Control of diabetic hyperglycaemia and insulin resistance through TSC22D4.

Nature communications (2016-11-09)
Bilgen Ekim Üstünel, Kilian Friedrich, Adriano Maida, Xiaoyue Wang, Anja Krones-Herzig, Oksana Seibert, Anke Sommerfeld, Allan Jones, Tjeerd P Sijmonsma, Carsten Sticht, Norbert Gretz, Thomas Fleming, Peter P Nawroth, Wolfgang Stremmel, Adam J Rose, Mauricio Berriel-Diaz, Matthias Blüher, Stephan Herzig
要旨

Obesity-related insulin resistance represents the core component of the metabolic syndrome, promoting glucose intolerance, pancreatic beta cell failure and type 2 diabetes. Efficient and safe insulin sensitization and glucose control remain critical therapeutic aims to prevent diabetic late complications Here, we identify transforming growth factor beta-like stimulated clone (TSC) 22 D4 as a molecular determinant of insulin signalling and glucose handling. Hepatic TSC22D4 inhibition both prevents and reverses hyperglycaemia, glucose intolerance and insulin resistance in diabetes mouse models. TSC22D4 exerts its effects on systemic glucose homeostasis-at least in part-through the direct transcriptional regulation of the small secretory protein lipocalin 13 (LCN13). Human diabetic patients display elevated hepatic TSC22D4 expression, which correlates with decreased insulin sensitivity, hyperglycaemia and LCN13 serum levels. Our results establish TSC22D4 as a checkpoint in systemic glucose metabolism in both mice and humans, and propose TSC22D4 inhibition as an insulin sensitizing option in diabetes therapy.

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Sigma-Aldrich
モノクローナル抗FLAG® M2抗体 マウス宿主抗体, clone M2, purified immunoglobulin (Purified IgG1 subclass), buffered aqueous solution (10 mM sodium phosphate, 150 mM NaCl, pH 7.4, containing 0.02% sodium azide)
Sigma-Aldrich
Anti-GLUT-4 Antibody, C-terminus, from rabbit, purified by affinity chromatography
Sigma-Aldrich
抗TSC22D4抗体 ウサギ宿主抗体, affinity isolated antibody

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