Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P56851 (epididymal)
 11,273 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pertussis toxin (PT), a protein produced by Bordetella pertussis, was studied for its effect on lipolysis in isolated rat epididymal adipocytes. Exposure of adipocytes to pertussis toxin resulted in a significant increase in cyclic AMP levels and lipolysis after a lag of 1-2 hr. Both the maximal rate of lipolysis and the time lag (beyond 1 hr) were PT concentration-dependent. Heat treatment (95 degrees C, 30 min) or incubation with specific antibody directed against PT eliminated the ability of toxin to increase lipolysis. Cell-free culture medium from B. pertussis, but not from nontoxigenic Bordetella species, had the same effect on lipolysis as purified toxin. Comparison of the PT effect with the known lipolytic effect of cholera toxin (CT) revealed that the two toxins elicited responses that were indistinguishable in time course and magnitude. In contrast, the adenylate cyclase (EC 4.6.1.1) activities in membranes prepared from PT- or CT-treated adipocytes were different. Adenylate cyclase activity in membranes from control (untreated) adipocytes was inhibited 35-64% by the adenosine analogue N6-(L-2-phenylisopropyl)-adenosine. As expected from previous studies, membranes from CT-treated adipocytes demonstrated an increased basal activity but showed the same proportional inhibition by N6-(L-2-phenylisopropyl)-adenosine as controls. On the other hand, membranes from adipocytes exposed to PT (400 ng/ml for 4 hr) showed no increase in basal adenylate cyclase activity but had reduced sensitivity to N6-(L-2-phenylisopropyl)-adenosine inhibition, with the maximal effect ranging from 11 to 30% at 10(-6) M N6-(L-2-phenylisopropyl)-adenosine. These data support the hypothesis that PT promotes cyclic AMP-dependent lipolysis in a manner quantitatively equivalent to CT, but by a different mechanism involving increased cyclic AMP levels resulting from loss of responsiveness to endogenous inhibitors such as adenosine.
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PMID:Promotion of lipolysis in rat adipocytes by pertussis toxin: reversal of endogenous inhibition. 619 60

Histamine-sensitizing factor (HSF) purified from Bordetella pertussis induced specifically the release of glycerol from rat epididymal adipocytes in vitro. The most sensitive and reproducible results were obtained by using 1 to 2 x 10(5) adipocytes/tube from rats weighing 150 to 200 g, and by incubation at 37 C for 180 min. After a lag period of about 60 min, HSF-treated adipocytes released glycerol in increasing amounts between 60 and 240 min, depending on the dose of HSF. A close correlation between the glycerol-releasing (GR) activity of HSF for adipocytes and histamine-sensitizing or leukocytosis-promoting activity in mice was observed. The GR activity was inactivated by heating at 56 C for 60 min, 63 C for 30 min or 96 C for 10 min. The adipocytes washed out with a Krebs-Ringer bicarbonate buffer immediately after being exposed to HSF for 1 to 3 min manifested about 75% of the total GR activity induced by HSF, and those washed out after being exposed for 30 min or longer had full activity. Anti-HSF serum neutralized the activity when it was added to adipocytes simultaneously with HSF, but did not when it was added 30 min after being exposed to HSF. By using both native and 125 I-labeled HSF, the ratio of binding of HSF to adipocytes was estimated to be 10 to 15% of the total HSF per 2 x 10(5) cells/tube, and to be about 1,000 molecules of HSF per cell to induce the release of glycerol. The GR activity induced with 10 ng of HSF was inhibited by addition of insulin at a dose of over 1 micro IU/tube, but not by concanavalin A.
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PMID:Glycerol-releasing activity of histamine-sensitizing factor of Bordetella pertussis for rat adipocytes in vitro. 629 84