TY - JOUR
T1 - Gut microbiota induces weight gain and inflammation in the gut and adipose tissue independent of manipulations in diet, genetics, and immune development
AU - Kulkarni, Devesha H.
AU - Rusconi, Brigida
AU - Floyd, Alexandria N.
AU - Joyce, Elisabeth L.
AU - Talati, Khushi B.
AU - Kousik, Hrishi
AU - Alleyne, Dereck
AU - Harris, Dalia L.
AU - Garnica, Lorena
AU - McDonough, Ryan
AU - Bidani, Shay S.
AU - Kulkarni, Hrishikesh S.
AU - Newberry, Elizabeth P.
AU - McDonald, Keely G.
AU - Newberry, Rodney D.
N1 - Publisher Copyright:
© 2023 The Author(s). Published with license by Taylor & Francis Group, LLC.
PY - 2023
Y1 - 2023
N2 - Obesity and the metabolic syndrome are complex disorders resulting from multiple factors including genetics, diet, activity, inflammation, and gut microbes. Animal studies have identified roles for each of these, however the contribution(s) specifically attributed to the gut microbiota remain unclear, as studies have used combinations of genetically altered mice, high fat diet, and/or colonization of germ-free mice, which have an underdeveloped immune system. We investigated the role(s) of the gut microbiota driving obesity and inflammation independent of manipulations in diet and genetics in mice with fully developed immune systems. We demonstrate that the human obese gut microbiota alone was sufficient to drive weight gain, systemic, adipose tissue, and intestinal inflammation, but did not promote intestinal barrier leak. The obese microbiota induced gene expression promoting caloric uptake/harvest but was less effective at inducing genes associated with mucosal immune responses. Thus, the obese gut microbiota is sufficient to induce weight gain and inflammation.
AB - Obesity and the metabolic syndrome are complex disorders resulting from multiple factors including genetics, diet, activity, inflammation, and gut microbes. Animal studies have identified roles for each of these, however the contribution(s) specifically attributed to the gut microbiota remain unclear, as studies have used combinations of genetically altered mice, high fat diet, and/or colonization of germ-free mice, which have an underdeveloped immune system. We investigated the role(s) of the gut microbiota driving obesity and inflammation independent of manipulations in diet and genetics in mice with fully developed immune systems. We demonstrate that the human obese gut microbiota alone was sufficient to drive weight gain, systemic, adipose tissue, and intestinal inflammation, but did not promote intestinal barrier leak. The obese microbiota induced gene expression promoting caloric uptake/harvest but was less effective at inducing genes associated with mucosal immune responses. Thus, the obese gut microbiota is sufficient to induce weight gain and inflammation.
KW - gut microbiome
KW - inflammation
KW - obesity
UR - http://www.scopus.com/inward/record.url?scp=85178503951&partnerID=8YFLogxK
U2 - 10.1080/19490976.2023.2284240
DO - 10.1080/19490976.2023.2284240
M3 - Article
C2 - 38036944
AN - SCOPUS:85178503951
SN - 1949-0976
VL - 15
JO - Gut microbes
JF - Gut microbes
IS - 2
M1 - 2284240
ER -