Implications of ADAM17 activation for hyperglycaemia,obesity and type 2 diabetes |
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Authors: | Jennifer Matthews Sofia Villescas Lakshini Herat Markus Schlaich Vance Matthews |
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Affiliation: | 1.Dobney Hypertension Centre, School of Biomedical Science - Royal Perth Hospital Unit, University of Western Australia, Crawley, WA 6009, Australia;2.Dobney Hypertension Centre, School of Medicine – Royal Perth Hospital Unit, University of Western Australia, Crawley, WA 6009, Australia;3.Department of Cardiology and Department of Nephrology, Royal Perth Hospital, Perth, WA 6000, Australia |
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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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Keywords: | ADAM17 hypertension metabolic syndromes obesity TACE type 2 diabetes |
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