β2-Adrenergic receptors in propranolol therapy: Does down-regulation do it?

Hepatology ◽  
1987 ◽  
Vol 7 (2) ◽  
pp. 398-400 ◽  
Author(s):  
Andrew K. Burroughs
1989 ◽  
Vol 121 (5) ◽  
pp. 705-713 ◽  
Author(s):  
Nobuyuki Sato ◽  
Minoru Irie ◽  
Hiroshi Kajinuma ◽  
Kazuo Suzuki

Abstract. Adipocytes from streptozotocin-diabetic rats showed a markedly reduced lipolytic response to glucagon concomitant with a 90% or greater decrease in the number of glucagon receptors per cell. In contrast, β-adrenergic receptors assessed by [3H]dihydroalprenolol binding and lipolysis stimulated by isoproterenol, dibutyryl 3′5′-cyclic AMP and 3-isobutyl-1-methylxanthine were reduced by only 10–25% in diabetic rats compared with controls. Furthermore, quantitative analysis of the relationship between the amount of cell-bound glucagon and the hormone-stimulated lipolysis revealed that the function of the remaining 10% of glucagon receptors remained intact in cells from diabetic animals. These findings suggest that the lipolytic cascades, including β-adrenergic receptors, in adipocytes are not greatly impaired by diabetes, and therefore, the unresponsiveness of these cells to glucagon is mostly due to a marked reduction in the number of glucagon receptors, probably as a result of a down-regulation by postprandial hyperglucagonemia.


1997 ◽  
Vol 82 (4) ◽  
pp. 1235-1242
Author(s):  
Stefan Engelhardt ◽  
Wolfgang Zieger ◽  
Jan Kassubek ◽  
Martin C. Michel ◽  
Martin J. Lohse ◽  
...  

1997 ◽  
Vol 337 (20) ◽  
pp. 1429-1434 ◽  
Author(s):  
André Lacroix ◽  
Johanne Tremblay ◽  
Guy Rousseau ◽  
Michel Bouvier ◽  
Pavel Hamet

2012 ◽  
Vol 36 (12) ◽  
pp. 1171-1183 ◽  
Author(s):  
Yulia Koryakina ◽  
Stacie M. Jones ◽  
Lawrence E. Cornett ◽  
Kathryn Seely ◽  
Lisa Brents ◽  
...  

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