Showing papers by "Martin Ridderstråle published in 1995"
TL;DR: The data suggest that GH-induced tyrosine phosphorylation of IRS-1 and the subsequent docking of PI 3-kinase are important postreceptor events in GH action.
134 citations
TL;DR: Reduction in cAMP levels by the activation of cGI-PDE may be sufficient to account for the antilipolytic action of insulin, as demonstrated in rat adipocytes with special reference to changes as cAMP-dependent protein kinase (cAMP-PK) activity ratios.
116 citations
TL;DR: It is concluded that tyrosine phosphorylation of JAK2 and the GH receptor seems to be involved in the signal transduction mechanism leading to the insulin-like effects of GH in adipocytes.
Abstract: The nature of tyrosine phosphorylations induced by GH in relation to the insulin-like metabolic effects in primary rat adipocytes was investigated. Unlike other cells, e.g. 3T3-F442A fibroblast, in which GH is believed to initiate cell differentiation through activation of the Janus tyrosine kinase-2 (JAK2), the adipocytes are metabolically active and fully differentiated cells that do not proliferate. Thus, it cannot be assumed that the same molecular mechanisms relay the acute insulin-like effects of GH. In adipocytes responsive to these effects, we found that GH induced tyrosine phosphorylation of a 114-kilodalton membrane protein, identified as the GH receptor, and a 130-kilodalton cytosolic protein, identified as JAK2. In contrast, these phosphorylations were not seen in adipocytes refractory to these effects of GH. The GH concentration dependency (ED50,1-2 nM) of these phosphorylations coincided with the increase in lipogenesis and the decrease in noradrenaline-induced lipolysis caused by the hormon...
22 citations
1 citations