scholarly journals Evidence that stimulation of plasma-membrane Ca2+ inflow is an early action of glucagon and dibutyryl cyclic AMP in rat hepatocytes

1993 ◽  
Vol 292 (1) ◽  
pp. 19-22 ◽  
Author(s):  
F L Bygrave ◽  
A Gamberucci ◽  
R Fulceri ◽  
A Benedetti
Keyword(s):  
Plasma Membrane ◽  
Cyclic Amp ◽  
Rat Hepatocytes ◽  
Fixed Time ◽  
Time Interval ◽  
Dibutyryl Cyclic Amp ◽  
Fixed Time Interval ◽  
Early Action ◽  
Co Addition ◽  
Stimulation Of

The ability of glucagon (1 nM) and of dibutyryl cyclic AMP (50 microM) to increase cytosolic free Ca2+ concentration ([Ca2+]i) in Fura-loaded rat hepatocytes was examined in a system wherein Ca2+ inflow was induced by the re-admission of excess Ca2+ to a nominally Ca(2+)-free medium. An increase in [Ca2+]i did not occur in the absence of either agonist, but did so after co-addition of either agonist with Ca2+. Increasing the time between addition of dibutyryl cyclic AMP (or of glucagon) and Ca2+ led to increases in [Ca2+]i; half-maximal and maximal increases were observed at 0 s (i.e. at co-addition) and 5-7 s respectively. Dibutyryl cyclic AMP and Ca2+ each exhibited a concentration-dependence when their respective concentrations were changed for a fixed time interval between additions. Half-maximal and maximal effects were obtained with 30 microM and 50 microM dibutyryl cyclic AMP and with 0.5 mM and approx. 1 mM Ca2+ respectively. The data demonstrate an early action of glucagon and dibutyryl cyclic AMP on [Ca2+]i. It is argued that the agonist-induced rise in [Ca2+]i results from an increase in plasma-membrane Ca2+ inflow, an effect that appears to occur much earlier than that on mobilization of internal stores of Ca2+.

scholarly journals Stimulation by glucocorticoids of protein degradation in hepatocyte monolayers

1981 ◽  
Vol 196 (1) ◽  
pp. 33-40 ◽  
Author(s):  
M F Hopgood ◽  
M G Clark ◽  
F J Ballard
Keyword(s):  
Cyclic Amp ◽  
Protein Degradation ◽  
Monolayer Culture ◽  
Rat Hepatocytes ◽  
Protein Breakdown ◽  
Dibutyryl Cyclic Amp ◽  
Intracellular Proteins ◽  
Autophagic Process ◽  
Soluble Material ◽  
Stimulation Of

1. Protein degradation in rat hepatocytes in stationary monolayer culture was measured as release of radioactive trichloroacetic acid-soluble material from intracellular proteins labelled with [3H]leucine. 2. Glucocorticoids, but not other steroids, stimulated protein breakdown in the hepatocyte monolayers. The effects observed were greater when the cells were preincubated with the hormones, indicating that the stimulation was not immediate. In addition, the stimulation by glucocorticoids persisted for up to 4 h after hormone removal. 3. Cycloheximide and the lysosomotropic agents leupeptin and ammonia effectively blocked glucocorticoid stimulation of protein degradation. 4. Insulin blocked dexamethasone stimulation when added at the same time as the steroid, but not when added 3 h later. 5. Stimulation of protein breakdown by dexamethasone was additive with that by glucagon or dibutyryl cyclic AMP, suggesting that its mechanism of action is different from that of the latter two agents. 6. Total activities of several lysosomal enzymes were unaffected under conditions where protein breakdown was stimulated by either glucagon or dexamethasone. 7. It is suggested that, whereas glucagon, dibutyryl cyclic AMP and insulin modulate protein breakdown in these cells via changes in autophagocytosis, the stimulation by glucocorticoids is exerted independently, perhaps by stimulating the synthesis of membrane proteins essential to the autophagic process.

scholarly journals Stimulation of hepatic inositol 1,4,5-trisphosphate kinase activity by Ca2+-dependent and -independent mechanisms

1988 ◽  
Vol 256 (3) ◽  
pp. 697-701 ◽  
Author(s):  
T J Biden ◽  
J G Altin ◽  
A Karjalainen ◽  
F L Bygrave
Keyword(s):  
Cyclic Amp ◽  
Kinase Activity ◽  
Rat Hepatocytes ◽  
Cytosolic Fraction ◽  
Dibutyryl Cyclic Amp ◽  
Assay Medium ◽  
Tetradecanoylphorbol Acetate ◽  
Inositol 1,4,5 Trisphosphate ◽  
Stimulation Of

A cytosolic fraction derived from rat hepatocytes was used to investigate the regulation of inositol 1,4,5-trisphosphate [Ins(1,4,5)P3] kinase, the enzyme which converts Ins(1,4,5)P3 to inositol 1,3,4,5-tetrakisphosphate [Ins(1,3,4,5)P4]. The activity was doubled by raising the free Ca2+ concentration of the assay medium from 0.1 microM to 1.0 microM. A 5 min preincubation of the hepatocytes with 100 microM-dibutyryl cyclic AMP (db.cAMP) plus 100 nM-tetradecanoylphorbol acetate (TPA) resulted in a 40% increase in Ins(1,4,5)P3 kinase activity when subsequently assayed at 0.1 microM-Ca2+. This effect was smaller at [Ca2+] greater than 0.5 microM, and absent at 1.0 microM-Ca2+. Similar results were obtained after preincubation with 100 microM-db.cAMP plus 300 nM-vasopressin (20% increase at 0.1 microM-Ca2+; no effect at 1.0 microM-Ca2+). Preincubation with vasopressin, db.cAMP or TPA alone did not alter Ins(1,4,5)P3 kinase activity. It is proposed that these results, together with recent evidence implicating Ins(1,3,4,5)P4 in the control of Ca2+ influx, could be relevant to earlier findings that hepatic Ca2+ uptake is synergistically stimulated by cyclic AMP analogues and vasopressin.

Control of brown adipose tissue lipolysis and respiration by adenosine

1983 ◽  
Vol 245 (6) ◽  
pp. E555-E559 ◽  
Author(s):  
D. Szillat ◽  
L. J. Bukowiecki
Keyword(s):  
Adipose Tissue ◽  
Cyclic Amp ◽  
Palmitic Acid ◽  
Brown Adipose Tissue ◽  
Brown Adipocyte ◽  
Tissue Respiration ◽  
Dibutyryl Cyclic Amp ◽  
Response Curves ◽  
Brown Adipose ◽  
Stimulation Of

Adenosine competitively inhibited the stimulatory effects of (-)-isoproterenol on lipolysis and respiration in hamster brown adipocytes. The low value of the apparent ki for respiratory inhibition by adenosine (7 nM) indicated that the nucleoside may control brown adipocyte function under physiological concentrations. Significantly, the dose-response curves for isoproterenol stimulation of lipolysis and respiration were both shifted by adenosine to higher agonist concentrations by the same order of magnitude, providing additional evidence for a tight coupling between lipolysis and respiration. The inhibitory effects of adenosine were rapidly reversed by a) adenosine deaminase, b) agents known to increase intracellular cyclic AMP levels (isoproterenol, isobutylmethylxanthine, dibutyryl cyclic AMP), and c) direct stimulation of respiration with palmitic acid. These results, combined with the fact that adenosine failed to affect respiration evoked either by dibutyryl cyclic AMP or by palmitic acid, strongly indicate that adenosine regulates brown adipose tissue respiration at an early metabolic step of the stimulus-thermogenesis sequence, most probably at the level of the adenylate cyclase complex.

scholarly journals Improved bounds for the availability and unavailability in a fixed time interval for systems of maintained, interdependent components

1980 ◽  
Vol 12 (01) ◽  
pp. 200-221 ◽  
Author(s):  
B. Natvig
Keyword(s):  
Lower Bound ◽  
System Reliability ◽  
Nuclear Reactors ◽  
Random Variables ◽  
Fixed Time ◽  
Time Interval ◽  
Coherent System ◽  
Exact Results ◽  
Fixed Time Interval ◽  
Special Case

In this paper we arrive at a series of bounds for the availability and unavailability in the time interval I = [t A , t B ] ⊂ [0, ∞), for a coherent system of maintained, interdependent components. These generalize the minimal cut lower bound for the availability in [0, t] given in Esary and Proschan (1970) and also most bounds for the reliability at time t given in Bodin (1970) and Barlow and Proschan (1975). In the latter special case also some new improved bounds are given. The bounds arrived at are of great interest when trying to predict the performance process of the system. In particular, Lewis et al. (1978) have revealed the great need for adequate tools to treat the dependence between the random variables of interest when considering the safety of nuclear reactors. Satyanarayana and Prabhakar (1978) give a rapid algorithm for computing exact system reliability at time t. This can also be used in cases where some simpler assumptions on the dependence between the components are made. It seems, however, impossible to extend their approach to obtain exact results for the cases treated in the present paper.

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