Nucleobindin-2 is a positive regulator for insulin-stimulated glucose transporter 4 translocation in fenofibrate treated E11 podocytes.

Abstract:

:The physiology of insulin signaling under normal and disease conditions is well studied in classical insulin target tissues, but not in podocytes. To examine insulin stimulation of podocyte GLUT4 translocation, we established a protocol involving treatment with the PPARα agonist fenofibrate to induce E11 podocyte differentiation within 48 hours rather than 7-10 days, which is required for differentiation under the reported protocol. This allowed us to transiently introduce GLUT4 reporter cDNA and RNAi and thereby to examine the regulatory pathway involved. Here we demonstrate that treatment with 200 μM fenofibrate for 36 hours following transfection had a dramatic effect on podocyte morphology, induced several podocyte specific protein expression markers (G protein-coupled receptor 137B, chloride intracellular channel 5, and nephrin) and resulted in insulin-stimulated GLUT4 translocation. In addition, Nucleobindin-2 was found to constitutively associate with Septin 7 (the repressor of GLUT4 translocation), and knockdown of Nucleobindin-2 was found to completely abrogate insulin-stimulated GLUT4 translocation. Together, these data suggest that Nucleobindin-2 may repress Septin7-induced inhibition of insulin-stimulated GLUT4 translocation in podocytes.

journal_name

Endocr J

journal_title

Endocrine journal

authors

Saito T,Yamada E,Okada S,Shimoda Y,Tagaya Y,Hashimoto K,Satoh T,Mori M,Okada J,Pessin JE,Yamada M

doi

10.1507/endocrj.ej14-0330

subject

Has Abstract

pub_date

2014-01-01 00:00:00

pages

933-9

issue

9

eissn

0918-8959

issn

1348-4540

pii

DN/JST.JSTAGE/endocrj/EJ14-0330

journal_volume

61

pub_type

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