D-(-)-beta-hydroxybutyrate inhibits catecholamine-stimulated lipolysis and decreases beta-adrenoceptors' affinity in human fat cells but not in lymphomonocytes.
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| Abstract |
The effect of D-(-)-beta-hydroxybutyrate, at concentrations commonly achieved during ketoacidosis in humans (10 mmol/l), on human fat cell lipolysis in vitro was the aim of this study. The basal lipolysis was not modified and beta-hydroxybutyrate did not affect forskolin- or dibutyryl-cAMP-stimulated glycerol release, whereas it markedly inhibited isoproterenol-stimulated lipolysis. In membranes of intact adipocytes exposed to D-(-)-beta-hydroxybutyrate for 1 h, we found a decrease in beta-adrenoceptor affinity in saturation experiments and a shift to the right of the isoproterenol-mediated radioligand [( 125I]-cyanopindolol) displacement curve. These findings suggest that beta-hydroxybutyrate inhibits catecholamine-stimulated lipolysis by decreasing beta-adrenoceptor affinity. No effect of beta-hydroxybutyrate was found on beta-adrenoceptor binding of intact mononuclear cells of peripheral blood. In conclusion, the beta-adrenoceptor affinity lowering effect of beta-hydroxybutyrate is seemingly specific to human fat cells and might represent a feed-back mechanism that prevents an uncontrolled breakdown of triglycerides and indirectly regulates its own production rate.
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| Authors | G De Pergola, M Cignarelli, M Corso, G Garruti, S Di Paolo, R Giorgino |
| Journal | Acta endocrinologica (Acta Endocrinol (Copenh)) Vol. 122 Issue 4 Pg. 450-4 (Apr 1990) ISSN: 0001-5598 [Print] Denmark |
| PMID | 2159203 (Publication Type: Journal Article) |
| Chemical References |
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