Decreased glucagon binding and glucagon-stimulated lipolysis in adipocytes from streptozotocin-diabetic rats

1989 ◽  
Vol 121 (5) ◽  
pp. 705-713 ◽  
Author(s):  
Nobuyuki Sato ◽  
Minoru Irie ◽  
Hiroshi Kajinuma ◽  
Kazuo Suzuki
Keyword(s):  
Quantitative Analysis ◽  
Cyclic Amp ◽  
Adrenergic Receptors ◽  
Marked Reduction ◽  
Diabetic Rats ◽  
Down Regulation ◽  
Streptozotocin Diabetic Rats ◽  
Β Adrenergic Receptors ◽  
Glucagon Receptors ◽  
The Relationship

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.

OESTRADIOL-INDUCED SYNTHESIS OF A SPECIFIC UTERINE PROTEIN IN PROPRANOLOL-TREATED RATS

1975 ◽  
Vol 65 (2) ◽  
pp. 215-218 ◽  
Author(s):  
N. DUPONT-MAIRESSE ◽  
P. GALAND
Keyword(s):  
Cyclic Amp ◽  
Adrenergic Receptors ◽  
Blocking Agent ◽  
Conflicting Evidence ◽  
Early Increase ◽  
Β Adrenergic Receptors ◽  
Adrenergic Blocking

SUMMARY While there is conflicting evidence concerning an effect of oestradiol on uterine cyclic AMP concentration, results from different laboratories (including ours) are in agreement that even when observed, the early increase in uterine cyclic AMP after oestradiol injection fails to occur when propranolol, a β-adrenergic blocking agent, is given (50 μg, i.p.) 20 min before the oestradiol. The present work shows that pretreatment with propranolol failed to inhibit an early uterine response to oestradiol, namely the synthesis after 1 h of uterine protein, or class of proteins, IP. It is concluded that the induction of IP by oestradiol does not depend on an increase in uterine cyclic AMP concentration and that β-adrenergic receptors do not have a role in this oestrogenic response.

Altered release of growth hormone from dispersed adenohypophysial cells of streptozotocin diabetic rats. II. Effects of a phorbol ester and secretagogues which increase cyclic AMP

1989 ◽  
Vol 67 (10) ◽  
pp. 1321-1325
Author(s):  
M. S. Sheppard ◽  
B. A. Eatock ◽  
R. M. Bala
Keyword(s):  
Growth Hormone ◽  
Cyclic Amp ◽  
Phorbol Ester ◽  
Phosphodiesterase Inhibitor ◽  
Adenosine Monophosphate ◽  
Diabetic Rats ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Growth Hormone Releasing Factor ◽  
Streptozotocin Diabetic Rats

We have shown in the companion paper that somatotrophs dispersed from streptozotocin diabetic rats exhibit altered sensitivity to the natural hypothalamic controlling hormones, growth hormone releasing factor and somatostatin. We have further studied the effects on growth hormone release from dispersed adenohypophysial cells of normal and streptozotocin diabetic rats of stimulation by compounds that increase cyclic 3′,5′-adenosine monophosphate formation or inhibit its breakdown and of a phorbol ester. The cells of the diabetic rats had no change in sensitivity in response to either cholera toxin or forskolin. A phosphodiesterase inhibitor caused an equal GH release from cells of both diabetic and normal animals after 60 min of incubation. There was no change in sensitivity of the cells of diabetic animals or in the maximal reponse of these cells to the phorbol ester 12-O-tetradecanoylphorbol 13-acetate when compared with normal cells. A low calcium medium that blocked growth hormone releasing factor stimulated growth hormone release from normal rat cells also blocked it from the cells of the diabetic rats. These results suggest that the defect in response of the somatotrophs of diabetic animals is specific and only occurs with the hypothalamic hormones and not with other secretagogues.Key words: growth hormone, diabetes, streptozotocin, cyclic AMP, phorbol ester.

scholarly journals Tocolytic Therapy with Fenoterol Induces Selective Down-Regulation of β-Adrenergic Receptors in Human Myometrium1

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

Regulation by progesterone of the high-affinity state of myometrial β-adrenergic receptor and of adenylate cyclase activity in the pregnant rat

1991 ◽  
Vol 6 (2) ◽  
pp. 137-145 ◽  
Author(s):  
J. Cohen-Tannoudji ◽  
V. Vivat ◽  
J. Heilmann ◽  
C. Legrand ◽  
J. P. Maltier
Keyword(s):  
Cyclic Amp ◽  
Adenylate Cyclase ◽  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Maximum Velocity ◽  
Cyclase Activity ◽  
Adenylate Cyclase Activity ◽  
Pregnant Rat ◽  
High Affinity ◽  
Β Adrenergic Receptors

ABSTRACT The effects of pregnancy or progesterone dominance on the β-adrenergic responsiveness of the uterus were studied in myometrial membranes from mid-and late-pregnant rats (day 15 and on the 16th h of day 22 of pregnancy respectively) or 24 h after administration of progesterone. Levels of the high (RH)- and low (RL)-affinity states of the β-adrenergic receptor were determined by competition experiments between 125I-labelled cyanopindolol binding and the selective β-agonist isoproterenol. The ratio KL/KH (respective dissociation constants) was determined since it also reflects the degree of formation of the high-affinity state of the β-adrenergic receptor. From day 15 to the 10th h of day 22 of pregnancy, two distinct affinity states were apparent: 80–55% RH (KH=0·31–0·21 μm) and 45–20% RL (KL=14–5 μm) with a ratio of KL/KH of 55–34. In the last 6 h before birth, β-adrenergic receptors underwent uncoupling which was paralleled by decreased responsiveness of myometrial adenylate cyclase to isoproterenol (maximum velocity (Vmax)=17±3 vs 44±3 fmol cyclic AMP/10 min per mg protein on day 15). At this stage of pregnancy, previous exposure to progesterone resulted in a 1·8-fold increase in 125I-labelled cyanopindolol-binding sites (Bmax) and the reappearance of the high-affinity state (67% RH, KH=0·19±0·04 (s.e.m.) μm, ratio KL/KH=81·1 ± 16·9). These results were reversed in the presence of the antiprogestin RU486 (100% RL, KL=24·6±4·1 μm, 41% reduction of Bmax). Moreover, after progesterone, adenylate cyclase activity was strongly stimulated by isoproterenol (Vmax=60±12 fmol cyclic AMP/10 min per mg protein vs 17±3 in controls). The data suggest (1) that progesterone may exert a permissive effect on β-adrenergic responsiveness of the pregnant rat myometrium and (2) that at term, both a desensitization mechanism involving uncoupling of β-adrenergic receptors and a decrease in activation of adenylate cyclase lead to a loss of myometrial response to β-agonists.

β-adrenergic receptors in brain microvessels of diabetic rats

Life Sciences ◽  
1984 ◽  
Vol 34 (11) ◽  
pp. 1095-1100 ◽  
Author(s):  
M.S. Magnoni ◽  
H. Kobayashi ◽  
E. Trezzi ◽  
A. Catapano ◽  
P.F. Spano ◽  
...  
Keyword(s):  
Adrenergic Receptors ◽  
Diabetic Rats ◽  
Brain Microvessels ◽  
Β Adrenergic Receptors

MECHANISM OF OESTRADIOL ACTION ON THE RAT UTERUS: INDEPENDENCE OF CYCLIC AMP, PROSTAGLANDIN E2 AND β-ADRENERGIC MEDIATION

1973 ◽  
Vol 58 (3) ◽  
pp. 525-533 ◽  
Author(s):  
U. ZOR ◽  
Y. KOCH ◽  
S. A. LAMPRECHT ◽  
J. AUSHER ◽  
H. R. LINDNER
Keyword(s):  
Cyclic Amp ◽  
Adrenergic Receptors ◽  
Tissue Concentration ◽  
Ovariectomized Rats ◽  
Minor Role ◽  
Prostaglandin E ◽  
Rat Uterus ◽  
Stimulatory Action ◽  
Β Adrenergic Receptors

SUMMARY The hypothesis that cyclic AMP plays an essential role in mediating the biological action of oestradiol on the uterus, was tested by determining the tissue concentration of the cyclic nucleotide after incubation of uteri of immature rats with oestradiol or after injection of this steroid into immature or ovariectomized rats. The effect of known stimulants of uterine adenyl cyclase, namely β-adrenergic drugs and prostaglandin E2 (PGE2), on the level of cyclic AMP in the uterus was also examined both in vitro and in vivo. In either system, oestradiol failed to enhance the concentration of cyclic AMP in the uterine tissue, whereas adrenaline or the almost purely β-adrenergic agonist isoprenaline (isoproterenol) caused cyclic AMP accumulation that was susceptible to inhibition by the β-adrenergic blocking agent propranolol. Prostaglandin E2, and to a much lesser degree prostaglandin F2α, increased cyclic AMP concentration in the uterus, but the effect of PGE2 was not inhibited by propranolol. It may be concluded that oestradiol does not cause appreciable stimulation of PGE2 synthesis or activation of β-adrenergic receptors in the rat uterus since, otherwise, increased cyclic AMP production should have been observed after the treatment with oestradiol. Isoprenaline mimicked the stimulatory action of oestradiol on uterine ornithine decarboxylase. However, this action of isoprenaline was abolished by propranolol, whereas that of oestradiol was only slightly, though significantly, inhibited. The present findings do not support the view that the action of oestradiol on the uterus is mediated by cyclic AMP, and also suggest that β-adrenergic receptors and PGE2 can have only a minor role, if any, in the mechanism of action of this hormone.

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