ArticleBMC pharmacology & toxicology2024
Dapagliflozin promotes white adipose tissue browning though regulating angiogenesis in high fat induced obese mice.
Article in BMC pharmacology & toxicology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 7 citations in OpenAlex.
- SGLT2 inhibitors and their role in reducing adiposopathy and inflammation in diabetes and non-diabetes CKD patients.International urology and nephrology · 2026Observational
- Illuminating Glucose: How to Unveil Organ-Specific Insulin Resistance and Guide Metabolic Strategies in Diabetes.Diabetes/metabolism research and reviews · 2026Review
- Heart matters: How glucose- and lipid-modulating drugs remodel epicardial adipose tissue accumulation, inflammatory patterns and browning.Diabetes, obesity & metabolism · 2026Review
- SGLT2 Inhibitors: Multifaceted Therapeutic Agents in Cardiometabolic and Renal Diseases.Metabolites · 2025Review
- Dapagliflozin attenuates metabolic dysfunction-associated steatotic liver disease by inhibiting lipid accumulation, inflammation and liver fibrosis.BMC pharmacology & toxicology · 2025Article
- SGLT2 inhibition and adipose tissue metabolism: current outlook and perspectives.Cardiovascular diabetology · 2024Review
- The Effects of SGLT2 Inhibitors on Blood Pressure and Other Cardiometabolic Risk Factors.International journal of molecular sciences · 2024 · on this mapReview
- The Role of Adipocytes Recruited as Part of Tumor Microenvironment in Promoting Colorectal Cancer Metastases.International journal of molecular sciences · 2024Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Browning of white adipose tissue (WAT) is become an appealing target for therapeutics in the treatment of obesity and related metabolic diseases. Dapagliflozin is widely used in the treatment of type 2 diabetes, and it is also found that the drug exhibits regulate systemic metabolism such as obesity, insulin resistance and hepatic steatosis. However, the precise role of dapagliflozin on WAT remodeling remains to be elucidated. The current study aimed to explore the role of dapagliflozin on WAT browning in high-fat diet (HFD)-induced obese mice. Male C57BL/6J mice (n = 6 per group) were used to establish obesity model by following feeding with HFD for 6 weeks. The mice were randomly treated with or without dapagliflozin for the experimental observation. The volume and fat fraction of WAT were quantified, H&E, UCP-1 staining and immunohistochemistry were conducted to investigate the white-to-brown fat conversion and angiogenesis in WAT respectively. Quantitative real-time polymerase chain reaction (qPCR) was employed to explore the mRNA expression levels of genes related to fat browning and angiogenesis in WAT. Subsequently, 3T3-L1 cells were used to explore the effect of dapagliflozin on preadipocytes differentiation in vitro. Our results demonstrated that dapagliflozin could reduce body weight gain and promote WAT browning in HFD induced obese mice via regulating lipogenesis and angiogenesis in WAT. Furthermore, dapagliflozin reduce cells differentiation, up-regulate the expression of WAT browning and angiogenesis genes in 3T3-L1 adipocytes in vitro. In conclusion, dapagliflozin can potentially promote WAT browning in HFD induced obese mice via improving lipogenesis and angiogenesis in WAT.
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