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The expression and antilipolytic role of phosphodiesterase 4 in rat adipocytes in vitro

Wang, Hong
http://rave.ohiolink.edu/etdc/view?acc_num=osu1124189520

Abstract Details

2005, Doctor of Philosophy, Ohio State University, Human Nutrition and Food Management.
Elevated concentrations of plasma free fatty acids (FFA) may cause insulin resistance. Inhibition of lipolysis reduces FFA availability and improves insulin sensitivity. Lipolysis is stimulated by increased concentration of cAMP. Phosphodiesterases (PDEs) hydrolyze cAMP and limit stimulation of lipolysis. PDE3B is the major isoform of PDE in rat adipocytes and mediates the antilipolytic effect of insulin. The present study showed that insulin inhibited lipolysis by 42.4% compared to the basal lipolysis (p<0.002). The specific PDE3 inhibitor cilostamide completely reversed insulin antilipolysis, whereas the specific PDE4 inhibitor rolipram did not reduce insulin antilipolysis. Korean ginseng extract (Panax ginseng; KGE) inhibited lipolysis by 49% compared to the basal lipolysis (p<0.002). Cilostamide and rolipram reduced KGE antilipolysis to 43% and 23.4% compared to basal conditions with the inhibitors, respectively. Moreover, combination of the PDE3 and PDE4 inhibitors completely reversed KGE antilipolysis. In contrast with insulin, KGE did not affect phosphorylation of protein kinase B (PKB). RT-PCR showed that four subtypes of PDE4 gene were expressed in rat adipocytes. Real-time quantitative PCR demonstrated that the gene expression of four PDE4 subtypes (A, B, C, D) relative to PDE3B was 7%, 19%, 19%, and 7%, respectively. Prostaglandin E2 (PGE2) and N6-(2-phenylisopropyl)adenosine (PIA) are two antilipolytic agents. PGE2 inhibited lipolysis by 84% compared to the basal condition (p<0.006). Cilostamide and rolipram reduced PGE2 antilipolysis to 76.3% and 46.6% compared to basal conditions with the inhibitors, respectively. The combination of cilostamide and rolipram reduced PGE2 antilipolysis to 17.5 %. PIA inhibited lipolysis by 92.2% compared to the basal lipolysis (p<0.006). Although cilostamide and rolipram alone did not affect PIA antilipolysis, combination of these two inhibitors reduced PIA antilipolysis to 56.8%. The results of PDE activity assay showed that PGE2 moderately increased the total PDE activity, PDE3 activity, and PDE4 activity in rat adipocytes. In contrast, PIA slightly decreased the total PDE activity and KGE did not change the total PDE activity. These data suggest that PDE4 plays an antilipolytic role in rat adipocytes. Both KGE and PGE2 antilipolysis are mediated by PDE4 in part. The signaling pathway for KGE antilipolysis is different from that activated by insulin.
Mark Failla (Advisor)
145 p.
Health Sciences, Nutrition
phosphodiesterase; free fatty acids; lipolysis; cAMP; ginseng

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Citations

  • Wang, H. (2005). The expression and antilipolytic role of phosphodiesterase 4 in rat adipocytes in vitro [Doctoral dissertation, Ohio State University]. OhioLINK Electronic Theses and Dissertations Center. http://rave.ohiolink.edu/etdc/view?acc_num=osu1124189520

    APA Style (7th edition)

  • Wang, Hong. The expression and antilipolytic role of phosphodiesterase 4 in rat adipocytes in vitro. 2005. Ohio State University, Doctoral dissertation. OhioLINK Electronic Theses and Dissertations Center, http://rave.ohiolink.edu/etdc/view?acc_num=osu1124189520.

    MLA Style (8th edition)

  • Wang, Hong. "The expression and antilipolytic role of phosphodiesterase 4 in rat adipocytes in vitro." Doctoral dissertation, Ohio State University, 2005. http://rave.ohiolink.edu/etdc/view?acc_num=osu1124189520

    Chicago Manual of Style (17th edition)

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This open access ETD is published by The Ohio State University and OhioLINK.