1989
DOI: 10.1016/0898-6568(89)90016-8
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Multiple defects occur in the guanine nucleotide regulatory protein system in liver plasma membranes of obese (fa/fa) but not lean (Fa/Fa) zucker rats: Loss of functional G1 and abnormal Gs function

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Cited by 41 publications
(29 citation statements)
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“…This takes advantage of the fact that Gi has a higher affinity for p[NH]ppG than Gs, thus allowing Gi to be selectively activated [1][2][3]16]. oe-Gi has also been detected in hepatocyte membranes using pertussis toxin-catalysed ADP-ribosylation [13,20]. Similarly, the presence of ce-Gi has been determined in hepatocytes using a specific antiserum (AS7) raised against the C-terminal decapeptide of the related G-protein, transducin [18].…”
Section: Resultsmentioning
confidence: 99%
“…This takes advantage of the fact that Gi has a higher affinity for p[NH]ppG than Gs, thus allowing Gi to be selectively activated [1][2][3]16]. oe-Gi has also been detected in hepatocyte membranes using pertussis toxin-catalysed ADP-ribosylation [13,20]. Similarly, the presence of ce-Gi has been determined in hepatocytes using a specific antiserum (AS7) raised against the C-terminal decapeptide of the related G-protein, transducin [18].…”
Section: Resultsmentioning
confidence: 99%
“…The concept that increased stimulation of cyclic AMP synthesis within the liver contributes to the diabetic state has gained favour in recent years from observations that plasma membranes from livers of diabetic animals possess abnormalities in the regulatory GTP-binding proteins that couple receptors to the stimulation (Gs) or inhibition (Gi) of adenylyl cyclase. It has been argued that animal models of both insulin-dependent and non-insulin dependent diabetes show impairments of G~ function in liver and hepatocyte plasma membranes [3][4][5][6]. These reports, however, have been challenged by others, who are unable to show changes in G~ function and expression in the diabetic state, but instead attribute increased cyclic AMP synthesis to the overexpression and stimulation of Gs protein function [7].…”
mentioning
confidence: 99%
“…Although this is similar to the pattern found in adipocyte membranes, it is surprising in view of the greater responsiveness of AC to the stimulatory action of catecholamines in liver membranes of obese than of lean mice and of their similar response to activation by glucagon (BeginHeick & Welsh, 1988 (Begin-Heick & Welsh, 1988). In other models of obesity and insulin resistance, a decrease in ADP-ribosylation of Gio2 was linked to loss of inhibition of AC and ascribed to increased phosphorylation of the peptide in vivo (Pyne et al, 1989;Houslay et al, 1989;Bushfield et al, 1990a,b). In the present case, the decrease in ADP-ribosylation is parallelled by a decrease in the immunodetectable peptides.…”
Section: Discussionmentioning
confidence: 99%
“…Many mutants of the AC system have been found (Haga et al, 1977;Bourne et al, 1982;Schimmer & Tsao, 1984) which alter the regulatory properties of AC. There are several examples showing that tissues differ in the proportion of regulatory components that they contain and that the relative amount of the subunits of the transducing G-proteins is subject to modulation (Bokoch, 1987;Carter et al, 1987;Milligan et al, 1987;Watkins et al, 1987;Hinsch et al, 1988;Houslay et al, 1989;Garcia-Sainz et al, 1989;Green & Johnson, 1989;Rapiejko et al, 1989).…”
Section: Introductionmentioning
confidence: 99%