Alterations in Lipolysis, Adenylate Cyclase and Adenosine 3',5'–Monophosphate Levels in Isolated Fat Cells Following Adrenalectomy1

Allen, Donald O.; Beck, R. R.

doi:10.1210/endo-91-2-504

Cited by 32 publications

(16 citation statements)

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“…Steroid hormones modulate the ability of cells and tissues to respond to hormones that act via the second messenger cyclic AMP. In adipose tissue, in particular, adrenalectomy has been shown to attenuate catecholamine-stimulated lipolysis (Allen & Beck, 1972;Lamberts et al, 1975;Exton et al, 1972). In liver, glucocorticoids also have been shown to exert permissive effects on the catecholamine-stimulated ureogenesis and glycogenolysis (Garcia-Sainz et al, 1988;Exton et al, 1972).…”

Section: Introductionmentioning

confidence: 99%

Adipocyte G-proteins and adenylate cyclase. Effects of adrenalectomy

Ros

Northup

Malbon

1989

Biochemical Journal

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Steroid hormones modulate the ability of cells to respond to hormones that act via cyclic AMP. In adipocytes of adrenalectomized rats, cyclic AMP accumulation and lipolysis in response to adrenaline are attenuated. However, the mechanism(s) of these effects are poorly understood. The effects of altered glucocorticoid status in vivo on the steady-state amounts of components of the hormone-sensitive adenylate cyclase were analysed in rat adipocytes. beta-Adrenergic receptors were analysed by using radioligand binding and immunoblotting with an anti-receptor antiserum. Neither the amount of radioligand binding nor the amount of beta-adrenergic-receptor peptide (Mr 67,000) was altered by adrenalectomy, whereas treatment of adrenalectomized rats with dexamethasone was found to increase both parameters by more than 25% with respect to the control. Forskolin-stimulated adenylated cyclase activity was unchanged in membranes isolated from adipocytes of adrenalectomized rats, but was decreased (50%) in those from dexamethasone-treated rats. The alpha-subunit of Gs was probed by using cholera-toxin-catalysed ADP-ribosylation. Immunoblotting was used to analyse the steady-state amounts of G-protein beta-subunits (beta-G35/36). Adrenalectomy was associated with decreases in the steady-state amounts of alpha-Gs (30%) and beta-G35/36 (50%). Dexamethasone treatment of adrenalectomized animals partially restored the lipolytic response of adipocytes to adrenaline and the amounts of alpha-Gs, increased the amounts of beta-G35/36 subunits from 50% to 150% of control values, increased beta-adrenergic receptors by more than 25% and decreased adenylate cyclase activity (50%). These results suggest that the steady-state amounts of components of hormone-sensitive adenylate cyclase are differentially regulated by glucocorticoids.

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Section: Introductionmentioning

confidence: 99%

Adipocyte G-proteins and adenylate cyclase. Effects of adrenalectomy

Ros

Northup

Malbon

1989

Biochemical Journal

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“…Until now, glucocorticoid manipulation by adrenalectomy of rats and/or dexamethasone administration had led to erratic and sometimes controversial results concerning the effect of these hormones on adipocyte corticotropin receptors and adipocyte responses [15][16][17][18][19]. Moreover, the differences observed between these studies raised questions as to whether glucocorticoid hormones had direct effects or whether some aspects of their physiological role were mediated by changes in counterregulatory hormones or metabolites.…”

Section: Discussionmentioning

confidence: 99%

Dexamethasone‐dependent expression of β^1–24 corticotropin stimulated adenylate cyclase during adipose conversion of 3T3‐F442A cells

Fève

Pairault

1987

FEBS Letters

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When 3T3-F442A preadipocytes were grown in culture media supplemented with corticosteroid poor fetal calf serum and insulin they differentiated into adipocytes. Glycerophosphate dehydrogenase, a marker of terminal differentiation, developed a 600-fold increase of activity whereas the adenylate cyclase system remained unresponsive to the synthetic ACTH(1-24) analog. In contrast, 3T3-F442A adipocytes, differentiated in the presence of dexamethasone, exhibited an adenylate cyclase activity which was stimulated 4-fold by ACTH(1-24). The stimulation of the adenylate cyclase activity by GTPyS remained unchanged (about 20-25-fold) suggesting that the G regulatory coupling protein was not functionally modified by dexamethasone. Binding studies with t25I-ACTH revealed that specific cellular binding could be evidenced in dexamethasone-treated cells while control adipocytes did not exhibit any specific binding of 125I-ACTH. These findings lend support to the hypothesis that the setting off of this ACTH responsiveness in 3T3-F442A cells is regulated by dexamethasone after cells are committed to adipose differentiation.

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“…It was also found that glucocorticoids were required for the normal lipolytic response to adrenaline or ACTH (Jeanrenaud and Renold, 1960;Allen and Beck, 1972;Exton et al, 1972). Various sites have been suggested for the biochemical lesions induced by adrenalectomy.…”

Section: Synopsismentioning

confidence: 99%

Studies on adrenaline-induced lipolysis in adrenalectomized rats.

et al. 1978

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Alterations in Lipolysis, Adenylate Cyclase and Adenosine 3',5'–Monophosphate Levels in Isolated Fat Cells Following Adrenalectomy1

Cited by 32 publications

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Adipocyte G-proteins and adenylate cyclase. Effects of adrenalectomy

Adipocyte G-proteins and adenylate cyclase. Effects of adrenalectomy

Dexamethasone‐dependent expression of β^1–24 corticotropin stimulated adenylate cyclase during adipose conversion of 3T3‐F442A cells

Studies on adrenaline-induced lipolysis in adrenalectomized rats.

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Alterations in Lipolysis, Adenylate Cyclase and Adenosine 3',5'–Monophosphate Levels in Isolated Fat Cells Following Adrenalectomy1

Cited by 32 publications

References 0 publications

Adipocyte G-proteins and adenylate cyclase. Effects of adrenalectomy

Adipocyte G-proteins and adenylate cyclase. Effects of adrenalectomy

Dexamethasone‐dependent expression of β1–24 corticotropin stimulated adenylate cyclase during adipose conversion of 3T3‐F442A cells

Studies on adrenaline-induced lipolysis in adrenalectomized rats.

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Dexamethasone‐dependent expression of β^1–24 corticotropin stimulated adenylate cyclase during adipose conversion of 3T3‐F442A cells