scholarly journals Insights into the Roles of Gut Microbes in Obesity

2008 ◽  
Vol 2008 ◽  
pp. 1-9 ◽  
Author(s):  
Yolanda Sanz ◽  
Arlette Santacruz ◽  
Giada De Palma
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Gut Microbiota ◽  
Metabolic Disorders ◽  
Cholesterol Metabolism ◽  
Body Weight Gain ◽  
Inflammatory Factors ◽  
Public Health Issue ◽  
Low Grade ◽  
Gut Microbes

Obesity is a major public health issue as it enhances the risk of suffering several chronic diseases of increasing prevalence. Obesity results from an imbalance between energy intake and expenditure, associated with a chronic low-grade inflammation. Gut microbes are considered to contribute to body weight regulation and related disorders by influencing metabolic and immune host functions. The gut microbiota as a whole improves the host's ability to extract and store energy from the diet leading to body weight gain, while specific commensal microbes seem to exert beneficial effects on bile salt, lipoprotein, and cholesterol metabolism. The gut microbiota and some probiotics also regulate immune functions, protecting the host form infections and chronic inflammation. In contrast, dysbiosis and endotoxaemia may be inflammatory factors responsible for developing insulin resistance and body weight gain. In the light of the link between the gut microbiota, metabolism, and immunity, the use of dietary strategies to modulate microbiota composition is likely to be effective in controlling metabolic disorders. Although so far only a few preclinical and clinical trials have demonstrated the effects of specific gut microbes and prebiotics on biological markers of these disorders, the findings indicate that advances in this field could be of value in the struggle against obesity and its associated-metabolic disorders.

scholarly journals Gut microbiota in obesity and metabolic disorders

2010 ◽  
Vol 69 (3) ◽  
pp. 434-441 ◽  
Author(s):  
Yolanda Sanz ◽  
Arlette Santacruz ◽  
Paola Gauffin
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Gut Microbiota ◽  
Metabolic Disorders ◽  
Dietary Intervention ◽  
Body Weight Gain ◽  
Human Subjects ◽  
Inflammatory Factors ◽  
Public Health Issue ◽  
Immune Functions

Obesity is a major public health issue as it is causally related to several chronic disorders, including type-2 diabetes, CVD and cancer. Novel research shows that the gut microbiota is involved in obesity and metabolic disorders, revealing that obese animal and human subjects have alterations in the composition of the gut microbiota compared to their lean counterparts. Moreover, transplantation of the microbiota of either obese or lean mice influences body weight in the germ-free recipient mice, suggesting that the gut ecosystem is a relevant target for weight management. Indigenous gut microbes may regulate body weight by influencing the host's metabolic, neuroendocrine and immune functions. The intestinal microbiota, as a whole, provides additional metabolic functions and regulates the host's gene expression, improving the ability to extract and store energy from the diet and contributing to body-weight gain. Imbalances in the gut microbiota and increases in plasma lipopolysaccharide may also act as inflammatory factors related to the development of atherosclerosis, insulin resistance and body-weight gain. In contrast, specific probiotics, prebiotics and related metabolites might exert beneficial effects on lipid and glucose metabolism, the production of satiety peptides and the inflammatory tone related to obesity and associated metabolic disorders. This knowledge is contributing to our understanding of how environmental factors influence obesity and associated diseases, providing new opportunities to design improved dietary intervention strategies to manage these disorders.

scholarly journals Deletion of miRNA-22 Induces Cardiac Hypertrophy in Females but Attenuates Obesogenic Diet-Mediated Metabolic Disorders

2020 ◽  
Vol 54 (6) ◽  
pp. 1199-1217
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Cardiac Hypertrophy ◽  
Mrna Expression ◽  
Metabolic Disorders ◽  
Body Weight Gain ◽  
Expression Profiles ◽  
Left Ventricular ◽  
Sequencing Analysis ◽  
Obesogenic Diet

Background/Aims: Obesity is a risk factor associated with cardiometabolic complications. Recently, we reported that miRNA-22 deletion attenuated high-fat diet-induced adiposity and prevented dyslipidemia without affecting cardiac hypertrophy in male mice. In this study, we examined the impact of miRNA-22 in obesogenic diet-induced cardiovascular and metabolic disorders in females. Methods: Wild type (WT) and miRNA-22 knockout (miRNA-22 KO) females were fed a control or an obesogenic diet. Body weight gain, adiposity, glucose tolerance, insulin tolerance, and plasma levels of total cholesterol and triglycerides were measured. Cardiac and white adipose tissue remodeling was assessed by histological analyses. Echocardiography was used to evaluate cardiac function and morphology. RNA-sequencing analysis was employed to characterize mRNA expression profiles in female hearts. Results: Loss of miRNA-22 attenuated body weight gain, adiposity, and prevented obesogenic diet-induced insulin resistance and dyslipidemia in females. WT obese females developed cardiac hypertrophy. Interestingly, miRNA-22 KO females displayed cardiac hypertrophy without left ventricular dysfunction and myocardial fibrosis. Both miRNA-22 deletion and obesogenic diet changed mRNA expression profiles in female hearts. Enrichment analysis revealed that genes associated with regulation of the force of heart contraction, protein folding and fatty acid oxidation were enriched in hearts of WT obese females. In addition, genes related to thyroid hormone responses, heart growth and PI3K signaling were enriched in hearts of miRNA-22 KO females. Interestingly, miRNA-22 KO obese females exhibited reduced mRNA levels of Yap1, Egfr and Tgfbr1 compared to their respective controls. Conclusion: This study reveals that miRNA-22 deletion induces cardiac hypertrophy in females without affecting myocardial function. In addition, our findings suggest miRNA-22 as a potential therapeutic target to treat obesity-related metabolic disorders in females.

Salvianolic acid B prevents body weight gain and regulates gut microbiota and LPS/TLR4 signaling pathway in high-fat diet-induced obese mice

2020 ◽  
Vol 11 (10) ◽  
pp. 8743-8756
Author(s):  
Lin Li ◽  
Rui Li ◽  
Ruyuan Zhu ◽  
Beibei Chen ◽  
Yimiao Tian ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Gut Microbiota ◽  
Body Weight Gain ◽  
Underlying Mechanism ◽  
Salvianolic Acid B ◽  
Obese Mice ◽  
Salvianolic Acid ◽  
Tlr4 Signaling Pathway ◽  
Metabolic Endotoxemia

Salvianolic acid B prevents body weight gain and improves insulin sensitivity in obese mice. The underlying mechanism behind these effects may be associated with the regulation of metabolic endotoxemia, gut microbiota homeostasis and LPS/TLR4 pathway.

scholarly journals Neoagarooligosaccharides modulate gut microbiota and alleviate body weight gain and metabolic syndrome in high-fat diet-induced obese rats

2022 ◽  
Vol 88 ◽  
pp. 104869
Author(s):  
Ju Kyoung Oh ◽  
Robie Vasquez ◽  
Sang Hoon Kim ◽  
Je Hyeon Lee ◽  
Eun Joo Kim ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Body Weight ◽  
Weight Gain ◽  
Gut Microbiota ◽  
High Fat Diet ◽  
Body Weight Gain ◽  
High Fat ◽  
Obese Rats

Abstract 295: Microsomal Prostaglandin E Synthase 1 Deficiency Attenuates Diet-Induced Obesity and Promotes the Formation of Brite Adipose Tissue

2012 ◽  
Vol 32 (suppl_1) ◽  
Author(s):  
Natalie J Moretz ◽  
Nicholas Hatch ◽  
Sarah Srodulski ◽  
Victoria L King
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Weight Gain ◽  
Marked Reduction ◽  
Body Weight Gain ◽  
Prostaglandin E ◽  
Low Grade ◽  
Prostaglandin E Synthase ◽  
Diet Induced Obesity ◽  
Microsomal Prostaglandin E Synthase

Mice deficient in adipocyte specific phospholipases A2 have a marked reduction in prostaglandin E2 (PGE2) levels and are resistant to the development of diet-induced obesity. Clinical data suggest that obesity is a chronic low grade inflammatory disease, characterized by the influx of inflammatory cells into the adipose tissue. During a chronic inflammatory state, microsomal prostaglandin E synthase-1 (mPGES-1) is the primary source of PGE2. We have previously demonstrated that mice deficient in mPGES-1 (KO) have a marked reduction in body weight gain and adiposity compared to littermate controls (WT) fed a high fat (HF) diet with a concomitant reduction in urinary PGE2 concentrations and an increase in urinary PGI2 concentrations. The reduction in weight gain is not for accounted by alterations in food intake or locomotor activity. However, resting metabolic rate, measured by indirect calorimetry, was increased in KO mice compared to WT fed a HF diet. Moreover, body temperature was also increased in KO mice compared to WT mice (37.0 ± 0.2 vs 35.8 ± 0.2; P < 0.05) fed a HF diet. Taken together these data suggest that mPGES-1 deficiency increases energy expenditure in response to feeding a HF diet. Analysis of white adipose tissue (WAT) depots demonstrated an increase in number of smaller adipocytes per unit area in the KO mice compared to WT mice. The WAT from KO mice also had a marked decrease in triglyceride content, F4/80 staining and CD86 staining with a concomitant increase in CD206 staining suggesting an attenuation in macrophage recruitment into the WAT as well as an M2 phenotype. Additionally, COX-2 and UCP-1 and PPAR-γ expression were increased in WAT depots with a concomitant localization of multi-locular adipocytes in WAT depots, demonstrating the presence of brown adipocytes in WAT depots in KO mice fed a HF diet. These data suggest that the reduction in body weight gain in the KO mice may be due an increase in thermogenesis mediated by the formation of brite adipose tissue in WAT depots.

scholarly journals Soy Protein Health Benefits Are in Part Dependent of the Gut Microbiota

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 669-669
Author(s):  
Armando Tovar ◽  
Monica Sanchez-Tapia ◽  
Daniela Moreno ◽  
Guillermo Ordaz ◽  
Martha Guevara ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Energy Expenditure ◽  
Glucose Tolerance ◽  
Gut Microbiota ◽  
Antibiotic Treatment ◽  
Soy Protein ◽  
High Fat Diet ◽  
Body Weight Gain ◽  
High Fat

Abstract Objectives Several studies have demonstrated that the consumption of soy protein decreases LDL-cholesterol, improves insulin sensitivity and attenuates body weight gain. Also, soy protein consumption can modify the gut microbiota, however it has not been established whether the changes in gut microbiota are in part responsible of the health effects of soy protein. Thus, the aim of the present study was to understand whether the metabolic effects of soy protein are reduced by the use of an antibiotic treatment. Methods Rats were fed for 16 weeks with one of the 4 experimental diets: 1) Casein control diet (C), 2) Soy protein diet (S), 3) C high-fat diet, and 4) S high-fat diet. Each group was sub-divided at the end of the 16 weeks in 2 groups. One subgroup continue with the same diet, and the other received the antibiotic treatment (Ampicillin/Neomycin) for 4 weeks. During the study body weight, food intake, body composition, energy expenditure and glucose tolerance were measured. Fecal samples were collected before and after the antibiotic treatment to determine the gut microbiota using the Illumina platform. At the end of the study blood samples were obtained to measure several biochemical variables. Also, liver and adipose tissue samples were obtained to assess the abundance of mRNA and proteins involved in lipid, glucose and thermogenesis. Results Rats fed S or S high fat diet had significant lower body weight gain, body fat, energy expenditure, glucose tolerance, blood lipids, increased expression of thermogenic genes and decreased serum lipopolisacharide than the control or high fat groups fed C diets. The antibiotic treatment abolished the health benefits observed in rats fed the S diets, particularly energy expenditure and weight gain. These changes were associated with changes in the gut microbiota, since S consumption increased the abundance of the Akkermansia and Bifidobacterium genus. This effect on the gut microbiota was prevented by the antibiotic treatment and rats developed metabolic endotoxemia. Finally, the antibiotic treatment reduced the expression of thermogenic genes, particularly in rats fed S high fat diet. Conclusions This study indicates that the beneficial effects of soy protein consumption on health are significantly dependent on the gut microbiota. Funding Sources CONACYT, INCMNSZ.

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