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. Author manuscript; available in PMC: 2018 Feb 1.
Published in final edited form as: Can J Diabetes. 2016 Sep 7;41(1):108–113. doi: 10.1016/j.jcjd.2016.07.002

Figure 7.

Figure 7

Activation of the endosomal IRK is sufficient to promote insulin signalling. Left, (bottom) IRK activity in ENS and PM following bpV(phen) administration to rats pretreated with colchicine to block recycling of IRK from ENS to PM. IRK activation is seen exclusively in the ENS; (top) IRS-1 phosphorylation is seen when only endosomal IRK is activated. Right, (bottom) bpV(phen) lowers blood glucose levels; (top) in the absence of any effect to increase glucose uptake as measured by 2-deoxyglucose (2-DG) accumulation in skeletal muscle exemplified by diaphragm (DIA). (bottom) Lowering of blood glucose levels by bpV(phen) in colchicine-treated rats. For details see reference (22).