The extracellular portion of the insulin receptor beta-subunit regulates the cellular trafficking of the insulin-insulin receptor complex. Studies on Chinese hamster ovary cells carrying the Cys 860--&gt;Ser insulin receptor mutation

Benzi, Luca; Cecchetti, P; Am, Ciccarone; Novelli, Sara; Paoli, Anna A. de; Bertacca, A; Maffei, Margherita; Maggi, Davide; Andraghetti, Gabriella; Prato, Stefano Del; Cordera, Renzo

doi:10.1530/eje.0.1480365

Cited by 3 publications

(1 citation statement)

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“…, 1990). The high concentration of insulin used in the present study and the time‐course of the internalization and recycling (Benzi et al. , 2003) suggest that desensitization could be the reason for the short‐lived effect of insulin observed.…”

Section: Discussionsupporting

confidence: 88%

Insulin induces cobalt uptake in a subpopulation of rat cultured primary sensory neurons

Sathianathan

Avelino

Charrua

et al. 2003

Eur J of Neuroscience

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Previous findings show that both the vanilloid receptor 1 and the insulin receptor are expressed on small primary sensory neurons. As insulin evokes activity in second messengers which could induce opening of the vanilloid receptor 1, we examined, by using the cobalt-uptake technique, whether or not insulin can activate cultured rat primary sensory neurons through activating the vanilloid receptor 1. Capsaicin (50, 100 and 500 nm) induced concentration-dependent labelling in primary sensory neurons. Preincubation of cells in insulin (10 micromoles) for 10 min followed by a 2-min wash did not produce significant change in the capsaicin-induced labelling. Coapplication of insulin (10 micromoles) with capsaicin, however, potentiated the 50 and 100 nm capsaicin-evoked staining. Insulin itself also produced cobalt labelling in a concentration-dependent manner. The size-frequency distributions of neurons showing capsaicin- or insulin-induced cobalt accumulation were similar. The insulin-induced cobalt labelling was significantly reduced by the tyrosine kinase inhibitor, tyrphostin AG1024, the vanilloid receptor 1 antagonists, ruthenium red and capsazepine, the protein kinase inhibitor, staurosporine and the phospholipase C inhibitor neomycin. Double immunostaining of cultured primary sensory neurons and sections from dorsal root ganglia revealed that about one-third of the cells coexpress the insulin receptor and vanilloid receptor 1. These findings suggest that insulin activates a subpopulation of primary sensory neurons, probably through phosphorylation- and/or phosphatidylinositol(4,5)biphosphate hydrolysis-evoked activation of the vanilloid receptor 1. Although the insulin-induced activation of vanilloid receptor 1 seems to be a short-lived effect in vitro, in vivo it might play a role in the development of burning pain sensation in hyperinsulinism.

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Section: Discussionsupporting

confidence: 88%