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Roux-en-Y Gastric Bypass and Vertical Banded Gastroplasty Induce Long-Term Changes on the Human Gut Microbiome Contributing to Fat Mass Regulation.

Tremaroli V, Karlsson F, Werling M, Ståhlman M, Kovatcheva-Datchary P, Olbers T, Fändriks L, le Roux CW, Nielsen J, Bäckhed F - Cell Metab. (2015)

Bottom Line: The two surgical procedures induced similar and durable changes on the gut microbiome that were not dependent on body mass index and resulted in altered levels of fecal and circulating metabolites compared with obese controls.By colonizing germ-free mice with stools from the patients, we demonstrated that the surgically altered microbiota promoted reduced fat deposition in recipient mice.These mice also had a lower respiratory quotient, indicating decreased utilization of carbohydrates as fuel.

View Article: PubMed Central - PubMed

Affiliation: The Wallenberg Laboratory and Sahlgrenska Center for Cardiovascular and Metabolic Research, Department of Molecular and Clinical Medicine, Institute of Medicine, University of Gothenburg, SE-413 45 Gothenburg, Sweden.

No MeSH data available.


Related in: MedlinePlus

The Gut Microbiota Influences Fat Accumulation and Metabolism in Colonized Mice(A) Fat gain in mice colonized with human stools from OBS, RYGB, and VBG women. Fat gain was calculated as the difference between fat content normalized over body weight at the end of the experiment (d14) and fat content normalized over body weight 1 day after colonization (d1). The results presented were obtained from colonization of GF mice with fecal microbiota from two patients in each of the RYGB, VBG, and OBS groups (four to five mice per donor microbiota).(B) RQ (ratio between CO2 produced and O2 consumed) calculated for the light and dark phases and for the overall 22 hr period in the Somedic chamber.(C) RQ in the resting phase (basal RQ, calculated as the average RQ for the lowest 10 min average of O2 consumption).The results presented in (B) and (C) were obtained from colonization of GF mice with fecal microbiota from three patients in each of the RYGB, VBG, and OBS groups (3–5 mice per donor microbiota).Bars show the results of colonization with the same donor microbiota, with black dots showing individual mice and lines indicating the mean. Statistical significance of differences between the means was tested by one-way ANOVA with Tukey’s correction for multiple comparisons (a p < 0.05 for RYGB compared to OBS, b p < 0.05 for VBG compared to OBS, and c p < 0.05 for RYGB compared to VBG). See also Figure S5.
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fig5: The Gut Microbiota Influences Fat Accumulation and Metabolism in Colonized Mice(A) Fat gain in mice colonized with human stools from OBS, RYGB, and VBG women. Fat gain was calculated as the difference between fat content normalized over body weight at the end of the experiment (d14) and fat content normalized over body weight 1 day after colonization (d1). The results presented were obtained from colonization of GF mice with fecal microbiota from two patients in each of the RYGB, VBG, and OBS groups (four to five mice per donor microbiota).(B) RQ (ratio between CO2 produced and O2 consumed) calculated for the light and dark phases and for the overall 22 hr period in the Somedic chamber.(C) RQ in the resting phase (basal RQ, calculated as the average RQ for the lowest 10 min average of O2 consumption).The results presented in (B) and (C) were obtained from colonization of GF mice with fecal microbiota from three patients in each of the RYGB, VBG, and OBS groups (3–5 mice per donor microbiota).Bars show the results of colonization with the same donor microbiota, with black dots showing individual mice and lines indicating the mean. Statistical significance of differences between the means was tested by one-way ANOVA with Tukey’s correction for multiple comparisons (a p < 0.05 for RYGB compared to OBS, b p < 0.05 for VBG compared to OBS, and c p < 0.05 for RYGB compared to VBG). See also Figure S5.

Mentions: To investigate whether the altered gut microbiota of bariatric surgery patients directly affects adiposity and metabolism, we transplanted the fecal microbiota of RYGB, VBG, and OBS patients into female GF mice. We observed that mice colonized with RYGB and VBG microbiota for 2 weeks accumulated 43% and 26% less body fat, respectively, than mice colonized with OBS microbiota (Figure 5A), while mice colonized with RYGB microbiota had the highest average increase in lean mass (Figures S5A–S5C); body weight gain and food intake did not differ between the groups during the 2-week colonization period (Figures S5D and S5E). In addition, we measured oxygen (O2) consumption and carbon dioxide (CO2) production in the mice colonized with RYGB, VGB, and OBS microbiota. Although O2 consumption, body weight gain, and food intake did not differ during the measurements (Figures S5F–S5I), GF mice colonized with RYGB microbiota had a lower respiratory quotient ([RQ]; ratio between CO2 produced and O2 consumed) than mice colonized with OBS microbiota (active phase, Night1, Figure 5B) or with VBG microbiota (resting phase, Figure 5C), thus indicating decreased utilization of carbohydrates and increased utilization of lipids as fuel in recipients of RYGB microbiota.


Roux-en-Y Gastric Bypass and Vertical Banded Gastroplasty Induce Long-Term Changes on the Human Gut Microbiome Contributing to Fat Mass Regulation.

Tremaroli V, Karlsson F, Werling M, Ståhlman M, Kovatcheva-Datchary P, Olbers T, Fändriks L, le Roux CW, Nielsen J, Bäckhed F - Cell Metab. (2015)

The Gut Microbiota Influences Fat Accumulation and Metabolism in Colonized Mice(A) Fat gain in mice colonized with human stools from OBS, RYGB, and VBG women. Fat gain was calculated as the difference between fat content normalized over body weight at the end of the experiment (d14) and fat content normalized over body weight 1 day after colonization (d1). The results presented were obtained from colonization of GF mice with fecal microbiota from two patients in each of the RYGB, VBG, and OBS groups (four to five mice per donor microbiota).(B) RQ (ratio between CO2 produced and O2 consumed) calculated for the light and dark phases and for the overall 22 hr period in the Somedic chamber.(C) RQ in the resting phase (basal RQ, calculated as the average RQ for the lowest 10 min average of O2 consumption).The results presented in (B) and (C) were obtained from colonization of GF mice with fecal microbiota from three patients in each of the RYGB, VBG, and OBS groups (3–5 mice per donor microbiota).Bars show the results of colonization with the same donor microbiota, with black dots showing individual mice and lines indicating the mean. Statistical significance of differences between the means was tested by one-way ANOVA with Tukey’s correction for multiple comparisons (a p < 0.05 for RYGB compared to OBS, b p < 0.05 for VBG compared to OBS, and c p < 0.05 for RYGB compared to VBG). See also Figure S5.
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fig5: The Gut Microbiota Influences Fat Accumulation and Metabolism in Colonized Mice(A) Fat gain in mice colonized with human stools from OBS, RYGB, and VBG women. Fat gain was calculated as the difference between fat content normalized over body weight at the end of the experiment (d14) and fat content normalized over body weight 1 day after colonization (d1). The results presented were obtained from colonization of GF mice with fecal microbiota from two patients in each of the RYGB, VBG, and OBS groups (four to five mice per donor microbiota).(B) RQ (ratio between CO2 produced and O2 consumed) calculated for the light and dark phases and for the overall 22 hr period in the Somedic chamber.(C) RQ in the resting phase (basal RQ, calculated as the average RQ for the lowest 10 min average of O2 consumption).The results presented in (B) and (C) were obtained from colonization of GF mice with fecal microbiota from three patients in each of the RYGB, VBG, and OBS groups (3–5 mice per donor microbiota).Bars show the results of colonization with the same donor microbiota, with black dots showing individual mice and lines indicating the mean. Statistical significance of differences between the means was tested by one-way ANOVA with Tukey’s correction for multiple comparisons (a p < 0.05 for RYGB compared to OBS, b p < 0.05 for VBG compared to OBS, and c p < 0.05 for RYGB compared to VBG). See also Figure S5.
Mentions: To investigate whether the altered gut microbiota of bariatric surgery patients directly affects adiposity and metabolism, we transplanted the fecal microbiota of RYGB, VBG, and OBS patients into female GF mice. We observed that mice colonized with RYGB and VBG microbiota for 2 weeks accumulated 43% and 26% less body fat, respectively, than mice colonized with OBS microbiota (Figure 5A), while mice colonized with RYGB microbiota had the highest average increase in lean mass (Figures S5A–S5C); body weight gain and food intake did not differ between the groups during the 2-week colonization period (Figures S5D and S5E). In addition, we measured oxygen (O2) consumption and carbon dioxide (CO2) production in the mice colonized with RYGB, VGB, and OBS microbiota. Although O2 consumption, body weight gain, and food intake did not differ during the measurements (Figures S5F–S5I), GF mice colonized with RYGB microbiota had a lower respiratory quotient ([RQ]; ratio between CO2 produced and O2 consumed) than mice colonized with OBS microbiota (active phase, Night1, Figure 5B) or with VBG microbiota (resting phase, Figure 5C), thus indicating decreased utilization of carbohydrates and increased utilization of lipids as fuel in recipients of RYGB microbiota.

Bottom Line: The two surgical procedures induced similar and durable changes on the gut microbiome that were not dependent on body mass index and resulted in altered levels of fecal and circulating metabolites compared with obese controls.By colonizing germ-free mice with stools from the patients, we demonstrated that the surgically altered microbiota promoted reduced fat deposition in recipient mice.These mice also had a lower respiratory quotient, indicating decreased utilization of carbohydrates as fuel.

View Article: PubMed Central - PubMed

Affiliation: The Wallenberg Laboratory and Sahlgrenska Center for Cardiovascular and Metabolic Research, Department of Molecular and Clinical Medicine, Institute of Medicine, University of Gothenburg, SE-413 45 Gothenburg, Sweden.

No MeSH data available.


Related in: MedlinePlus