Abstract
Atriplex gmelinii is an edible halophyte that has been suggested to possess various health benefits. In the present study, 3,5-dicaffeoyl-epi-quinic acid (DEQA) isolated from A. gmelinii was tested for its ability to prevent adipogenesis in 3T3-L1 cells. Also, the molecular mechanisms by which DEQA affects differentiation of 3T3-L1 cells were investigated. The introduction of DEQA to differentiating 3T3-L1 preadipocytes resulted in suppressed adipogenesis and lowered expression of adipogenesis-related factors, PPARγ, C/EBPα, and SREBP-1c. Treatment of 3T3-L1 adipocytes with DEQA notably decreased the levels of phosphorylated p38, ERK, and JNK. In addition, presence of DEQA upregulated the levels of both inactive and phosphorylated adenosine monophosphate-activated protein kinase (AMPK) and its substrate, acetyl-CoA carboxylase (ACC). Taken together, current results indicated that DEQA exhibited a significant antiadipogenesis activity by activation of AMPK and downregulation of MAPK signal pathways in 3T3-L1 preadipocytes.
Highlights
Obesity is a worldwide health problem and many diseases such as cardiovascular disease, liver and kidney diseases, diabetes, and cancer are considered to be linked with the prior cases of excess body fat accumulation [1,2,3]
Prior to assays regarding the ability of dicaffeoyl-epi-quinic acid (DEQA) hindering differentiation and adipocyte profile of 3T3-L1 preadipocytes, its biocompatibility was tested by MTT assay
It has been demonstrated that DEQA attenuated stimulated adipogenesis without showing any cytotoxic outcome on differentiating preadipocytes indicated by lowering the amount of accumulated lipid droplets
Summary
Obesity is a worldwide health problem and many diseases such as cardiovascular disease, liver and kidney diseases, diabetes, and cancer are considered to be linked with the prior cases of excess body fat accumulation [1,2,3]. Adipose tissue that stores the excessive fat in the body plays pivotal roles in controlling body homeostasis [4]. It secretes hormones and interacts with regulation of several important organs. Current studies revealed the role of adipocyte dysfunction in the progression of obesity, cardiovascular diseases, and various metabolic diseases including type 2-diabetes [5,6,7]. Formation of new adipocyte cells, adipogenesis, takes place in two stages which can be called the determination and differentiation phases. The change of mesenchymal stem cells into adipocyte lineage is called the determination stage while the decisive differentiation of these preadipocytes into mature adipocytes is regarded as the differentiation stage [8]
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