Abstract
Adipocytes are important players in metabolic health and disease, and disruption of adipocyte development or function contributes to metabolic dysregulation. Hence, adipocytes are significant targets for therapeutic intervention in obesity and metabolic syndrome. Plants have long been sources for bioactive compounds and drugs. In previous studies, we screened botanical extracts for effects on adipogenesis in vitro and discovered that an ethanolic extract of Artemisia scoparia (SCO) could promote adipocyte differentiation. To follow up on these studies, we have used various separation methods to identify the compound(s) responsible for SCO's adipogenic properties. Fractions and subfractions of SCO were tested for effects on lipid accumulation and adipogenic gene expression in differentiating 3T3-L1 adipocytes. Fractions were also analyzed by Ultra Performance Liquid Chromatography- Mass Spectrometry (UPLC-MS), and resulting peaks were putatively identified through high resolution, high mass accuracy mass spectrometry, literature data, and available natural products databases. The inactive fractions contained mostly quercetin derivatives and chlorogenates, including chlorogenic acid and 3,5-dicaffeoylquinic acid, which had no effects on adipogenesis when tested individually, thus ruling them out as pro-adipogenic bioactives in SCO. Based on these studies we have putatively identified the principal constituents in SCO fractions and subfractions that promoted adipocyte development and fat cell gene expression as prenylated coumaric acids, coumarin monoterpene ethers, 6-demethoxycapillarisin and two polymethoxyflavones.
Highlights
Obesity, one of the great public health challenges of our time, is a major risk factor for type 2 diabetes mellitus (T2DM) and cardiovascular disease [1, 2]
We identified an extract of Artemisia scoparia (SCO) as having positive effects on adipocyte differentiation and endocrine function both in vitro and in vivo [10, 11]
We predict that the metabolically beneficial effects of SCO in vivo might be mediated by its ability to increase adipogenesis
Summary
One of the great public health challenges of our time, is a major risk factor for type 2 diabetes mellitus (T2DM) and cardiovascular disease [1, 2]. Inhibition of adipocyte differentiation was once viewed as a promising therapeutic strategy for preventing or treating obesity and its metabolic consequences. It is known that obese and insulin resistant states are associated with impaired adipogenesis and that limiting adipose tissue expansion leads to ectopic lipid deposition and metabolic dysregulation [3,4,5,6]. Clinical use of TZDs has declined substantially since 2007, in response to concerns over safety and side effects that may not occur from botanical alternatives of TZDs. adipocyte differentiation continues to be a therapeutic target of interest for intervention in metabolic related diseases including obesity and T2DM
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