Groundsel Bush (Baccharis halimifolia) Extract Promotes Adipocyte Differentiation In Vitro and Increases Adiponectin Expression in Mature Adipocytes.

Anik Boudreau,Jacqueline Stephens,Allison Richard,Scott Fuller,David Ribnicky

doi:10.3390/biology7020022

Abstract

An ethanolic extract of Baccharis halimifolia (groundsel bush, GB), which is a native Louisiana plant with documented use in Creole folk medicine, has been shown to inhibit lipopolysaccharide (LPS)-induced inflammation in cultured macrophages. Here, we examine the effects of GB on adipocyte development and function, as these processes are attractive targets for intervention in insulin resistance. Oil Red O neutral lipid staining, reverse transcription-quantitative polymerase chain reaction (RT-qPCR), and immunoblotting were used to measure GB effects on lipid accumulation, gene expression, and protein abundance, respectively. In differentiating 3T3-L1 adipocytes, GB enhanced lipid accumulation and increased expression of several adipogenic genes (GLUT4, aP2, ADPN, CEBPα, FAS, and PPARγ). Protein levels of two of these adipogenic markers (aP2 and adiponectin) were examined and found to be induced by GB treatment. In mature adipocytes, GB reduced the gene expression of resistin, a pro-inflammatory endocrine factor, increased the adiponectin protein levels in a time-dependent manner, and substantially attenuated the TNF-alpha-induced reduction in adiponectin. In macrophages, GB reduced the expression of pro-inflammatory genes that were induced by LPS. GB produces metabolically favorable changes in differentiating adipocytes, mature adipocytes, and macrophages in vitro, suggesting its potential use as a dietary supplement or nutraceutical to support metabolic health and resiliency.

Highlights

Metabolic syndrome, which is a collection of risk factors, including insulin resistance and obesity, has emerged as a major public health challenge in the 21st century [1,2]
10% fetal bovine serum (FBS) and 0.425 μM insulin for cells induced with standard MDI cocktail, or 0.21 μM insulin for cells induced with 0.5× MDI cocktail, and cells were treated again with the groundsel bush (GB) extract. 48 h later, cells were fed with Dulbecco’s Modified Eagle’s Medium (DMEM) plus 10% FBS and treated with GB
In a follow-up experiment, differentiating 3T3-L1 adipocytes were treated with 5, 20, or 50 μg/mL of GB, and lipid accumulation was assessed by Oil Red O (ORO) staining

Summary

Introduction

Metabolic syndrome, which is a collection of risk factors, including insulin resistance and obesity, has emerged as a major public health challenge in the 21st century [1,2]. We know that in obesity, adipocyte differentiation is often impaired, and that the inability of adipose tissue to expand is associated with poor metabolic outcomes [4] In addition to their well-established function as safe storage for lipids, adipocytes are understood to be indispensable endocrine regulators of insulin sensitivity and glucose homeostasis [5,6], in large part through their. Biology 2018, 7, 22 capacity to synthesize and secrete adiponectin, which promotes insulin sensitivity in peripheral tissues, such as skeletal muscle and liver, thereby mediating whole-body glucose homeostasis [7] This endocrine action of adipose tissue is disrupted in obese states [8], which, in turn, further exacerbates the features of metabolic syndrome. Obesity and metabolic disease are known to be associated with the activation of inflammatory pathways within adipose tissue, where adipocytes and immune cells (principally macrophages) interact and promote insulin resistance, contributing to the vicious cycle of metabolic dysfunction and impaired adipose tissue function

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