AI Article Synopsis
- - The review examines the role of ADAM17, a metalloproteinase, in developing and progressing metabolic syndrome, linking it to obesity, inflammation, and diabetes through its interaction with TNF-α.
- - Research shows that mice lacking ADAM17 are significantly leaner and exhibit notable hypermetabolism, emphasizing its importance in energy regulation.
- - Understanding ADAM17's mechanisms could reveal it as a promising target for therapies aimed at treating obesity and diabetes.
Article Abstract
In this review, we focus specifically on the role that the metalloproteinase, A Disintegrin and Metalloproteinase 17 [ADAM17] plays in the development and progression of the metabolic syndrome. There is a well-recognised link between the ADAM17 substrate tumour necrosis factor α (TNF-α) and obesity, inflammation and diabetes. In addition, knocking out ADAM17 in mice leads to an extremely lean phenotype. Importantly, ADAM17-deficient mice exhibit one of the most pronounced examples of hypermetabolism in rodents to date. It is vital to further understand the mechanistic role that ADAM17 plays in the metabolic syndrome. Such studies will demonstrate that ADAM17 is a valuable therapeutic target to treat obesity and diabetes.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8128101 | PMC |
| http://dx.doi.org/10.1042/BSR20210029 | DOI Listing |
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