title: Ginsenoside Rb1 promotes browning through regulation of PPARγ in 3T3-L1 adipocytes.
abstract: Browning of white adipocyte tissue (WAT) has received considerable attention due to its potential implication in preventing obesity and related comorbidities. Ginsenoside Rb1 is reported to improve glycolipid metabolism and reduce body weight in obese animals. However whether the body reducing effect mediates by browning effect remains unclear. For this purpose, 3T3-L1 adipocytes were used to study the effect of ginsenoside Rb1 on browning adipocytes specific genes and oxygen consumptions. The results demonstrate that 10 μM of ginsenoside Rb1 increases basal glucose uptake and promoted browning evidenced by significant increases in mRNA expressions of UCP-1, PGC-1α and PRDM16 in 3T3-L1 mature adipocytes. Further, ginsenoside Rb1 also increases PPARγ activity. And the browning effect is abrogated by GW9692, a PPARγ antagonist. In addition, ginsenoside Rb1 increases basal respiration rate, ATP production and uncoupling capacity in 3T3-L1 adipocytes. Those effects are also blunted by GW9692. The results suggest that ginsenoside Rb1 promote browning of 3T3-L1 adipocytes through induction of PPARγ. Our finding offer a new source to discover browning agonists and also useful to understand and extend the applications of ginseng and its constituents.
authors.affiliation: Preclinical Medicine School, Beijing University of Chinese Medicine, Beijing 100029, China.
authors.forename: Qianqian
authors.initials: Q
authors.lastname: Mu
authors.affiliation: Preclinical Medicine School, Beijing University of Chinese Medicine, Beijing 100029, China.
authors.forename: Xin
authors.initials: X
authors.lastname: Fang
authors.affiliation: Preclinical Medicine School, Beijing University of Chinese Medicine, Beijing 100029, China.
authors.forename: Xiaoke
authors.initials: X
authors.lastname: Li
authors.affiliation: Diabetes Research Center, Beijing University of Chinese Medicine, Beijing 100029, China.
authors.forename: Dandan
authors.initials: D
authors.lastname: Zhao
authors.affiliation: Diabetes Research Center, Beijing University of Chinese Medicine, Beijing 100029, China.
authors.forename: Fangfang
authors.initials: F
authors.lastname: Mo
authors.affiliation: Diabetes Research Center, Beijing University of Chinese Medicine, Beijing 100029, China.
authors.forename: Guangjian
authors.initials: G
authors.lastname: Jiang
authors.affiliation: Preclinical Medicine School, Beijing University of Chinese Medicine, Beijing 100029, China.
authors.forename: Na
authors.initials: N
authors.lastname: Yu
authors.affiliation: Preclinical Medicine School, Beijing University of Chinese Medicine, Beijing 100029, China.
authors.forename: Yi
authors.initials: Y
authors.lastname: Zhang
authors.affiliation: Preclinical Medicine School, Beijing University of Chinese Medicine, Beijing 100029, China.
authors.forename: Yubo
authors.initials: Y
authors.lastname: Guo
authors.affiliation: The Research Institute of McGill University Health Center, Montreal, Quebec H4A 3J1, Canada.
authors.forename: Min
authors.initials: M
authors.lastname: Fu
authors.affiliation: The Research Institute of McGill University Health Center, Montreal, Quebec H4A 3J1, Canada.
authors.forename: Jun-Li
authors.initials: JL
authors.lastname: Liu
authors.affiliation: Diabetes Research Center, Beijing University of Chinese Medicine, Beijing 100029, China. Electronic address: dongwei1006@gmail.com.
authors.forename: Dongwei
authors.initials: D
authors.lastname: Zhang
authors.affiliation: Diabetes Research Center, Beijing University of Chinese Medicine, Beijing 100029, China. Electronic address: gaosihua1216@163.com.
authors.forename: Sihua
authors.initials: S
authors.lastname: Gao
mesh_terms: D041721:3T3-L1 Cells; D052437:Adipocytes, Brown / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism*; D052438:Adipocytes, White / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism*; D000813:Anilides / Q000494:pharmacology; D000818:Animals; D002454:Cell Differentiation; D004268:DNA-Binding Proteins / Q000235:genetics; D004734:Energy Metabolism / Q000187:drug effects; D036145:Ginsenosides / Q000494:pharmacology*; D005947:Glucose / Q000378:metabolism; D007473:Ion Channels / Q000235:genetics; D051379:Mice; D024101:Mitochondrial Proteins / Q000235:genetics; D010101:Oxygen Consumption / Q000187:drug effects; D047495:PPAR gamma / Q000819:agonists / Q000037:antagonists & inhibitors / Q000378:metabolism*; D000071248:Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D014157:Transcription Factors / Q000235:genetics; D000071256:Uncoupling Protein 1
chemical_list: C457499:2-chloro-5-nitrobenzanilide; D000813:Anilides; D004268:DNA-Binding Proteins; D036145:Ginsenosides; D007473:Ion Channels; D024101:Mitochondrial Proteins; D047495:PPAR gamma; D000071248:Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha; C485290:Ppargc1a protein, mouse; C521133:Prdm16 protein, mouse; D012333:RNA, Messenger; D014157:Transcription Factors; C000604372:Ucp1 protein, mouse; D000071256:Uncoupling Protein 1; C442759:ginsenoside Rb1; D005947:Glucose
keywords: 3T3-L1 adipocytes; Browning; Ginsenoside Rb1; Mitochondrial respiration; PPARγ