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Honokiol Alleviates High-Fat Diet-Induced Obesity of Mice by Inhibiting Adipogenesis and Promoting White Adipose Tissue Browning.

ABSTRACT: Honokiol (HON) is one of the main biological active components of the traditional Chinese medicine Magnolia officinalis and has many health benefits. The aim of this study was to investigate whether HON could alleviate obesity in mice by inhibiting adipogenesis and promoting the browning of white adipose tissue (WAT). C57BL/6 mice were divided into five groups and fed with a normal diet (ND), high-fat diet (HFD), or HFD supplemented with 200 (H200), 400 (H400), or 800 (H800) mg/kg BW HON for 8 weeks. The results showed that the mice fed HFD plus HON had lower body fat ratios (BFRs) and smaller adipocyte diameters in the epididymal WAT compared with those of the HFD group. With a proteomics analysis, the HON group upregulated 30 proteins and downregulated 98 proteins in the epididymal WAT of mice, and the steroid O-acyltransferase 1 (SOAT1) was screened as a key protein. The HON supplement prevented HFD-induced adipogenesis by reduced the mRNA and protein expression of SOAT1 and CCAAT/enhancer-binding protein-α (C/EBPα), suggesting that SOAT1 might play an important role in regulating adipogenesis. Moreover, HON treatment increased the expression of proteins related to the classical pathways of energy and lipid metabolism, such as AMP-activated kinase (AMPK) and acetyl-CoA carboxylase (ACC), and promoted the browning of epididymal WAT by upregulation of the protein expression of uncoupling protein 1 (UCP1) in the HFD mice. In conclusion, these results suggest that HON supplements could prevent increases in body fat for HFD mice by suppressing adipogenesis and promoting WAT browning.

SUBMITTER: Ding Y

PROVIDER: S-EPMC8224378 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Aims/hypothesisDespite a similar fat storing function, visceral (intra-abdominal) white adipose tissue (WAT) is detrimental, whereas subcutaneous WAT is considered to protect against metabolic disease. Recent findings indicate that thermogenic genes, expressed in brown adipose tissue (BAT), can be induced primarily in subcutaneous WAT. Here, we investigate the hypothesis that the Wilms tumour gene product (WT1), which is expressed in intra-abdominal WAT but not in subcutaneous WAT and BAT, suppresses a thermogenic program in white fat cells.MethodsHeterozygous Wt1 knockout mice and their wild-type littermates were examined in terms of thermogenic and adipocyte-selective gene expression. Glucose tolerance and hepatic lipid accumulation in these mice were assessed under normal chow and high-fat diet conditions. Pre-adipocytes isolated from the stromal vascular fraction of BAT were transduced with Wt1-expressing retrovirus, induced to differentiate and analysed for the expression of thermogenic and adipocyte-selective genes.ResultsExpression of the thermogenic genes Cpt1b and Tmem26 was enhanced and transcript levels of Ucp1 were on average more than tenfold higher in epididymal WAT of heterozygous Wt1 knockout mice compared with wild-type mice. Wt1 heterozygosity reduced epididymal WAT mass, improved whole-body glucose tolerance and alleviated severe hepatic steatosis upon diet-induced obesity in mice. Retroviral expression of WT1 in brown pre-adipocytes, which lack endogenous WT1, reduced mRNA levels of Ucp1, Ppargc1a, Cidea, Prdm16 and Cpt1b upon in vitro differentiation by 60-90%. WT1 knockdown in epididymal pre-adipocytes significantly lowered Aldh1a1 and Zfp423 transcripts, two key suppressors of the thermogenic program. Conversely, Aldh1a1 and Zfp423 mRNA levels were increased approximately five- and threefold, respectively, by retroviral expression of WT1 in brown pre-adipocytes.Conclusion/interpretationWT1 functions as a white adipocyte determination factor in epididymal WAT by suppressing thermogenic genes. Reducing Wt1 expression in this and other intra-abdominal fat depots may represent a novel treatment strategy in metabolic disease.

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Honokiol Alleviates High-Fat Diet-Induced Obesity of Mice by Inhibiting Adipogenesis and Promoting White Adipose Tissue Browning.

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