Regulation of glucose transport by insulin, bombesin, and bradykinin in Swiss 3T3 fibroblasts: Involvement of protein kinase C-dependent and -independent mechanisms☆

摘要: Abstract Glucose transport stimulation by insulin, bombesin, and bradykinin in Swiss 3T3 fibroblasts was compared with the phosphoinositide hydrolysis effects of same stimulants a variety experimental paradigms known to affect generation and/or functioning intracellular second messengers: short- long-term treatments phorbol dibutyrate, that cause activation down-regulation protein kinase C, respectively; cell loading high [quin2], causes clamping [Ca2+]i near resting level; poisoning pertussis toxin, affects GTP binding proteins Go Gi class; treatment Ca2+ ionophores. maximal [insulin] affected neither toxin nor C down-regulation. The latter, however, partially blocked action suboptimal [insulin]; moreover, acute dibutyrate caused responses more than additive at all [insulin]. Thus, insulin on glucose cells appears be synergistically potentiated C-dependent mechanism, not directly mediated enzyme. This result correlates lack effect hydrolysis. In contrast, part induced bombesin appeared proportion these peptides C-independent portion response found inhabitable toxin. latter might suggest an interaction between receptor transporter, class.