Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.4.1 (phosphodiesterase)
 18,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The goal of the present study was to examine cellular mechanisms that regulate adipose cell metabolism in ovariectomized (OVX) and intact rats that were subjected to long-term (27 weeks) treatment with dehydroepiandrosterone (DHEA). Forty-eight 16-month-old female rats were divided into 4 groups of 9 to 11 animals (intact, intact-DHEA, OVX, OVX-DHEA). Adipose tissue lipoprotein lipase (LPL), hormone-sensitive lipase (HSL), and cyclic adenosine monophosphate (cAMP)-dependent phosphodiesterase (cAMP-PDE) activities were determined, and alpha2-, beta1/beta2-, and beta3-adrenoceptors (ARs) were quantified. DHEA did not affect body weight, fat, or muscle mass in intact rats. The similar retroperitoneal fat pad weight of intact-DHEA rats compared to intact animals was in agreement with the lack of difference in the enzyme activities and AR densities. The increased body weight of OVX rat was paralleled by a greater retroperitoneal adipose tissue mass (P <.01), which was in turn associated with a marked rise in LPL activity (P <.005) and a slight decrease in HSL activity (P <.05) compared to intact animals. OVX-DHEA rats, compared to untreated OVX animals, had a smaller retroperitoneal fat depot, which correlated with a decrease in LPL activity (P <.005) and moderate increase in both HSL activity and beta3-AR density (P <.05). DHEA-treatment lowered fasting insulin and triglyceride levels in both intact and OVX rats (P <.05). Plasma testosterone, androsterone, androstenedione, and androstenediol levels were also significantly increased in both intact-DHEA and OVX-DHEA rats compared to untreated animals (P <.0001). These findings suggest that the antiobesity action of DHEA may be related in part to changes in lipase activities and in beta3-AR density, and that it is dependent on the ovarian status of the animal.
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PMID:Chronic effects of dehydroepiandrosterone on rat adipose tissue metabolism. 1264 61

The effects of vanadate on lipoprotein lipase (LPL), a lipid-metabolizing enzyme, were tested using isolated rat fat pads. Vanadate increased the cellular LPL content through the stimulation of intracellular transport of the enzyme for activation, probably glycosylation. The stimulated release of LPL from the fat pads by vanadate was due to the increase in intracellular Ca2+ concentration, leading to the fusion of plasma membrane with vehicle included active LPL. Although vanadate shows insulin- and heparin-mimicking effects, it appears to differ from both insulin and heparin with regard to the mechanism of action. In isolated mouse fat pads, vanadate decreased the cellular leptin content and secretion by the increased degradation via a cAMP/PKA-dependent process involving proteasome activation and/or ubiquitination. This was the reverse of the action of insulin. In hepatocytes, cAMP phosphodiesterase type 3 activity was stimulated via the increased mitogen-activated protein kinase activity by vanadate. On the other hand, the stimulation by insulin was dependent on Akt kinase activation. The effects of vanadate were additive to those of insulin, suggesting that vanadate differs from insulin with regard to the receptor-signaling cascade. Furthermore, vanadate showed antiplatelet and antithrombin activity, leading to the prolongation of blood clotting time.
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PMID:[New biological actions of vanasium]. 1293 59


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