Abstract
Sinapic acid is a plant-derived phenolic compound, which acts as an antioxidant, anticancer, and anti-inflammatory agent. Although sinapic acid is valuable in a variety of therapeutic applications, its role in the improvement of obesity-related metabolic disease is relatively unexplored. Brown-like adipocytes (beige adipocytes) are characterized by a high concentration of mitochondria and high expression of uncoupling protein 1 (UCP1), which has specific functions in energy expenditure and thermogenesis. This study assessed the browning effects of sinapic acid in 3T3-L1 adipocytes. We investigated the expression of beige marker genes in 3T3-L1 adipocytes treated with sinapic acid. Sinapic acid increased the expression of peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) and UCP1. Sinapic acid also promoted mitochondrial biogenesis by dose-dependently upregulating the oxygen consumption rate and enhancing the expression of representative subunits of oxidative phosphorylation complexes. In addition, treatment with p38 mitogen-activated protein kinase (MAPK) inhibitor and cAMP response element binding (CREB) inhibitor decreased the expressions of genes associated with thermogenesis, mitochondrial biogenesis, and oxidative phosphorylation. In summary, sinapic acid initiates browning 3T3-L1 adipocytes via the p38 MAPK/CREB signaling pathway. Thus, sinapic acid may have potential therapeutic implication in obesity.
Highlights
Obesity arising from overaccumulation of fat in the body is caused by the imbalance between energy absorption and release
We determined whether sinapic acid had an adverse effect on adipocyte viability. 3T3-L1 cells were treated with sinapic acid at concentrations of 1 to 20 μM, and cell viability was measured
To investigate whether sinapic acid induces the transformation of white adipocytes to beige adipocytes, genes expressed in beige adipocytes were examined. e mRNA levels of uncoupling protein 1 (UCP1) and PGC-1α, thermogenic genes, were investigated in 3T3-L1 cells treated with sinapic acid
Summary
Obesity arising from overaccumulation of fat in the body is caused by the imbalance between energy absorption and release. Adipose tissue is functionally composed of two types of fat: white fat and brown fat [1]. Unlike white adipose cells, which store fat as an energy source, brown fat cells break down stored fat to release heat [2, 3]. Brown adipocytes express uncoupling protein 1 (UCP1), which promotes mitochondrial thermogenesis [3]. In addition to white and brown adipocytes, when the sympathetic nerves or β-adrenergic receptors are activated by exercise and cold or spicy foods, white adipocytes are converted into beige adipocytes through the expression of UCP1 and PGC-1α [4, 5]. Beige fat cells contain large numbers of mitochondria and small lipid droplets and oxidize fat to generate heat [6, 7]
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