β3‐Adrenergic activation of adenylyl cyclase in mouse white adipocytes: modulation by GTP and effect of obesity

N Bégin‐Heick - Journal of cellular biochemistry, 1995 - Wiley Online Library
N Bégin‐Heick
Journal of cellular biochemistry, 1995Wiley Online Library
Lipolysis and adenylyl cyclase (AC) activation in response to β‐adrenergic agents are
abnormally low in white epididymal adipose tissue (WAT) of the ob/ob mouse. The
abundance of G‐proteins (Gsα and Giα) linked to AC is also abnormally low. By contrast, β‐
adrenergic receptor (β‐AR) levels were previously found to be normal in WAT and elevated
in liver. The relative importance of various forms of the β‐AR in mouse WAT was reassessed
in view of the discovery of the β3‐AR. The results show that (1) the β3‐AR is mainly …
Abstract
Lipolysis and adenylyl cyclase (AC) activation in response to β‐adrenergic agents are abnormally low in white epididymal adipose tissue (WAT) of the ob/ob mouse. The abundance of G‐proteins (Gsα and Giα) linked to AC is also abnormally low. By contrast, β‐adrenergic receptor (β‐AR) levels were previously found to be normal in WAT and elevated in liver. The relative importance of various forms of the β‐AR in mouse WAT was reassessed in view of the discovery of the β3‐AR. The results show that (1) the β3‐AR is mainly responsible for AC activation in lean‐mouse WAT; (2) the β3‐AR is only partly responsible for AC activation in obese mouse WAT; and (3) GTP modulates β3—‐but not β1—‐or β2‐AR activation of AC in a biphasic manner. Therefore, the β3‐AR appears responsible for the well‐known bimodal effect of GTP on β‐adrenergic receptor‐mediated AC activity in WAT.
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