Trans-anethole ameliorates obesity via induction of browning in white adipocytes and activation of brown adipocytes

May 28, 2018Biochimie

Trans-anethole reduces obesity by turning white fat into calorie-burning fat and activating brown fat

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Regenerative Health on OpenScience ↗PubMed ↗DOI ↗

Abstract

Trans-anethole (TA) alleviated high fat diet-induced obesity in mice by increasing the expression of beige-specific genes.

TA elevated the expression of beige-specific genes including Ppargc1α, Prdm16, and Ucp1.
The compound reduced adipogenesis and lipogenesis while increasing lipolysis and fat oxidation in white adipocytes.
TA enhanced thermogenic activity by promoting mitochondrial biogenesis in white adipocytes.
Molecular docking analysis predicted interactions of TA with key proteins involved in fat browning, such as β3-adrenergic receptor and sirtuin1.
TA induced browning of adipocytes through activation of β3-AR and the AMPK-mediated SIRT1 pathway.

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To treat obesity, suppression of white adipose tissue (WAT) expansion and activation of brown adipose tissue (BAT) are considered as potential therapeutic targets. Recent advances have been made in the induction of brown fat-like adipocytes (beige) in WAT, which represents an attractive potential strategy for the management and treatment of obesity. Use of natural compounds for browning of white adipocytes can be considered as a safe and novel strategy against obesity. Here, we report that trans-anethole (TA), a flavoring substance present in the essential oils of various plants, alleviated high fat diet (HFD)-induced obesity in mice models via elevation of the expression of beige-specific genes such as Ppargc1α, Prdm16, Ucp1, Cd137, Cited1, Tbx1, and Tmem26. TA also regulated lipid metabolism in white adipocytes via reduction of adipogenesis and lipogenesis as well as elevation of lipolysis and fat oxidation. Moreover, TA exhibited thermogenic activity by increasing mitochondrial biogenesis in white adipocytes and activating brown adipocytes. In addition, molecular docking analysis enabled us to successfully predict core proteins for fat browning such as β3-adrenergic receptor (β3-AR) and sirtuin1 (SIRT1) based on their low binding energy interactions with TA for promotion of regulatory mechanisms. Indeed, agonistic and antagonistic studies demonstrated that TA induced browning of 3T3-L1 adipocytes through activation of β3-AR as well as the AMPK-mediated SIRT1 pathway regulating PPARα and PGC-1α. In conclusion, TA possesses potential therapeutic implications for treatment of obesity by playing multiple modulatory roles in the induction of white fat browning, activation of brown adipocytes, and promotion of lipid catabolism.

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Trans-anethole ameliorates obesity via induction of browning in white adipocytes and activation of brown adipocytes

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