Treatment of Metabolic Syndrome and Obesity
Categories: Other Disorders
Reference #: 2022-019
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Georgetown University researchers discovered a potential drug treatment that inhibits the activity of a neutral amino acid transporter in fat cells, preventing the development of adipocyte exuberance, resulting in weight loss and reduced adipocyte hypertrophy in mice under a chronic high fat diet. This innovation reveals potential methods and compositions for treating obesity or reducing weight or fat mass in a subject.
Adipocytes, or fat cells, serve as a sink for lipid storage in our bodies. However, when lipid accumulation far exceeds their breakdown, adipocytes, in response, will enlarge, expand, and ultimately recruit immune cells to adipose tissues and promote inflammation. There are no effective drugs to prevent this pathological metabolic response, “adipocyte exuberance,” which can lead to obesity and chronic health problems if not regulated. Therefore, strategies to temper adipocyte exuberance might restore adipocyte homeostasis and prevent the development of obesity and associated diseases.
- Potential for preventing or reducing weight gain/obesity and the development of diet-associated metabolic syndrome and diseases
- Ability to be used in treatments of diseases such as type 2 diabetes, heart disease, and stroke
- Possible methods of reducing body weight, reducing white adipose tissue, and reducing inflammation in adipose tissue
- Possible application in preventing an increase in fat mass and inhibiting weight gain
- Possible application of converting white adipose tissue to brown adipose tissue
- Pharmaceutical composition administered systemically with little to no adverse side effects
- New use for known compounds or class
Stage of Development
To confirm the pharmacological study, researchers are currently examining the effect of the genetic deletion of a specific amino acid transporter, specifically in adipocytes in mice under a high-fat diet.
Provisional application has been filed.
Jeffrey Huang, PhD
Mi-Hye Lee, PhD