ArticleAnnals of translational medicine2022
Jian Pi Tiao Gan Yin alleviates obesity phenotypes through mTORC1/SREBP1 signaling
Article in Annals of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed, 7 citations in OpenAlex.
- Dapagliflozin promotes white adipose tissue browning though regulating angiogenesis in high fat induced obese mice.BMC pharmacology & toxicology · 2024Article
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Authors and funding
6 authors at 5 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
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
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