Evidence that levels of malate dehydrogenase and fumarase are increased by cAMP in rat myotubes

1984 ◽  
Vol 247 (1) ◽  
pp. C33-C38 ◽  
Author(s):  
J. C. Lawrence ◽  
W. J. Salsgiver
Keyword(s):  
Energy Metabolism ◽  
Malate Dehydrogenase ◽  
Potential Role ◽  
Primary Cultures ◽  
Phosphodiesterase Inhibitors ◽  
Dibutyryl Camp ◽  
Rat Skeletal Muscle ◽  
Oxidative Energy Metabolism ◽  
Enzymes Of Energy Metabolism

We have investigated the potential role of adenosine 3',5'-cyclic monophosphate (cAMP) in controlling levels of enzymes of energy metabolism in primary cultures of rat skeletal muscle cells. Incubating myotubes with cholera toxin or forskolin (2 persistent activators of adenylate cyclase) significantly increased the levels of two enzymes of oxidative metabolism, fumarase and malate dehydrogenase. These enzymes were also increased (1.5- to 2.0-fold) by phosphodiesterase inhibitors (caffeine, theophylline, theobromine, 3-isobutyl-1-methylxanthine, papaverine, MJ 1988, Ro 20–1724, or SQ 20009) and the cAMP derivatives: 8-bromo-cAMP or dibutyryl cAMP. In contrast two enzymes of glycolytic metabolism, lactate dehydrogenase and pyruvate kinase, were not consistently affected by these agents. The results presented provide strong evidence that an increase in cAMP can lead to an increase in certain enzymes of oxidative energy metabolism.

Stimulation of Ca(2+)-dependent exocytosis of the sperm acrosome by cAMP acting downstream of phospholipase A2

Reproduction ◽  
2000 ◽  
pp. 57-68 ◽  
Author(s):  
J Garde ◽  
ER Roldan
Keyword(s):  
Arachidonic Acid ◽  
Phospholipase A2 ◽  
Phospholipase C ◽  
Phosphodiesterase Inhibitors ◽  
Dibutyryl Camp ◽  
Camp Phosphodiesterase ◽  
Ram Sperm ◽  
Camp Formation ◽  
Stimulation Of

Spermatozoa undergo exocytosis in response to agonists that induce Ca2+ influx and, in turn, activation of phosphoinositidase C, phospholipase C, phospholipase A2, and cAMP formation. Since the role of cAMP downstream of Ca2+ influx is unknown, this study investigated whether cAMP modulates phospholipase C or phospholipase A2 using a ram sperm model stimulated with A23187 and Ca2+. Exposure to dibutyryl-cAMP, phosphodiesterase inhibitors or forskolin resulted in enhancement of exocytosis. However, the effect was not due to stimulation of phospholipase C or phospholipase A2: in spermatozoa prelabelled with [3H]palmitic acid or [14C]arachidonic acid, these reagents did not enhance [3H]diacylglycerol formation or [14C]arachidonic acid release. Spermatozoa were treated with the phospholipase A2 inhibitor aristolochic acid, and dibutyryl-cAMP to test whether cAMP acts downstream of phospholipase A2. Under these conditions, exocytosis did not occur in response to A23187 and Ca2+. However, inclusion of dibutyryl-cAMP and the phospholipase A2 metabolite lysophosphatidylcholine did result in exocytosis (at an extent similar to that seen when cells were treated with A23187/Ca2+ and without the inhibitor). Inclusion of lysophosphatidylcholine alone, without dibutyryl-cAMP, enhanced exocytosis to a lesser extent, demonstrating that cAMP requires a phospholipase A2 metabolite to stimulate the final stages of exocytosis. These results indicate that cAMP may act downstream of phospholipase A2, exerting a regulatory role in the exocytosis triggered by physiological agonists.

Evidence for cAMP as a mediator of gonadotropin secretion from male pituitaries

1987 ◽  
Vol 253 (3) ◽  
pp. E296-E299
Author(s):  
G. A. Bourne ◽  
D. M. Baldwin
Keyword(s):  
Protein Synthesis ◽  
Potential Role ◽  
De Novo ◽  
Follicle Stimulating Hormone ◽  
Gonadotropin Releasing Hormone ◽  
Dibutyryl Camp ◽  
Camp Production ◽  
Gonadotropin Secretion ◽  
De Novo Protein Synthesis

The purpose of this study was to use sodium flufenamate, a compound that inhibits gonadotropin-releasing hormone (GnRH)-stimulated adenosine 3',5'-cyclic monophosphate (cAMP) production in the pituitary, to evaluate the potential role of cAMP as a mediator of GnRH-stimulated gonadotropin secretion from male pituitaries. Quartered male pituitaries were perifused at 37 degrees C and sequential effluent fractions collected every 10 min. Infusions of GnRH resulted in a twofold increase in luteinizing hormone (LH) and follicle-stimulating hormone (FSH) secretion. Cycloheximide, 5 microM, completely inhibited the GnRH-stimulated LH and FSH secretion. Infusions of 0.1 mM flufenamate had similar effects on gonadotropin secretion as cycloheximide, whereas the administration of 5 mM dibutyryl cAMP in combination with GnRH and flufenamate restored the secretory responses of both hormones. The flufenamate-inhibited GnRH stimulated LH and FSH release, which was restored by DBcAMP and appeared to be protein synthesis dependent and specific for cAMP. These results suggest an indirect role for cAMP as a mediator of gonadotropin secretion from male pituitaries. However, in contrast to female pituitaries, the secretion of these hormones from male pituitaries is completely dependent on cAMP and de novo protein synthesis.

scholarly journals Study Progression of Apelin/APJ Signaling and Apela in Different Types of Cancer

2021 ◽  
Vol 11 ◽  
Author(s):  
Longfei Liu ◽  
Xiaoping Yi ◽  
Can Lu ◽  
Yong Wang ◽  
Qiao Xiao ◽  
...  
Keyword(s):  
Stress Response ◽  
Energy Metabolism ◽  
G Protein ◽  
Potential Role ◽  
Cardiovascular Regulation ◽  
Cancer Development ◽  
Endogenous Ligand ◽  
Different Types ◽  
G Protein Coupled

Apelin is an endogenous ligand that binds to the G protein-coupled receptor angiotensin-like-receptor 1 (APJ). Apelin and APJ are widely distributed in organs and tissues and are involved in multiple physiological and pathological processes including cardiovascular regulation, neuroendocrine stress response, energy metabolism, etc. Additionally, apelin/APJ axis was found to play an important role in cancer development and progression. Apela is a newly identified endogenous ligand for APJ. Several studies have revealed the potential role of Apela in cancers. In this article, we review the current studies focusing on the role of apelin/APJ signaling and Apela in different cancers. Potential mechanisms by which apelin/APJ and Apela mediate the regulation of cancer development and progression were also mentioned. The Apelin/APJ signaling and Apela may serve as potential therapeutic candidates for treatment of cancer.

scholarly journals Potential Role of Acetyl-CoA Synthetase (acs) and Malate Dehydrogenase (mae) in the Evolution of the Acetate Switch in Bacteria and Archaea

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Elliott P. Barnhart ◽  
Marcella A. McClure ◽  
Kiki Johnson ◽  
Sean Cleveland ◽  
Kristopher A. Hunt ◽  
...  
Keyword(s):  
Malate Dehydrogenase ◽  
Potential Role ◽  
Acetyl Coa

Disturbed energy metabolism and lipid profile after a 4 week high oral fructose challenge: potential role of bile acids?

2015 ◽  
Vol 53 (05) ◽  
Author(s):  
C Kienbacher ◽  
S Traussnigg ◽  
E Halilbasic ◽  
C Fuchs ◽  
W Dolak ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Lipid Profile ◽  
Bile Acids ◽  
Potential Role

scholarly journals Mitochondria in Sepsis-Induced AKI

2019 ◽  
Vol 30 (7) ◽  
pp. 1151-1161 ◽  
Author(s):  
Jian Sun ◽  
Jingxiao Zhang ◽  
Jiakun Tian ◽  
Grazia Maria Virzì ◽  
Kumar Digvijay ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Potential Role ◽  
Regional Blood Flow ◽  
Flow Distribution ◽  
Endothelial Activation ◽  
Therapeutic Approaches ◽  
Potential Therapeutic Target ◽  
Human Sepsis ◽  
Effective Drugs

AKI is a common clinical condition associated with the risk of developing CKD and ESKD. Sepsis is the leading cause of AKI in the intensive care unit (ICU) and accounts for nearly half of all AKI events. Patients with AKI who require dialysis have an unacceptably high mortality rate of 60%–80%. During sepsis, endothelial activation, increased microvascular permeability, changes in regional blood flow distribution with resulting areas of hypoperfusion, and hypoxemia can lead to AKI. No effective drugs to prevent or treat human sepsis-induced AKI are currently available. Recent research has identified dysfunction in energy metabolism as a critical contributor to the pathogenesis of AKI. Mitochondria, the center of energy metabolism, are increasingly recognized to be involved in the pathophysiology of sepsis-induced AKI and mitochondria could serve as a potential therapeutic target. In this review, we summarize the potential role of mitochondria in sepsis-induced AKI and identify future therapeutic approaches that target mitochondrial function in an effort to treat sepsis-induced AKI.

Control of enzyme activities in individual myotubes cultured without nerve

1985 ◽  
Vol 249 (3) ◽  
pp. C313-C317 ◽  
Author(s):  
P. M. Nemeth ◽  
L. Solanki ◽  
J. C. Lawrence
Keyword(s):  
Skeletal Muscle ◽  
Lactate Dehydrogenase ◽  
Malate Dehydrogenase ◽  
Enzyme Activities ◽  
Adenylate Kinase ◽  
Contractile Activity ◽  
Primary Cultures ◽  
Rat Skeletal Muscle

The activities of lactate dehydrogenase, malate dehydrogenase, phosphorylase, and adenylate kinase were measured in single myotubes dissected from primary cultures of rat skeletal muscle. For a given enzyme, activities among the spontaneously contracting cells varied as much as eightfold. When the myotubes were paralyzed with tetrodotoxin, the variability in enzyme levels was markedly decreased. These and other findings suggest that differences in enzyme levels among individual myotubes may arise as a result of differences in their pattern of contractile activity.

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