scholarly journals Absence of intestinal microbiota does not protect mice from diet-induced obesity

2010 ◽  
Vol 104 (6) ◽  
pp. 919-929 ◽  
Author(s):  
Christine K. Fleissner ◽  
Nora Huebel ◽  
Mohamed Mostafa Abd El-Bary ◽  
Gunnar Loh ◽  
Susanne Klaus ◽  
...  
Keyword(s):  
Body Weight ◽  
Gut Microbiota ◽  
Body Fat ◽  
Energy Homeostasis ◽  
Body Weight Gain ◽  
Microbial Composition ◽  
Male Adult ◽  
Low Fat Diet ◽  
Diet Induced Obesity ◽  
C3h Mice

The gut microbiota has been implicated in host nutrient absorption and energy homeostasis. We studied the influence of different diets on body composition in germ-free (GF) and conventional (CV) mice. GF and CV male adult C3H mice were fedad libituma semi-synthetic low-fat diet (LFD; carbohydrate–protein–fat ratio: 41:42:17; 19·8 kJ/g), a high-fat diet (HFD; 41:16:43; 21·4 kJ/g) or a commercial Western diet (WD; 41:19:41; 21·5 kJ/g). There was no difference in body weight gain between GF and CV mice on the LFD. On the HFD, GF mice gained more body weight and body fat than CV mice, and had lower energy expenditure. GF mice on the WD gained significantly less body fat than GF mice on the HFD. GF mice on both HFD and WD showed increased intestinal mRNA expression of fasting-induced adipose factor/angiopoietin-like protein 4 (Fiaf/Angptl4), but they showed no major changes in circulating Fiaf/Angptl4 compared with CV mice. The faecal microbiota composition of the CV mice differed between diets: the proportion of Firmicutes increased on both HFD and WD at the expense of the Bacteroidetes. This increase in the Firmicutes was mainly due to the proliferation of one family within this phylum: the Erysipelotrichaceae. We conclude that the absence of gut microbiota does not provide a general protection from diet-induced obesity, that intestinal production of Fiaf/Angptl4 does not play a causal role in gut microbiota-mediated effects on fat storage and that diet composition affects gut microbial composition to larger extent than previously thought.

scholarly journals A Metagenomics Investigation of Intergenerational Effects of Non-nutritive Sweeteners on Gut Microbiome

2022 ◽  
Vol 8 ◽  
Author(s):  
Weilan Wang ◽  
Jodi E. Nettleton ◽  
Michael G. Gänzle ◽  
Raylene A. Reimer
Keyword(s):  
Body Weight ◽  
Body Fat ◽  
Body Weight Gain ◽  
Lactate Production ◽  
16S Rrna Gene Sequencing ◽  
Liver Weight ◽  
Rrna Gene ◽  
Metagenomic Sequencing ◽  
Microbial Composition ◽  
Maternal Consumption

To identify possible mechanisms by which maternal consumption of non-nutritive sweeteners increases obesity risk in offspring, we reconstructed the major alterations in the cecal microbiome of 3-week-old offspring of obese dams consuming high fat/sucrose (HFS) diet with or without aspartame (5–7 mg/kg/day) or stevia (2–3 mg/kg/day) by shotgun metagenomic sequencing (n = 36). High throughput 16S rRNA gene sequencing (n = 105) was performed for dams, 3- and 18-week-old offspring. Maternal consumption of sweeteners altered cecal microbial composition and metabolism of propionate/lactate in their offspring. Offspring daily body weight gain, liver weight and body fat were positively correlated to the relative abundance of key microbes and enzymes involved in succinate/propionate production while negatively correlated to that of lactose degradation and lactate production. The altered propionate/lactate production in the cecum of weanlings from aspartame and stevia consuming dams implicates an altered ratio of dietary carbohydrate digestion, mainly lactose, in the small intestine vs. microbial fermentation in the large intestine. The reconstructed microbiome alterations could explain increased offspring body weight and body fat. This study demonstrates that intense sweet tastants have a lasting and intergenerational effect on gut microbiota, microbial metabolites and host health.

scholarly journals Effect ofLactobacillus acidophilusNCDC 13 supplementation on the progression of obesity in diet-induced obese mice

2012 ◽  
Vol 108 (8) ◽  
pp. 1382-1389 ◽  
Author(s):  
Tulika Arora ◽  
Jelena Anastasovska ◽  
Glen Gibson ◽  
Kieran Tuohy ◽  
Raj Kumar Sharma ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Body Fat ◽  
Energy Homeostasis ◽  
Dietary Intervention ◽  
Body Weight Gain ◽  
Starter Cultures ◽  
Whole Body ◽  
Fat Composition ◽  
Muscle Adiposity ◽  
Mri Changes

There is an increased interest in investigating the relationship between the gut microbiota and energy homeostasis. Probiotics are health beneficial microbes mainly categorised under the genusLactobacillusandBifidobacterium, which when administered in adequate amounts confer health benefits to the host, and have been implicated in various physiological functions. The potential role of probiotics in energy homeostasis is a current and an emerging area of research. In the present study,Lactobacillus acidophilusNCDC 13 was used to evaluate its anti-obesity potential in diet-induced obese (C57BL/6) mice. The probiotic bacterial culture was administered in Indian yogurt preparation called ‘dahi’, prepared using native starter cultures, and compared with control dahi containing only dahi starter cultures. The dietary intervention was followed for 8 weeks, and whole-body fat composition, and liver and muscle adiposity were measured using MRI. Changes in gut microbiota were assessed by fluorescentin situhybridisation in faeces and caecal contents. The feeding of the probiotic brought no changes in body-weight gain, food and dahi intake when compared with the control dahi-fed animals. No significant changes in body fat composition, liver and muscle adiposity were also observed. At the end of the dietary intervention, a significant increase (P < 0·05) in the number of totalBifidobacteriumwas observed in both faeces and caecal contents of mice as a result of probiotic dahi administration. Thus,L. acidophilusNCDC 13 supplementation could be beneficial in shifting the gut microbiota balance positively. However, its anti-obesity potential could not be established in the present study and warrants further exploration.

scholarly journals THE ROLE OF THE INTESTINAL MICROBIOTA IN THE MODULATION OF FOOD INTAKE AND BODY WEIGHT

2017 ◽  
Author(s):  
Matthew John Dalby
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Body Fat ◽  
Intestinal Microbiota ◽  
High Fat Diet ◽  
High Fat ◽  
Low Fat ◽  
Low Fat Diet ◽  
Diet Induced Obesity

This research investigated the role of the intestinal microbiota in shaping host food intake and body weight through immunomodulation, the impact of refined and unrefined diets, and though fermentable fibre induced gastrointestinal hormone secretion. Gut-derived lipopolysaccharide activating TLR4 has been proposed to contribute to obesity. To investigate this, TLR4-/- or CD14-/- mice and C57BL/6J controls were fed a high-fat or low-fat diet. Neither TLR4-/- or CD14-/- were protected against high-fat diet-induced obesity. High-fat diet increased hypothalamic expression of SerpinA3N and SOCS3 regardless of genotype; however, inflammatory gene expression was not increased. To investigate the use of chow control diets in obesity-associated microbiota changes, C57BL/6J mice were fed a chow diet, refined high-fat, or low-fat diet. Both high-fat and low-fat refined diets resulted in similar dramatic alterations in the composition of the intestinal microbiota at the phylum, family, and species level compared to chow, while only high-fat diet feeding resulted in obesity and glucose intolerance. The roles of colonic GLP-1 and PYY in mediating fermentable fibre in reducing food intake and body fat were investigated using GLP-1R-/- and PYY-/- mice fed a high-fat diet supplemented with inulin or cellulose. Inulin supplementation reduced body fat and food intake in C57BL/6J control mice while GLP-1R-/- and PYY-/- mice showed an attenuated response to dietary inulin. In summary, this research questions the role of TLR4 and LPS in diet-induced obesity. These results demonstrate the importance of the control diet used in studies of obesity in mice and indicate that many of the obesity-associated changes in the gut microbiota are due to comparing refined high-fat diets with chow diets. These results also provide evidence for an essential role for both GLP-1 and PYY in mediating the food intake and bodyweight-reducing effects of fermentable fibre.

scholarly journals Oral Supplements of Combined Bacillus licheniformis Zhengchangsheng® and Xylooligosaccharides Improve High-Fat Diet-Induced Obesity and Modulate the Gut Microbiota in Rats

2020 ◽  
Vol 2020 ◽  
pp. 1-17
Author(s):  
Yuyuan Li ◽  
Man Liu ◽  
He Liu ◽  
Xiaoqing Wei ◽  
Xianying Su ◽  
...  
Keyword(s):  
Body Weight ◽  
Lipid Metabolism ◽  
Gut Microbiota ◽  
Bacillus Licheniformis ◽  
High Fat Diet ◽  
Body Weight Gain ◽  
Low Grade ◽  
Microbiota Composition ◽  
High Fat ◽  
Diet Induced Obesity

Gut dysbiosis induced by high-fat diet (HFD) may result in low-grade inflammation leading to diverse inflammatory diseases. The beneficial effects of probiotics and prebiotics on obesity have been reported previously. However, their benefits in promoting human health and the underlying mechanisms still need to be further characterized. This study is aimed at understanding how probiotic Bacillus licheniformis Zhengchangsheng® (BL) and prebiotic xylooligosaccharides (XOS) influence the health of a rat model with HF (60 kcal %) diet-induced obesity. Five groups of male Sprague Dawley (SD) rats were fed a normal fat diet (CON) or an HFD with or without BL and XOS supplementation for 3 weeks. Lipid profiles, inflammatory biomarkers, and microbiota composition were analyzed at the end of the experiment. Rats fed an HFD exhibited increased body weight and disordered lipid metabolism. In contrast, combined BL and XOS supplementation inhibited body weight gain and returned lipid metabolism to normal. Furthermore, BL and XOS administration changed the gut microbiota composition and modulated specific bacteria such as Prevotellaceae, Desulfovibrionaceae, and Ruminococcaceae. In addition, supplements of combined BL and XOS obviously reduced the serum LPS level, which was significantly related to microbial variations. Our findings suggest that modulation of the gut microbiota as a result of probiotic BL and prebiotic XOS supplementation has a positive effect on HFD-induced obesity in rats.

scholarly journals Distinct Changes in Gut Microbiota Are Associated with Estradiol-Mediated Protection from Diet-Induced Obesity in Female Mice

Metabolites ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 499
Author(s):  
Kalpana D. Acharya ◽  
Hye L. Noh ◽  
Madeline E. Graham ◽  
Sujin Suk ◽  
Randall H. Friedline ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Energy Homeostasis ◽  
Whole Body ◽  
Glucose Turnover ◽  
Female Mice ◽  
Adult Mice ◽  
Diet Induced Obesity ◽  
Metabolic Dysregulation ◽  
Regulation Of Metabolism ◽  
Junction Protein

A decrease in ovarian estrogens in postmenopausal women increases the risk of weight gain, cardiovascular disease, type 2 diabetes, and chronic inflammation. While it is known that gut microbiota regulates energy homeostasis, it is unclear if gut microbiota is associated with estradiol regulation of metabolism. In this study, we tested if estradiol-mediated protection from high-fat diet (HFD)-induced obesity and metabolic changes are associated with longitudinal alterations in gut microbiota in female mice. Ovariectomized adult mice with vehicle or estradiol (E2) implants were fed chow for two weeks and HFD for four weeks. As reported previously, E2 increased energy expenditure, physical activity, insulin sensitivity, and whole-body glucose turnover. Interestingly, E2 decreased the tight junction protein occludin, suggesting E2 affects gut epithelial integrity. Moreover, E2 increased Akkermansia and decreased Erysipleotrichaceae and Streptococcaceae. Furthermore, Coprobacillus and Lactococcus were positively correlated, while Akkermansia was negatively correlated, with body weight and fat mass. These results suggest that changes in gut epithelial barrier and specific gut microbiota contribute to E2-mediated protection against diet-induced obesity and metabolic dysregulation. These findings provide support for the gut microbiota as a therapeutic target for treating estrogen-dependent metabolic disorders in women.

scholarly journals Neither Agouti-Related Protein nor Neuropeptide Y Is Critically Required for the Regulation of Energy Homeostasis in Mice

2002 ◽  
Vol 22 (14) ◽  
pp. 5027-5035 ◽  
Author(s):  
Su Qian ◽  
Howard Chen ◽  
Drew Weingarth ◽  
Myrna E. Trumbauer ◽  
Dawn E. Novi ◽  
...  
Keyword(s):  
Body Weight ◽  
Neuropeptide Y ◽  
Energy Homeostasis ◽  
Arcuate Nucleus ◽  
Body Weight Gain ◽  
Physiological Role ◽  
Related Protein ◽  
Double Knockout ◽  
Orexigenic Peptide ◽  
Agouti Related Protein

ABSTRACT Agouti-related protein (AgRP), a neuropeptide abundantly expressed in the arcuate nucleus of the hypothalamus, potently stimulates feeding and body weight gain in rodents. AgRP is believed to exert its effects through the blockade of signaling by α-melanocyte-stimulating hormone at central nervous system (CNS) melanocortin-3 receptor (Mc3r) and Mc4r. We generated AgRP-deficient (Agrp−/− ) mice to examine the physiological role of AgRP. Agrp−/− mice are viable and exhibit normal locomotor activity, growth rates, body composition, and food intake. Additionally, Agrp−/− mice display normal responses to starvation, diet-induced obesity, and the administration of exogenous leptin or neuropeptide Y (NPY). In situ hybridization failed to detect altered CNS expression levels for proopiomelanocortin, Mc3r, Mc4r, or NPY mRNAs in Agrp−/− mice. As AgRP and the orexigenic peptide NPY are coexpressed in neurons of the arcuate nucleus, we generated AgRP and NPY double-knockout (Agrp−/− ;Npy−/− ) mice to determine whether NPY or AgRP plays a compensatory role in Agrp−/− or NPY-deficient (Npy−/− ) mice, respectively. Similarly to mice deficient in either AgRP or NPY, Agrp−/− ;Npy−/− mice suffer no obvious feeding or body weight deficits and maintain a normal response to starvation. Our results demonstrate that neither AgRP nor NPY is a critically required orexigenic factor, suggesting that other pathways capable of regulating energy homeostasis can compensate for the loss of both AgRP and NPY.

scholarly journals Neonatal nutritional programming impairs adiponectin effects on energy homeostasis in adult life of male rats

2018 ◽  
Vol 315 (1) ◽  
pp. E29-E37 ◽  
Author(s):  
Mariana Peduti Halah ◽  
Paula Beatriz Marangon ◽  
Jose Antunes-Rodrigues ◽  
Lucila L. K. Elias
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Weight Gain ◽  
Food Intake ◽  
White Adipose Tissue ◽  
Energy Homeostasis ◽  
Body Weight Gain ◽  
Adult Life ◽  
Male Rats ◽  
Nutritional Programming

Neonatal nutritional changes induce long-lasting effects on energy homeostasis. Adiponectin influences food intake and body weight. The aim of this study was to investigate the effects of neonatal nutritional programming on the central stimulation of adiponectin. Male Wistar rats were divided on postnatal (PN) day 3 in litters of 3 (small litter, SL), 10 (normal litter, NL), or 16 pups/dam (large litter, LL). We assessed body weight gain for 60 days, adiponectin concentration, and white adipose tissue weight. We examined the response of SL, NL, and LL rats on body weight gain, food intake, oxygen consumption (V̇o2), respiratory exchange ratio (RER), calorimetry, locomotor activity, phosphorylated-AMP-activated protein kinase (AMPK) expression in the hypothalamus, and uncoupling protein (UCP)-1 in the brown adipose tissue after central stimulus with adiponectin. After weaning, SL rats maintained higher body weight gain despite similar food intake compared with NL rats. LL rats showed lower body weight at weaning, with a catch up afterward and higher food intake. Both LL and SL groups had decreased plasma concentrations of adiponectin at PN60. SL rats had increased white adipose tissue. Central injection of adiponectin decreased body weight and food intake and increased V̇o2, RER, calorimetry, p-AMPK and UCP- 1 expression in NL rats, but it had no effect on SL and LL rats, compared with the respective vehicle groups. In conclusion, neonatal under- and overfeeding induced an increase in body weight gain in juvenile and early adult life. Unresponsiveness to central effects of adiponectin contributes to the imbalance of the energy homeostasis in adult life induced by neonatal nutritional programming.

Defense of differfing body weight set points in diet-induced obese and resistant rats

1998 ◽  
Vol 274 (2) ◽  
pp. R412-R419 ◽  
Author(s):  
Barry E. Levin ◽  
Richard E. Keesey
Keyword(s):  
Body Weight ◽  
Diet Composition ◽  
Energy Homeostasis ◽  
Energy Content ◽  
Sprague Dawley ◽  
Fat Pad ◽  
Insulin Levels ◽  
Diet Induced Obesity ◽  
Sprague Dawley Rats ◽  
Plasma Leptin

Among outbred Sprague-Dawley rats, approximately one-half develop diet-induced obesity (DIO) and one-half are diet resistant (DR) on a diet relatively high in fat and energy content (HE diet). Here we examined the defense of body weight in these two phenotypes. After HE diet for 13 wk, followed by chow for 6 wk, DR rats gained weight comparably but their plasma leptin levels fell to 54% of chow-fed controls. When a palatable liquid diet (Ensure) was added for 13 wk, other DR rats became obese. But when switched to chow, their intakes fell by 60%, and body and retroperitoneal (RP) fat pad weights and plasma leptin and insulin levels all declined for 2 wk and then stabilized at control levels after 6 wk. In contrast, comparably obese DIO rats decreased their intake by only 20%, and their weights plateaued when they were switched to chow after 13 wk on HE diet. When a subgroup of these DIO rats was restricted to 60% of prior intake, their weights fell to chow-fed control levels over 2 wk. But their leptin and insulin levels both fell disproportionately to 30% of controls. When no longer restricted, their intake and feed efficiency rose immediately, and their body and RP pad weights and leptin and insulin levels rose to those of unrestricted DIO rats within 2 wk. Thus diet and genetic background interact to establish high (DIO) or low (DR) body weight set points, which are then defended against subsequent changes in diet composition and/or energy availability. If leptin affects energy homeostasis, it does so differentially in DIO vs. DR rats since comparably low and high levels were associated with differing patterns of weight change between the two phenotypes.

Dietary fat and adiposity: a dose-response relationship in adult male rats fed isocalorically

1995 ◽  
Vol 268 (4) ◽  
pp. E546-E550 ◽  
Author(s):  
C. N. Boozer ◽  
G. Schoenbach ◽  
R. L. Atkinson
Keyword(s):  
Body Weight ◽  
Body Fat ◽  
Adult Male ◽  
Dietary Fat ◽  
Male Rats ◽  
Control Group ◽  
Low Fat Diet ◽  
Mesenteric Fat ◽  
Total Body Fat ◽  
Total Body

This study examined the effects of increasing levels of dietary fat fed isocalorically on body weight, body composition, and adipose distribution. Adult male rats were weight matched into four groups. One group that was fed a low-fat diet (12%) served as reference controls. The other three groups were fed diets of 24, 36, or 48% fat in amounts to equal the energy intake of the control group. After 6 wk, body weights of the four groups were not significantly different. Intrascapular brown fat did not differ between groups. Total body fat and adipose depot weights, however, increased in proportion to the level of fat in the diet. Total body fat and retroperitoneal and mesenteric depot weights of the 48% fat group were greater than controls (P < 0.05). Mesenteric fat in this group was also significantly increased over all other groups (P < 0.05). These results show that high-fat diets fed to adult animals cause increased body fat in the absence of significant changes in body weight and that mesenteric fat is increased disproportionately.

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