Abstract
Browning is the process of increasing the number of brite cells, which helps to increase energy expenditure and reduce obesity. Consumption of natural and non-toxic herbal extracts that possess the browning effect is an attractive anti-obesity strategy. In this study, we examined the browning effect of cinnamon extract. We found that cinnamon extract (CE) induced typical brown adipocyte multiocular phenotype in 3T3-L1 adipocytes. The treatment also increased brown adipocytes markers and reduced white adipocytes markers in the 3T3-L1 adipocytes. In ex vivo studies, we found that CE increased brown adipocytes markers in the subcutaneous adipocytes isolated from db/db mice and diet-induced obesity (DIO) mice. However, CE did not significantly affect UCP1 expression in the adipocytes isolated from perinephric adipose tissue and epididymal adipose tissue. β3-adernergic receptor (β3-AR) antagonist reduced the CE-enhanced UCP1 expression, suggesting an involvement of the β3-AR activity. Oral administration of CE significantly increased UCP1 expression in the subcutaneous adipose tissue in vivo and reduced the body weight of the DIO mice. Taken together, our data suggest that CE has a browning effect in subcutaneous adipocytes. Our study suggests a natural non-toxic herbal remedy to reduce obesity.
Highlights
Obesity has become a public health crisis
Our data clearly demonstrated that cinnamon extract (CE) significantly increased the expressions of uncoupling protein 1 (UCP1) and other brown adipocyte markers in subcutaneous adipocytes and 3T3-L1 adipocytes
We found that CE increased UCP1 expression in subcutaneous adipocytes in vivo and reduced the body weight of the diet-induced obesity (DIO) mice
Summary
Obesity has become a public health crisis. Obese people are predisposed to a number of diseases, including cardiovascular disease, type 2 diabetes, hypertension, stroke and many types of cancers[1]. CE increased the expressions of other brown adipocyte marker genes including cell death-inducing DFFA-like effector A (Cidea), PR domain containing 16 (Prdm16), peroxisome proliferator-activated receptor gamma (PPARγ), PPARγ coactivator-1 (Pgc) and the fatty acid oxidation marker gene carnitine palmitoyltransferase 1 (Cpt1) (Fig. 4a). We found that CE increased UCP1 protein (Fig. 5a and Fig. S3) and mRNA (Fig. 5b) expressions in these subcutaneous adipocytes, and other brown adipocyte markers including Cidea and Prdm[16] (Fig. 5b). The CE treatment did not increase UCP1 expression in epididymal adipocytes isolated from these mice (Fig. 5c and Fig. S4).
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