Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.5.4.4 (adenosine deaminase)
 5,136 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Leptin, which is secreted from adipocytes, has a role in the regulation of appetite and energy expenditure. The thyrotropin receptor (TSH-R) was recently found in adipocytes. We examined the effects of TSH on leptin production and lipolysis in rat epididymal adipocytes. TSH decreased the concentration of leptin in the medium time (approximately 24 hours)- and dose (approximately 10(-7) mol/L)-dependently (half-maximal inhibition [IC50] approximately 10(-9) mol/L). TSH also decreased the ob mRNA level approximately 55% in adipocytes. We confirmed the presence of TSH-R mRNA in the adipocytes by reverse transcription-polymerase chain reaction (RT-PCR). TSH stimulated glycerol release dose-dependently (IC50 approximately 10(-8) mol/L) in adipocytes. This TSH-induced glycerol release was further enhanced by adenosine deaminase (ADA). In summary, TSH reduced leptin production and stimulated lipolysis in rat epididymal adipocytes. Although the pathophysiological relevance of the regulation of leptin production and lipolysis by TSH is unknown, we speculate that TSH may affect the regulation of appetite and energy expenditure in pathophysiological states.
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PMID:Thyrotropin decreases leptin production in rat adipocytes. 1059 90

The aim of the present study was to gain insight into the signaling pathway used by leptin to stimulate lipolysis. The lipolytic rate of white adipocytes from sex- and age-matched lean (+/+) and fa/fa rats was determined in the absence or presence of leptin together with a number of agents acting at different levels of the signaling cascade. Leptin did not modify FSK-, dbcAMP-, and IBMX-stimulated lipolysis. Lipolysis can also be maximally stimulated by lowering media adenosine levels with adenosine deaminase (ADA), i.e., in the ligand-free state. Although ADA produced near maximal lipolysis in adipocytes of lean animals, only half of the maximal lipolytic rate (50.9+/-3.2%) was achieved in fat cells from fa/fa rats (P=0.0034). In adipocytes from lean animals preincubated with ADA, leptin caused a concentration-related stimulation of lipolysis (P=0.0001). However, leptin had no effect on the lipolytic activity of adipocytes in the ligand-free state from fa/fa rats. The adenosine A1 receptor agonist CPA effectively inhibited basal lipolysis in both lean and obese adipocytes (P=0.0001 and P=0.0090, respectively). Leptin had no effect on the lipolytic rate of adipocytes isolated from fa/fa rats and preincubated with CPA. When adipocytes were incubated with the A1 receptor antagonist DPCPX, a significant increase in glycerol release was observed in fa/fa fat cells (P=0.009), whereas cells isolated from lean rats showed no differences to ADA-stimulated lipolysis. After pretreatment with PTX, which inactivates receptor-mediated Gi function, adipocytes of obese rats became as responsive to the stimulatory actions of ISO as cells from lean rats (P=0.0090 vs. ISO in fa/fa rats; P=0.2416 vs. lean rats, respectively). PTX treatment of lean cells, however, did not alter their response to this lipolytic agent. It can be concluded that the lipolytic effect of leptin is located at the adenylate cyclase/Gi proteins level and that leptin-induced lipolysis opposes the tonic inhibition of endogenous adenosine in white adipocytes.
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PMID:Leptin-induced lipolysis opposes the tonic inhibition of endogenous adenosine in white adipocytes. 1115 49

Direct effects of recombinant ovine leptin on adipose metabolism in sheep were investigated. Lipolytic and lipogenic rates were assessed following preincubation of subcutaneous adipose tissue explants with recombinant ovine leptin. Leptin had no consistent effect on the basal (unstimulated) lipolytic rate in adipose tissue from wethers. Lipolytic rate measured in the presence of combinations of adenosine deaminase, isoprenaline, and N6-phenylisopropyl adenosine was unaffected by pretreatment with leptin. In lactating ewes, there was no relationship between increasing concentrations of leptin and basal lipolytic rate. Leptin had no effect on basal (unstimulated) lipogenesis, or on insulin-stimulation or growth hormone inhibition of lipogenesis in adipose tissue from wethers. Lipogenesis in adipose tissue from lactating ewes was also unaffected by preincubation with leptin; however, at supraphysiological concentrations of leptin, there was a small reduction in the rate of insulin-stimulated lipogenesis. Leptin failed to induce phosphorylation of the signal transducers and activators of transcription, STAT 3 and STAT 5, in sheep adipocytes. These results suggest that leptin does not have a direct physiological effect on subcutaneous adipose tissue metabolism in sheep.
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PMID:Effects of recombinant ovine leptin on in vitro lipolysis and lipogenesis in subcutaneous adipose tissue from lactating and nonlactating sheep. 1121 54

It is suggested that leptin may be involved in inflammation. Although relation between leptin levels and active pulmonary tuberculosis has been studied, there is no information about relation between leptin levels and tuberculous pleural effusions (TPE). We evaluated the diagnostic value of pleural fluid and serum leptin levels in TPE and compared them with adenosine deaminase (ADA). Forty-five patients, 17 tuberculous effusion and 28 nontuberculous effusion, with exudative pleural effusions were included. Leptin and ADA levels were measured from serum and pleural fluid in all patients. There were no statistically significant differences between tuberculous and nontuberculous groups with respect to the serum ADA activity and pleural fluid/serum leptin ratio. On the contrary, pleural fluid leptin level, pleural fluid ADA activity, serum leptin level and pleural fluid/serum ADA activity ratio were statistically different between tuberculous and nontuberculous groups. When leptin levels were corrected for body mass index, serum leptin levels did not reach statistical significance. Cut-off points to predict tuberculosis were calculated as 9.85 ng/ml and 35.55 U/l for pleural fluid leptin level and pleural fluid ADA activity, respectively. Sensitivity, specificity and area under the curve +/- standard error were 82.4%, 82.1%, 0.83 +/- 0.07 for pleural fluid leptin levels and 100%, 100%, 1.00 +/- 0.00 for pleural fluid ADA activity, respectively; the difference between these curves was significant (p = 0.01). Pleural fluid leptin levels were lower in tuberculous effusions than in other exudates. Pleural fluid leptin has a diagnostic value for TPE but not as good as that of ADA.
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PMID:Diagnostic value of leptin in tuberculous pleural effusions. 1666 25