition of the gut microbiota in relation to host age and dietary fat content, but not the protein/sucrose ratio. Accordingly, dietary fat rather than the protein/sucrose ratio or adiposity is a major driver shaping the gut microbiota, whereas the effect of a high-fat diet on survival is dependent on the protein/sucrose ratio.

scholarly journals Altered Gut Microbiota Is a Novel Mechanism for the Adverse Effects Induced by Foodborne Titanium Dioxide Nanoparticles in Obese and Non-obese Mice (P21-021-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Hengjun Du ◽  
Xiaoqiong Cao ◽  
Yanhui Han ◽  
Min Gu ◽  
Hang Xiao
Keyword(s):  
Titanium Dioxide ◽  
Adverse Effects ◽  
Gut Microbiota ◽  
High Fat Diet ◽  
Obese Mice ◽  
High Fat ◽  
Low Fat ◽  
Colonic Inflammation ◽  
Tio2 Nps ◽  
Low Fat Diet

Abstract Objectives Many food products contain inorganic nanoparticles (NPs), such as titanium dioxide (TiO2) NPs. There is increasing concern about the potential unintended health risks associated with foodborne TiO2 NPs in certain populations, such as the obese. The purpose of this study was to determine the adverse effects of TiO2 NPs in obese individuals, the molecular mechanism involved and the potential role of gut microbiota in mediating the adverse effects. Methods Two types of TiO2 (30 nm and E171-Food grade TiO2) were mixed with mouse diet at 0.1 wt% and fed to two populations of mice (high-fat diet-fed obese mice and non-obese mice). Meanwhile, fecal samples from the above groups of mice were collected weekly for transplanting to four groups of mice fed a low-fat diet for 10 weeks. 16 s rRNA gene amplicon sequencing, histological analysis, immunohistochemistry, ELISA and SCFAs analysis were utilized to characterize the composition of the microbiota, inflammation status, and the effects of altered gut microbiota on the inflammation status of the mouse colon. Results TiO2 NPs significantly altered the composition of gut microbiota with stronger alterations in the high-fat diet-fed obese mice than the low-fat diet-fed non-obese mice. The abundance of inflammation-related cytokines (e.g., IL-10, IL-12p70, and IL-17) and myeloperoxidase (MPO) in the mouse colonic mucosa were significantly altered by TiO2 NPs to produce an inflammatory state. TiO2 NPs decreased the cecal levels of SCFAs such as butyrate. Moreover, the magnitude of the above alteration was higher in the obese mice than in the non-obese mice. After 10 weeks of microbial transplant, microbiota from the mice consuming a high-fat diet with TiO2 NPs led to an increase of pro-inflammatory cytokines, loss of healthy colonic morphology, and infiltration of immune cells in the colon of the low-fat diet-fed recipient mice, indicating a significant colonic inflammation. Conclusions TiO2 NPs altered gut microbiota in both obese and non-obese mice, with stronger effects in the obese mice, and the alteration of gut microbiota led to colonic inflammation in the mice. Overall, these findings provided a valuable new perspective on the potential adverse effects and appropriate mechanisms of foodborne TiO2 NPs among populations with different obese status. Funding Sources USDA/NIFA competitive grants to Hang Xiao.

scholarly journals Shrimp oil extracted from the shrimp processing waste reduces the development of insulin resistance and metabolic phenotypes in diet-induced obese rats

2017 ◽  
Vol 42 (8) ◽  
pp. 841-849 ◽  
Author(s):  
Sandhya Nair ◽  
Jacques Gagnon ◽  
Claude Pelletier ◽  
Nadia Tchoukanova ◽  
Junzeng Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Glucose Tolerance ◽  
Chronic Inflammation ◽  
High Fat Diet ◽  
High Fat ◽  
Low Fat ◽  
Low Fat Diet ◽  
Obese Rats ◽  
Shrimp Oil

Diet-induced obesity, insulin resistance, impaired glucose tolerance, chronic inflammation, and oxidative stress represent the main features of type 2 diabetes mellitus. The present study was conducted to examine the efficacy and mechanisms of shrimp oil on glucose homeostasis in obese rats. Male CD rats fed a high-fat diet (52 kcal% fat) and 20% fructose drinking water were divided into 4 groups and treated with the dietary replacement of 0%, 10%, 15%, or 20% of lard with shrimp oil for 10 weeks. Age-matched rats fed a low-fat diet (10 kcal% fat) were used as the normal control. Rats on the high-fat diet showed impaired (p < 0.05) glucose tolerance and insulin resistance compared with rats fed the low-fat diet. Shrimp oil improved (p < 0.05) oral glucose tolerance, insulin response, and homeostatic model assessment-estimated insulin resistance index; decreased serum insulin, leptin, hemoglobin A1c, and free fatty acids; and increased adiponectin. Shrimp oil also increased (p < 0.05) antioxidant capacity and reduced oxidative stress and chronic inflammation. The results demonstrated that shrimp oil dose-dependently improved glycemic control in obese rats through multiple mechanisms.

scholarly journals Chitosan Oligosaccharide Ameliorates Metabolic Syndrome Induced by Overnutrition via Altering Intestinal Microbiota

2021 ◽  
Vol 8 ◽  
Author(s):  
Yihua Wang ◽  
Shili Liu ◽  
Di Tang ◽  
Rui Dong ◽  
Qiang Feng
Keyword(s):  
Metabolic Syndrome ◽  
Gut Microbiota ◽  
Intestinal Microbiota ◽  
High Fat Diet ◽  
Lipid Lowering ◽  
Positive Interactions ◽  
High Fat ◽  
Low Fat ◽  
Low Fat Diet ◽  
Clostridium Paraputrificum

Chitosan oligosaccharides (COS) play a prebiotic role in many ways, whereas its function on microbiota is not fully understood. In this study, the effects of COS on metabolic syndrome were initially investigated by testing changes in the physiological indicators after adding COS to the diet of mice with high fat (group H) and low fat (group L). The results showed that COS markedly inhibited the accumulation of body weight and liver fat induced by high-fat diet, as well as restored the elevated concentration of blood glucose and fasting insulin to normal levels. Next, changes of the murine intestinal microbiota were examined. The results exhibited that COS reduced with-in-sample diversity, while the between-sample microbial diversity enhanced. Specifically, COS enriched Clostridium paraputrificum and Clostridium ramosum in the mice on a high-fat diet, while the abundance of Clostridium cocleatum was reduced. As a comparison, Parabacteroides goldsteinii and Bacteroides uniformis increased their abundance in response to COS in the low-fat diet group. Noticeably, a large amount of Akkermansia muciniphila was enriched in both high-fat or low-fat diet groups. Among the differential fecal bacteria, Clostridium ramosume was found to be positively interacted with Faecalibacterim prausnitzii and Clostridium paraputrificum; Clostridium paraputrificum had a positive interactions with Lactococcus chungangensis and Bifidobacterium mongoliense, suggesting that COS probably ameliorate metabolic syndrome through the microbiota in view of the lipid-lowering effects of these interacted bacteria. Furthermore, the gene expression data revealed that COS improved the functions related to intestinal barrier and glucose transport, which could be the trigger and consequence of the variations in gut microbiota induced by COS. Additionally, correlation analysis found that intestinal bacteria are related to physiological parameters, which further supports the mediating role of gut microbiota in the beneficial effect of COS. In summary, our research results provide new evidence for the prebiotic effects of COS.

scholarly journals Distinct Effects of a High Fat Diet on Bone in Skeletally Mature and Developing Male C57BL/6J Mice

Nutrients ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1666
Author(s):  
Dean S. Ross ◽  
Tzu-Hsuan Yeh ◽  
Shalinie King ◽  
Julia Mathers ◽  
Mark S. Rybchyn ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Bone Formation ◽  
Glucose Intolerance ◽  
High Fat Diet ◽  
Age Groups ◽  
Oral Glucose ◽  
Rna Expression ◽  
High Fat ◽  
Mineral Density ◽  
Skeletal Fragility

Increased risks of skeletal fractures are common in patients with impaired glucose handling and type 2 diabetes mellitus (T2DM). The pathogenesis of skeletal fragility in these patients remains ill-defined as patients present with normal to high bone mineral density. With increasing cases of glucose intolerance and T2DM it is imperative that we develop an accurate rodent model for further investigation. We hypothesized that a high fat diet (60%) administered to developing male C57BL/6J mice that had not reached skeletal maturity would over represent bone microarchitectural implications, and that skeletally mature mice would better represent adult-onset glucose intolerance and the pre-diabetes phenotype. Two groups of developing (8 week) and mature (12 week) male C57BL/6J mice were placed onto either a normal chow (NC) or high fat diet (HFD) for 10 weeks. Oral glucose tolerance tests were performed throughout the study period. Long bones were excised and analysed for ex vivo biomechanical testing, micro-computed tomography, 2D histomorphometry and gene/protein expression analyses. The HFD increased fasting blood glucose and significantly reduced glucose tolerance in both age groups by week 7 of the diets. The HFD reduced biomechanical strength, both cortical and trabecular indices in the developing mice, but only affected cortical outcomes in the mature mice. Similar results were reflected in the 2D histomorphometry. Tibial gene expression revealed decreased bone formation in the HFD mice of both age groups, i.e., decreased osteocalcin expression and increased sclerostin RNA expression. In the mature mice only, while the HFD led to a non-significant reduction in runt-related transcription factor 2 (Runx2) RNA expression, this decrease became significant at the protein level in the femora. Our mature HFD mouse model more accurately represents late-onset impaired glucose tolerance/pre-T2DM cases in humans and can be used to uncover potential insights into reduced bone formation as a mechanism of skeletal fragility in these patients.

Abstract 480: Exacerbation of Arterial Stiffness in Obese Adiponectin Deficient Mice

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Megha Murali ◽  
Carla Taylor ◽  
Peter Zahradka ◽  
Jeffrey Wigle
Keyword(s):  
Arterial Stiffness ◽  
Pulse Wave Velocity ◽  
Wave Velocity ◽  
High Fat Diet ◽  
Pulse Wave ◽  
High Fat ◽  
Low Fat ◽  
Low Fat Diet ◽  
High Fat Diets ◽  
Fat Diets

Background and Objective: Arterial stiffness is recognized as being an independent predictor of incipient vascular disease associated with obesity and metabolic syndrome. In obese subjects, the decrease in the plasma level of adiponectin, an anti-diabetic and anti-atherogenic adipokine, is well known. Hence the aim of our study was to examine the effect of loss of adiponectin on the development of arterial stiffness in response to a high fat diet. Methods and Results: Male 8-week old adiponectin knockout (APN KO) and C57BL/6 (control) mice were fed a high fat diet (60% Calories from fat) for 12 weeks to induce obesity and insulin resistance (n=10/group). APN KO and C57BL/6 mice were fed a low fat diet (10% Calories from fat) and used as lean controls (n=10/group). After 12 weeks on the high fat diet, the APN KO mice weighed significantly more than the C57BL/6 mice (45.1±1.3 g vs 40.1±1.1 g, p=0.0008) but there was no difference in the final weights between genotypes fed the low fat diet. APN KO mice on both high and low fat diets for 12 weeks developed insulin resistance as measured by oral glucose tolerance test (Area under curve (AUC) mmol/L х min = 437±70 and 438±57) as compared to the C57BL/6 mice fed low or high fat diets (AUC mmol/L х min = 251±27 and 245±43). Arterial stiffness was determined by Doppler pulse wave velocity analysis of the femoral artery. Pulse wave velocity was increased in APN KO mice fed a high fat diet relative to those fed the low fat diet (12.56±0.78 cm/s vs 9.47±0.95 cm/s, p=0.0035; n=8-10). Pulse wave velocity was not different between C57BL/6 control mice on the low or high fat diets (10.63±0.73 cm/s and 10.86±0.50 cm/s), thus revealing that only mice deficient in adiponectin developed arterial stiffness in response to high fat diet. Conclusions: Potentiation of the vascular stiffness in diet-induced obese APN KO mice indicates that adiponectin has a role in modulating vascular structure and the APN KO mouse models the vascular changes that occur in human obesity and metabolic disorders. Morphometric analysis of the aortic tissues for vessel thickness and expression of extracellular proteins will further validate the potential role of adiponectin on the maintenance of arterial elasticity in addition to its known effect on eNOS mediated vasoprotection.

scholarly journals Influence of gender on OVA-induced airway inflammation in C57/B6J mice on a high-fat diet

2018 ◽  
Vol 16 ◽  
pp. 205873921876094 ◽  
Author(s):  
Gang Yu ◽  
Lili Zhu ◽  
Haiyan Li ◽  
Youyou Shao ◽  
Lei Chong ◽  
...  
Keyword(s):  
Body Weight ◽  
High Fat Diet ◽  
Inflammatory Cells ◽  
Normal Weight ◽  
Male Mice ◽  
High Fat ◽  
Low Fat ◽  
Control Male ◽  
Low Fat Diet ◽  
Asthma Group

Overweight/obesity has been suggested as a risk factor for asthma development, and prospective studies have confirmed that high body weight precedes asthma symptoms. However, the nature of the association between overweight/obese status and asthma remains unclear. Animal models of obesity-related asthma are very useful for understanding disease pathophysiology. Although C57/B6J mice are the most widely used animal model for researching obesity-related asthma, gender differences are not always taken into consideration. Therefore, to explore the effect of gender on the development of obesity-related asthma, both female and male C57/B6J mice were used in this study. The mice were fed with a high-fat diet or a low-fat diet as control. Body weight, body length, liver weight, and Lee’s Index were used to evaluate obesity status, and lung histology, lung inflammatory cells infiltration, and inflammatory cytokines in bronchoalveolar lavage fluid (BALF) were examined for asthma evaluation. We found that the mean body weight of male mice on a high-fat diet gradually increased and was significantly higher than control male mice on a low-fat diet ( P < 0.01), while no significant differences were found between female mice at the end of 12 weeks of feeding. Furthermore, the obese asthma group female and male mice exhibited significantly high inflammatory cells infiltration than normal weight or obese female and male mice ( P < 0.01). However, the obese asthma group presented higher Neu infiltration, Th1 cytokine, and interferon gamma (IFNγ) concentrations in BALF than the asthma group in both the genders ( P < 0.01). In conclusion, both female and male mice are suitable for the obesity-related asthma model, although male mice might be more stable. Besides, obesity-related asthma is not Th2 type asthma.

scholarly journals SERUM LIPID PROFILE;

2008 ◽  
Vol 15 (04) ◽  
pp. 500-507
Author(s):  
MUHAMMAD ANWAR BURIRO ◽  
MUHAMMAD TAYYAB
Keyword(s):  
Sunflower Oil ◽  
High Fat Diet ◽  
Serum Lipid ◽  
Nigella Sativa ◽  
Albino Rats ◽  
High Fat ◽  
Low Fat ◽  
Control Groups ◽  
Low Fat Diet ◽  
Lipid Fractions

Objective: To determine the effects of Nigella sativa and sunflower oil diet intake on serum lipid profile in albino rats. Material& Methods: Eighty four albino rats with equal number of males and females were selected for the study, they were divided into six differentgroups, Control groups1,111,V,were given low fat diet(3%),high fat diet(20%), high fat diet supplemented with bile salt (1% colic acid) andantithyroid drug (0.5% propylthiouracil). The Experimental groups were given the above diets with supplemented Nigella sativa. Low fat dietincreased all the lipid fractions significantly when given at12 and 24 weeks duration as compared to 0 week. Results: The high fat diet whengiven at different intervals decreased all lipid fractions significantly as compared to baseline level. The high fat diet with propylthiouracil andbile salt also increased all the lipid fractions and the increase was more as compared to previous groups. The supplements of Nigella sativain the groups decreased all the lipid fractions significantly as compared to the control groups except HDL-c, which was significantly increasedin all the experimental groups as compared to control groups. Conclusion: On the basis of these findings conclusions are made, that Nigellasativa has got TG,TC, and LDL-c lowering and HDL-c raising effects.3% sunflower oil low fat diet has got TG,TC,HDL-c, and LDL-c raisingeffects.20% sunflower oil high fat diet has got TG,TC,HDL-c and LDL-c lowering effects. Both Nigella sativa and sunflower oil have got lowatherogenic index (TC/HDL) and may be recommended in hyperlipidaemic patients or normal individuals.

Whole body insulin sensitivity in Osborne-Mendel and S 5B/Pl rats eating a low- or high-fat diet

1992 ◽  
Vol 263 (4) ◽  
pp. R785-R789 ◽  
Author(s):  
T. A. Buchanan ◽  
J. S. Fisler ◽  
S. Underberger ◽  
G. F. Sipos ◽  
G. A. Bray
Keyword(s):  
Insulin Sensitivity ◽  
High Fat Diet ◽  
Whole Body ◽  
High Fat ◽  
Low Fat ◽  
Low Fat Diet ◽  
High Fat Diets ◽  
Glucose Clearance ◽  
Fat Diets ◽  
Fat Feeding

To determine whether whole body insulin sensitivity differs between a rat strain that does not (S 5B/Pl) and a strain that does [Osborne-Mendel (OM)] become obese when eating a high-fat diet, we performed euglycemic clamp studies in animals from each strain during low- and high-fat feeding. Clamps were performed after 2 days ("initial clamp") and 9 days ("final clamp") on each diet. Plasma glucose and insulin levels during the final 60 min of initial and final clamps were similar in S 5B/Pl and OM rats regardless of diet. Insulin sensitivity, measured as the glucose clearance rate during the final 60 min of the clamp, averaged 35 +/- 3 ml.kg-1.min-1 in S 5B/Pl rats after 2 days on a low-fat diet. This did not change significantly during an additional 7 days on the low-fat diet. The high-fat diet was associated with a 13% reduction in insulin sensitivity after 2 days and a 30% reduction after 9 days in S 5B/Pl rats. OM rats exhibited similar patterns of insulin sensitivity during low- and high-fat diets, albeit at lower insulin sensitivity overall (P < 0.0005 vs. S 5B/Pl). Mean glucose clearance after 2 days on the low-fat diet was 27 +/- 2 mg.kg-1.min-1 and did not change significantly during seven more days of low-fat feeding. The high-fat diet was associated with a 19% reduction in glucose clearance after 2 days and a 38% reduction after 9 days in OM rats. The magnitude of reduction in insulin sensitivity during high-fat diets did not differ significantly between strains.(ABSTRACT TRUNCATED AT 250 WORDS)

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