Ginseng extract inhibits lipolysis in rat adipocytes in vitro by activating phosphodiesterase 4.

Elevated concentrations of plasma free fatty acids (FFA) may cause insulin resistance. Inhibition of lipolysis reduces FFA availability and improves insulin sensitivity. Ginseng extract (Panax spp., GE) was shown to improve glycemia in Type 2 diabetes. In the present study, the antilipolytic effect of GE in rat adipocytes and the signaling pathway for GE antilipolysis were investigated. Adipocytes were isolated from rat fat tissue by collagenase digestion. The ability of GE to inhibit lipolysis was assessed by measuring glycerol and FFA release into the incubation medium. Phosphatidylinositol 3-kinase (PI3-K) inhibitor and various phosphodiesterase (PDE) inhibitors were applied to investigate the signaling pathway for GE antilipolysis. The present study showed that insulin and GE inhibited lipolysis by 42.4 and 49% compared with basal, respectively (P < 0.05). Unlike insulin, the PI3-K inhibitor wortmannin did not reverse GE antilipolysis, and GE did not affect phosphorylation of protein kinase B (PKB). The nonselective PDE inhibitor enprofylline reversed both insulin and GE antilipolysis. The specific phosphodiesterase 3 (PDE3) inhibitor cilostamide reversed insulin antilipolysis completely, but did not significantly affect GE antilipolysis. The specific phosphodiesterase 4 (PDE4) inhibitor rolipram did not significantly affect insulin antilipolysis, but almost completely reversed GE antilipolysis. Moreover, the combination of PDE3 and PDE4 inhibitors completely reversed GE antilipolysis. None of the ginsenosides (Rb1, Re, Rg1, Rc, Rb2, and Rd) were responsible for GE antilipolysis. The results suggest that ginseng exerts its antilipolytic effect through a signaling pathway different from that of insulin. GE antilipolysis is mediated in part by activating PDE4 in rat adipocytes.

Yeast extract stimulates glucose metabolism and inhibits lipolysis in rat adipocytes in vitro.

Foods contain bioactive components that contribute to optimal health. Food-grade yeast may contain components that enhance cellular glucose metabolism. We tested the effect of brewer's yeast (Saccharomyces cerevisiae) extract (YE), in vitro on rat fat cell glucose transport, glucose metabolism to lipid, and lipolysis. YE was fractionated by reverse-phase chromatography on a C18 open column using ammonium acetate (0.05 mol/L, pH 5.8), with acetonitrile (40%) elution solvent into fraction 1 (Fx1), fraction 2 (Fx2) and fraction 3 (Fx3). Isolated rat adipocytes were preincubated with insulin (51 pmol/L), YE (10 mg/L) or both; transport of U-(14)C-glucose was measured. Adipocytes were incubated with insulin and YE fractions (10 mg/L); glucose metabolism to lipid was measured by incorporation of U-(14)C-glucose into total lipids. Lipolysis was measured by glycerol release. Insulin stimulated glucose transport to sevenfold the basal value (P < 0.05). YE did not affect glucose transport. Insulin stimulated glucose metabolism to 2.6-fold the basal value (P < 0.001); YE stimulated glucose metabolism 14% (P < 0.005). YE potentiated the action of insulin 30% (P < 0.002). YE Fx2 and Fx3 stimulated glucose metabolism 25-40% (P < 0.05). Insulin inhibited lipolysis 47% (P < 0.001). YE alone inhibited lipolysis 63% (P < 0.001). YE and insulin inhibited lipolysis 81% (P < 0.001). Fractions of YE inhibited lipolysis in the presence of insulin (P < 0.05); the order of potency was Fx2 = Fx3 >> Fx1. A novel yeast extract (YE) and its fractions affect pathways of adipocyte metabolism differentially. YE and its fractions are good candidates for in vivo study.