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The Metalloproteinase ADAM28 Promotes Metabolic Dysfunction in Mice
Lakshini Herat1, Caroline Rudnicka2, Yasunori Okada3
1Dobney Hypertension Centre, School of Medicine and Pharmacology, University of Western Australia, Crawley WA 6009, Australia. lakshini.weerasekera@uwa.edu.au.
International Journal of Molecular Sciences
|April 22, 2017
Summary
A Disintegrin And Metalloproteinase 28 (ADAM28) is elevated in metabolic syndrome. Inhibiting ADAM28 reduced obesity, improved insulin sensitivity, and lowered liver inflammation in mice, suggesting it as a therapeutic target.
Area of Science:
- Biochemistry
- Metabolic Diseases
- Molecular Biology
Background:
- Obesity and type 2 diabetes are significant global health burdens.
- Previous studies linked A Disintegrin And Metalloproteinase 28 (ADAM28) to human obesity and type 2 diabetes pathogenesis.
Purpose of the Study:
- To characterize ADAM28 expression in a mouse model of metabolic syndrome.
- To investigate the functional role of ADAM28 in high-fat diet-induced obesity using molecular inhibition.
Main Methods:
- Assessed ADAM28 mRNA and protein expression in mouse liver.
- Utilized siRNA to downregulate ADAM28 in a diet-induced obesity model.
- Studied ADAM28 knockout mice.
- Measured metabolic parameters, including weight, glucose tolerance, insulin sensitivity, and liver enzymes.
Main Results:
- ADAM28 expression was significantly increased in the livers of mice with metabolic syndrome.
- Noradrenaline elevated ADAM28 mRNA in human monocytes.
- ADAM28 downregulation via siRNA led to reduced weight gain, improved insulin sensitivity, decreased liver TNF-α, and normalized liver enzymes.
- ADAM28 knockout mice showed lower body weight, improved lipid profiles, and reduced liver enzymes.
Conclusions:
- ADAM28 plays a significant pathogenic role in metabolic syndrome.
- Targeting ADAM28 may offer a novel therapeutic strategy for metabolic syndrome and associated conditions like obesity and diabetes.
