Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:4.6.1.1 (adenylate cyclase)
 19,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The cellular basis for the cold-induced increase in lipoprotein lipase activity in rat brown adipose tissue was investigated. Rats were treated with inhibitory agents and either exposed to cold for 4 h or injected with isoprenaline. Lipoprotein lipase activity was followed in acetone-ether extracts of the tissue. Besides cold, both the beta-adrenergic agonist isoprenaline and the adenylate cyclase activator cholera toxin were able to increase lipoprotein lipase activity in the tissue. The protein synthesis inhibitor cycloheximide fully abolished this response; the half-life of lipoprotein lipase activity was both in control and in the cold-exposed state approximately 2 h. Also the mRNA synthesis inhibitor actinomycin D fully abolished the cold-, the isoprenaline-, and the cholera toxin-induced increases in lipoprotein lipase activity; the half-life of lipoprotein lipase mRNA was estimated to be 20-30 h. However, in animals returned to control conditions after a 4-h cold stress, the decline in activity corresponded to a half-life of only 4 h. It was concluded that the increase in lipoprotein lipase activity in the brown adipose tissue of cold-exposed rats is not due to an activation of preexisting enzyme nor due to an increased half-life of functional enzyme. Rather it is suggested that in brown adipose tissue the rate of lipoprotein lipase gene transcription is positively regulated by the cellular level of cAMP and that this increase in lipoprotein lipase mRNA leads directly to an increased rate of enzyme synthesis and hence to the increase in activity.
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PMID:Cold-induced beta-adrenergic recruitment of lipoprotein lipase in brown fat is due to increased transcription. 245 Apr 67

The antihypertensive drug-induced changes in serum lipoproteins can be attributed to two major mechanisms, namely an increased hepatic lipoprotein synthesis and a disturbed lipoprotein catabolism. Thiazides, by inhibiting phosphodiesterase, increase the intracellular concentration of cyclic AMP leading to a stimulation of lipolysis. beta-Blockers may reduce the adenylate cyclase activity in liver cells, leading to a reduced inhibition of the liver triglyceride synthesis and a higher secretion of VLDL triglyceride particles. alpha-Blockade through phosphodiesterase inhibition and an increased cAMP level, can result in a blockade of the liver triglyceride synthesis and a reduced serum triglyceride concentration. Lipoprotein lipase activity is reduced by beta-blockers and stimulated by alpha-blockers, leading, respectively, to a lower and a higher plasma HDL cholesterol. Besides these two major mechanisms, a direct effect of antihypertensive drugs on intracellular cholesterol synthesis can also be postulated.
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PMID:Possible biochemical mechanisms involved in the antihypertensive drug-induced changes in serum lipoproteins. 265 25

Lipoprotein lipase (LPL) activity is known to be synthesized, active and functional in the 1-day-old rat liver: it peaks just at birth triggered by parturition. During suckling LPL mRNA, LPL synthesis and LPL activity are still high at 5 days and then fade reaching adult values at weaning. How LPL expression is gradually extinguished is not known. Therefore we studied the effect of different doses of several hormones on LPL activity released by incubated hepatocytes from 5-day-old rats. In the presence of heparin the release of LPL activity in the medium was linear until 3 h and was always significantly increased vs. without heparin. At 3 h in the presence of heparin the main hormonal effects were: dose-dependent increase (30-60%) with dexamethasone; dose-dependent increase (20-60%) with glucagon; dose-independent decrease (50-60%) with ethinylestradiol, testosterone, progesterone and prolactin; no effect with insulin; 20-40% increase with adrenaline < 1 mM but 40-50% decrease with noradrenaline < 10 microM. Increase of LPL release by glucagon and adrenaline agrees with the increased LPL expression we previously found in an undifferentiated hepatoma cell line when the adenylate cyclase/protein kinase A pathway was activated. The effect of glucagon is concordant with our previous observations that fasting increases liver LPL activity in neonatal rats. The high estradiol levels known to be present in male and female 9-19-day-old rats might contribute to liver LPL extinction during suckling.
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PMID:Hormonal regulation of lipoprotein lipase activity from 5-day-old rat hepatocytes. 882 70