Jian Pi Tiao Gan Yin alleviates obesity phenotypes through mTORC1/SREBP1 signaling in vitro and in vivo

Xiaoming Song; Lulu Han; Xiaowan Lin; Minghui Tian; Fenglei Sun; Bo Feng

doi:10.21037/atm-22-685

Jian Pi Tiao Gan Yin alleviates obesity phenotypes through mTORC1/SREBP1 signaling in vitro and in vivo

Ann Transl Med. 2022 Mar;10(6):291. doi: 10.21037/atm-22-685.

Authors

Xiaoming Song^#¹, Lulu Han^#², Xiaowan Lin³, Minghui Tian³, Fenglei Sun⁴, Bo Feng¹

Affiliations

¹ Department of Geriatrics, the First Affiliated Hospital of Shandong First Medical University, Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan, China.
² Neurology Ward 3, the Fifth People's Hospital of Jinan, Jinan, China.
³ First Clinical Medical College, Shandong University of Traditional Chinese Medicine, Jinan, China.
⁴ General Medicine, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, China.

^# Contributed equally.

Abstract

Background: Obesity has been considered as a leading cause of multiple metabolic syndromes, such as type 2 diabetes and hypertension cardiovascular diseases. Jian Pi Tiao Gan Yin (JPTGY), a Chinese herb preparation, is used to treat obesity of liver qi stagnation and spleen deficiency. The mechanism of action of JPTGY in obesity remains unclear. This study evaluated the effect of JPTGY on obesity.

Methods: The mechanism of action of JPTGY on obesity was investigated in high-fat diet (HFD)-induced obese mice and palmitic acid-treated 3T3-L1 cells. Lipid droplet accumulation was detected using oil red O staining. Factors associated with lipid accumulation were detected by western blotting.

Results: Treatment with JPTGY reduced HFD-induced adiposity and body weight gain. JPTGY increased the levels of brown adipose tissue biomarkers in obese mice and palmitic acid-treated 3T3-L1 cells, including peroxisome proliferator-activated receptor gamma coactivator-1-alpha (PGC-1α) and uncoupling protein-1 (UCP-1). Meanwhile, the protein expression of white adipose tissue biomarkers, such as AGT, primary subtalar arthrodesis (PSTA), and endothelin receptor type A (EDNRA), was decreased in obese mice and palmitic acid-treated 3T3-L1 cells. JPTGY affects browning of 3T3-L1 cells through mechanistic target of rapamycin complex 1 (mTORC1) signaling. JPTGY decreased the expression levels of key adipogenic-specific proteins and lipogenic enzymes, including peroxisome proliferator-activated receptor γ (PPARγ), CCAAT/enhancer binding protein α (C/EBPα), sterol regulatory element binding protein (SREBP), and FAS. Treatment with the mTOR activator MHY reversed JPTGY-mediated protein expression.

Conclusions: We concluded that JPTGY relieved obesity phenotypes through mTORC1/SREBP1 signaling in vitro and in vivo. JPTGY may benefit the attenuation of obesity.

Keywords: Jian Pi Tiao Gan Yin (JPTGY); Obesity; mechanistic target of rapamycin complex 1 (mTORC1); sterol regulatory element-binding protein 1 (SREBP1).