Open Forum Infect Dis. 2015 Feb 4;2(1):ofv004. doi: 10.1093/ofid/ofv004. eCollection 2015 Jan.
Weight gain after fecal microbiota transplantation.
Alang N1, Kelly CR2.
Abstract
Fecal microbiota transplantation (FMT) is a promising treatment for recurrent Clostridium difficile infection. We report a case of a woman successfully treated with FMT who developed new-onset obesity after receiving stool from a healthy but overweight donor. This case may stimulate further studies on the mechanisms of the nutritional-neural-microbiota axis and reports of outcomes in patients who have used nonideal donors for FMT.
Gut. 2017 Mar;66(3):429-437. doi: 10.1136/gutjnl-2015-310283. Epub 2016 Jan 6.
Microbiota-induced obesity requires farnesoid X receptor.
Parséus A1, Sommer N1, Sommer F1, Caesar R1, Molinaro A1, Ståhlman M1, Greiner TU1, Perkins R1, Bäckhed F1,2.
Abstract
OBJECTIVE:
The gut microbiota has been implicated as an environmental factor that modulates obesity, and recent evidence suggests that microbiota-mediated changes in bile acid profiles and signalling through the bile acid nuclear receptor farnesoid X receptor (FXR) contribute to impaired host metabolism. Here we investigated if the gut microbiota modulates obesity and associated phenotypes through FXR.
DESIGN:
We fed germ-free (GF) and conventionally raised (CONV-R) wild-type and Fxr-/- mice a high-fat diet (HFD) for 10 weeks. We monitored weight gain and glucose metabolism and analysed the gut microbiota and bile acid composition, beta-cell mass, accumulation of macrophages in adipose tissue, liver steatosis, and expression of target genes in adipose tissue and liver. We also transferred the microbiota of wild-type and Fxr-deficient mice to GF wild-type mice.
RESULTS:
The gut microbiota promoted weight gain and hepatic steatosis in an FXR-dependent manner, and the bile acid profiles and composition of faecal microbiota differed between Fxr-/- and wild-type mice. The obese phenotype in colonised wild-type mice was associated with increased beta-cell mass, increased adipose inflammation, increased steatosis and expression of genes involved in lipid uptake. By transferring the caecal microbiota from HFD-fed Fxr-/- and wild-type mice into GF mice, we showed that the obesity phenotype was transferable.
CONCLUSIONS:
Our results indicate that the gut microbiota promotes diet-induced obesity and associated phenotypes through FXR, and that FXR may contribute to increased adiposity by altering the microbiota composition.
Thank you Kirkwood, Are you able to post the links to the information that you found?
I would point out that the first case you mentioned was a report of one individual who experienced weight gain after a fecal transplant... seemingly the same woman we had already been discussing since my first reply to you.
The second report was a study of mice... how they transferred the gut microbes from mouse to mouse was not clear to me from what was written. Was anyone arguing here that gut microbes do not have an effect on digestion? And that digestion is not a factor in weight gain? That was certainly not my intent.
I am not going to go back and repeat all that I have said here. Fecal transplants should obviously not be made from donors who are likely to have abnormal processes taking place in their digestive systems. Obesity would be an indicator of this type of problem.
I objected to your statement, “I found it interesting that doing a stool transplant from an obese person to a thin person will cause the thin person to become obese and never regain their thin body type despite dieting.” This is an inaccurate characterization even of the publicized single case that we have been discussing. It distorts one case into some sort of urban legend.
No one knows if the poop transplant from this woman's 16 year old daughter will cause her to be forever obese. We do not know what her activity level and diet were after the procedure. Did her previous problem go away? Did she ever have problems with weight gain previously? This was not a study... this is a single case. Both of the women lived in the same household so their are other factors that could be in play and there were no controls and no records of food consumed etc... Just the end results as recorded by their doctor.