Abstract
The relation between gut microbiota and the host has been suggested to benefit metabolic homeostasis. Brown adipose tissue (BAT) and beige adipocytes facilitate thermogenesis to maintain host core body temperature during cold exposure. However, the potential impact of gut microbiota on the thermogenic process is confused. Here, we evaluated how BAT and white adipose tissue (WAT) responded to temperature challenges in mice lacking gut microbiota. We found that microbiota depletion via treatment with different cocktails of antibiotics (ABX) or in germ-free (GF) mice impaired the thermogenic capacity of BAT by blunting the increase in the expression of uncoupling protein 1 (UCP1) and reducing the browning process of WAT. Gavage of the bacterial metabolite butyrate increased the thermogenic capacity of ABX-treated mice, reversing the deficit. Our results indicate that gut microbiota contributes to upregulated thermogenesis in the cold environment and that this may be partially mediated via butyrate.
| Original language | English |
|---|---|
| Pages (from-to) | 2720-2737 |
| Number of pages | 18 |
| Journal | Cell Reports |
| Volume | 26 |
| Issue number | 10 |
| Early online date | 5 Mar 2019 |
| DOIs | |
| Publication status | Published - 5 Mar 2019 |
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Keywords
- brown adipose tissue
- beige adipocytes
- brite adipocytes
- white adipose tissue
- hermogenesis
- UCP1
- gut microbiota
- butyrate
- antibiotics
- germ free mice
- macrophage
- IL-4
- CELLS
- COMMENSAL BACTERIA
- CATECHOLAMINES
- GUT MICROBIOTA
- DIET-INDUCED OBESITY
- ALTERNATIVELY ACTIVATED MACROPHAGES
- ENERGY-EXPENDITURE
- DEACETYLATION
- METABOLISM
- SODIUM-BUTYRATE
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)
Cite this
Microbiota Depletion Impairs Thermogenesis of Brown Adipose Tissue and Browning of White Adipose Tissue. / Li, Baoguo; Li, Li; Li, Min; Lam, Sin Man; Wang, Guanlin; Wu, Yingga; Zhang, Hanlin; Niu, Chaoqun; Zhang, Xueying; Liu, Xue; Hambly, Catherine; Jin, Wanzhu; Shui, Guanghou; Speakman, John R.
In: Cell Reports, Vol. 26, No. 10, 05.03.2019, p. 2720-2737.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Microbiota Depletion Impairs Thermogenesis of Brown Adipose Tissue and Browning of White Adipose Tissue
AU - Li, Baoguo
AU - Li, Li
AU - Li, Min
AU - Lam, Sin Man
AU - Wang, Guanlin
AU - Wu, Yingga
AU - Zhang, Hanlin
AU - Niu, Chaoqun
AU - Zhang, Xueying
AU - Liu, Xue
AU - Hambly, Catherine
AU - Jin, Wanzhu
AU - Shui, Guanghou
AU - Speakman, John R
N1 - This work was supported by the Strategic Priority Research Program of the Chinese Academy of Sciences (XDB13030000) and Natural Science Foundation of China (NSFC; 91649108), the Chinese Academy of Sciences-Novo Nordisk Foundation, as well as grants from the Chinese Academy of Sciences “1000 Talents” recruitment program and a “Great-Wall Professorship” from the Chinese Academy of Sciences-Novo Nordisk Foundation. J.R.S. was also supported by a Wolfson merit professorship from The UK Royal Society. We are grateful to all of the members of the Molecular Energetics Group for their support and discussion of the results. We would like to thank Dr. Jia and Dr. Sun from the Core Facility for Protein Research from the Institute of Biophysics, Chinese Academy of Sciences for flow cytometry, and Peter Thomson and Marina Samatiou for technical assistance with the DLW measurements.
PY - 2019/3/5
Y1 - 2019/3/5
N2 - The relation between gut microbiota and the host has been suggested to benefit metabolic homeostasis. Brown adipose tissue (BAT) and beige adipocytes facilitate thermogenesis to maintain host core body temperature during cold exposure. However, the potential impact of gut microbiota on the thermogenic process is confused. Here, we evaluated how BAT and white adipose tissue (WAT) responded to temperature challenges in mice lacking gut microbiota. We found that microbiota depletion via treatment with different cocktails of antibiotics (ABX) or in germ-free (GF) mice impaired the thermogenic capacity of BAT by blunting the increase in the expression of uncoupling protein 1 (UCP1) and reducing the browning process of WAT. Gavage of the bacterial metabolite butyrate increased the thermogenic capacity of ABX-treated mice, reversing the deficit. Our results indicate that gut microbiota contributes to upregulated thermogenesis in the cold environment and that this may be partially mediated via butyrate.
AB - The relation between gut microbiota and the host has been suggested to benefit metabolic homeostasis. Brown adipose tissue (BAT) and beige adipocytes facilitate thermogenesis to maintain host core body temperature during cold exposure. However, the potential impact of gut microbiota on the thermogenic process is confused. Here, we evaluated how BAT and white adipose tissue (WAT) responded to temperature challenges in mice lacking gut microbiota. We found that microbiota depletion via treatment with different cocktails of antibiotics (ABX) or in germ-free (GF) mice impaired the thermogenic capacity of BAT by blunting the increase in the expression of uncoupling protein 1 (UCP1) and reducing the browning process of WAT. Gavage of the bacterial metabolite butyrate increased the thermogenic capacity of ABX-treated mice, reversing the deficit. Our results indicate that gut microbiota contributes to upregulated thermogenesis in the cold environment and that this may be partially mediated via butyrate.
KW - brown adipose tissue
KW - beige adipocytes
KW - brite adipocytes
KW - white adipose tissue
KW - hermogenesis
KW - UCP1
KW - gut microbiota
KW - butyrate
KW - antibiotics
KW - germ free mice
KW - macrophage
KW - IL-4
KW - CELLS
KW - COMMENSAL BACTERIA
KW - CATECHOLAMINES
KW - GUT MICROBIOTA
KW - DIET-INDUCED OBESITY
KW - ALTERNATIVELY ACTIVATED MACROPHAGES
KW - ENERGY-EXPENDITURE
KW - DEACETYLATION
KW - METABOLISM
KW - SODIUM-BUTYRATE
UR - http://www.scopus.com/inward/record.url?scp=85061958692&partnerID=8YFLogxK
UR - http://www.mendeley.com/research/microbiota-depletion-impairs-thermogenesis-brown-adipose-tissue-browning-white-adipose-tissue
U2 - 10.1016/j.celrep.2019.02.015
DO - 10.1016/j.celrep.2019.02.015
M3 - Article
VL - 26
SP - 2720
EP - 2737
JO - Cell Reports
JF - Cell Reports
SN - 2211-1247
IS - 10
ER -