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Updated: Jul 13, 2026

Measuring the Rate of Lipolysis in Ex Vivo Murine Adipose Tissue and Primary Preadipocytes Differentiated In Vitro
Published on: March 17, 2023
Cathepsin L activity controls adipogenesis and glucose tolerance
Min Yang1, Yaou Zhang, Jiehong Pan
1Cardiovascular Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA.
Cathepsin L (CatL) degrades key proteins involved in fat cell development and glucose regulation. Inhibiting CatL improves adipogenesis, glucose uptake, and metabolic health, suggesting CatL as a therapeutic target for obesity and diabetes.
Area of Science:
- Biochemistry
- Metabolic research
- Pathobiology
Background:
- Cysteine proteases are crucial in human diseases.
- Cathepsin L (CatL) is implicated in metabolic dysregulation.
Purpose of the Study:
- To investigate the role of CatL in adipogenesis and glucose intolerance.
- To explore CatL as a potential therapeutic target for metabolic disorders.
Main Methods:
- In vitro studies on pre-adipocytes.
- Analysis of CatL-deficient mice.
- Pharmacological inhibition of CatL in obese mouse models.
Main Results:
- CatL degrades fibronectin, insulin receptor (IR), and IGF-1R.
- CatL inhibition reduces adipogenesis and lipid accumulation, enhancing glucose uptake.
- CatL-deficient and CatL-inhibited mice exhibit improved metabolic profiles, including reduced body weight and improved glucose tolerance.
Conclusions:
- CatL plays a significant role in adipogenesis and glucose metabolism.
- Targeting CatL offers a promising therapeutic strategy for obesity and type 2 diabetes.
- Elevated CatL levels in obese and diabetic patients underscore its relevance in metabolic diseases.
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