Project: Research project

Project Details


Insulin shifts the steady state subcellular distribution of IGF-II
receptors from a large intracellular pool to the plasma membrane in the rat
adipose cell. In the present study, the counterregulatory effects of
adrenergic stimulation, adenosine deaminase (ADA), and cAMP on this process
have been studied. The results suggest that beta-adrenergic stimulation,
through a cAMP-dependent mechanism, markedly alters the insulin-stimulated
redistribution of IGF-II receptors. This effect is additional to the potent
antagonistic action of cAMP on insulin's signaling mechanism. We have also
examined the modulation of protein kinase C-mediated stimulation of glucose
transport activity in the rat adipose cell by 1) ligands for receptors that
mediate stimulation (R(s); lipolytic) or inhibition (R(i); antilipolytic)
of adenylate cyclase and 2) pertussis and cholera toxins which regulate the
inhibitory (G(i)) and stimulatory (G(i)) and stimulatory (G(s),) guanyl
nucleotide-binding proteins of adenylate cyclase, respectively. The results
suggest that 1) C-proteins modulate protein kinase C-mediated stimulation
of glucose transport activity by altering the intrinsic activity of glucose
transporters residing in the plasma membrane and 2) a functional G(i)
protein is required for stimulation of glucose transport activity by
phorbol esters and vasopressin.
StatusNot started