Inhibition of Aurora-A improves insulin resistance by ameliorating islet inflammation and controlling interleukin-6 in a diabetic mouse model. (1st January 2020)

• Record Type: Journal Article
• Authors: Meng, Fandong; Sun, Qiangwei; Zhou, Dongmei; Li, Qiang; Han, Jing; Liu, Deshan; Yang, Jing
• Is Part Of: Adipocyte. Volume 9:Number 1(2020)
• Page Start: 609
• Page End: 619
• Publication Date: 2020-01-01
• Subjects: Aurora-A -- IL-6 -- macrophages -- insulin resistance -- inflammation; Fat cells -- Periodicals; Adipocytes -- Periodicals; 611.018276
• DOI: 10.1080/21623945.2020.1829851
• Languages: English
• ISSNs: 2162-3945

Abstract

ABSTRACT: Aurora-A kinase, a serine/threonine mitotic kinase, is reportedly upregulated in skin tissues of individuals with type 2 diabetes mellitus, although its function in diabetes is unclear. C57BL/6 J mice were utilized to establish a type 2 diabetic model and explore the functions of Aurora-A in diabetes. Aurora-A was highly expressed in the pancreas of the diabetic mice as confirmed by western blot. Inhibition of Aurora-A did not affect fasting blood glucose and body weight, but did improve insulin resistance, as indicated by improved oral glucose tolerance, insulin tolerance, and the Homoeostasis Model Assessment-Insulin Resistance index. Blockade of Aurora-A dramatically decreased the number of infiltrating macrophages in the pancreas in parallel with decreases in the levels of serum insulin and interleukin-6 (IL-6) mRNA. The levels of phosphorylated forms of protein kinase B, which are the key mediators of in insulin resistance, were not induced in liver, adipocyte tissues, and skeletal muscle by alisertib treatment. Our findings indicate that suppression of Aurora-A could at least partially enhance insulin sensitivity by decreasing the number of infiltrating macrophages and IL-6 level in a type 2 diabetic mouse model.