Abstract
Simple SummaryThe browning of white adipose tissue can change the body’s energy distribution and improve the disorder of energy metabolism through the expression of the iconic protein UCP1 to achieve beneficial effects on the body. As a natural plant functional component, polyphenols have been found to induce the browning of white adipose tissue, such as resveratrol and catechin. Honokiol is one of the main components in Magnolia officinalis, a traditional Chinese medicine in China. Modern pharmacological tests have proven that, like many plant functional components, honokiol has broad-spectrum antibacterial, anti-tumor, anti-inflammatory, and anti-oxidation effects. However, the effect of honokiol on inducing the browning of white adipose tissue and improving energy metabolism disorder has not been reported. In this study, a high-fat diet-induced obese model was established, and proteomic analysis was performed. It was found that honokiol could promote the browning of white adipose tissue in high-fat fed mice. The AMPK-ACC-CPT1A and C/EBPα-SOAT1 pathways may be the important molecular mechanisms of the browning induced by honokiol.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.
Highlights
Obesity has become a public health issue, generally increasing in the past few decades, which is often associated with a variety of metabolic disorders such as type 2 diabetes, dyslipidemia, and cardiovascular disease [1]
brown adipose tissue (BAT) mitochondria are distinct from their counterparts in white adipose tissue (WAT) in that adenosine triphosphate (ATP) production is not their primary physiologic role
Compared with the high-fat diet (HFD) group, HON (200, 400, and 800 mg/kg) treatment did not significantly decrease the total calorie intake (TCI), suggesting that the lowering of the body fat ratios (BFRs) was not caused by the decrease in energy intake (Figure 1B)
Summary
Obesity has become a public health issue, generally increasing in the past few decades, which is often associated with a variety of metabolic disorders such as type 2 diabetes, dyslipidemia, and cardiovascular disease [1]. The essence of obesity was believed to the growing size of adipose tissue due to excessive energy intake, secularly resulting in body fat accumulation [2]. Adipose tissue is a metabolic organ in the regulation of whole-body energy homeostasis, receiving excess energy and mobilizing stored energy [3]. Two major types of adipose tissue were previously identified: WAT and brown adipose tissue (BAT). The WAT functions as a key energy reservoir for other organs, whereas the brown adipose tissue dissipates chemical energy as heat [4]. BAT mitochondria are distinct from their counterparts in WAT in that ATP production is not their primary physiologic role
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