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Caffeic acid phenethyl ester inhibits the basal and drug-induced lipolysis in the rat mature adipocytes
Other Title
Caffeic acid phenethyl ester inhibits the basal and drug-induced lipolysis in the rat mature adipocytes
Type
thesis
Date Issued
2022-11-29
Author(s)
NGUYEN THI THU TRANG
Advisor
張榮善 ; 馮琮涵
Subjects
系所名稱：細胞治療與再生醫學國際博士學位學程
Description
學位別：博士
語文別：英文
口試委員：張榮善 CHANG, JUNGSHAN;馮琮涵 FONG, TSORNG-HARN ;蕭哲志 HSIAO, GEORGE;王嘉銓 WANG, CHIA-CHUAN;傅毓秀 FU, YU-SHOW
授權範圍：網際網路,開放日期為2022-12-05
語文別：英文
口試委員：張榮善 CHANG, JUNGSHAN;馮琮涵 FONG, TSORNG-HARN ;蕭哲志 HSIAO, GEORGE;王嘉銓 WANG, CHIA-CHUAN;傅毓秀 FU, YU-SHOW
授權範圍：網際網路,開放日期為2022-12-05
Abstract
ABSTRACT
Introduction: Caffeic acid phenethyl ester (CAPE), a natural compound which is extracted from honeybee hives, has been found to have a positive effect on metabolic syndrome. Abnormal lipolysis is one of the main process which strongly correlate with the change in lipid metabolism. However, it did not elucidate the effect of CAPE on lipolysis and lipid droplet-associated proteins as well as related pathway.
Methods: We separated the epididymal fat pad of male rats and isolated mature adipocytes from adipose tissues. Isolated adipocytes was incubated with CAPE or other lipolysis stimulated drugs to determine glycerol release which worked as scale for lipolysis process. Lipid droplet-associated proteins such as perilipin-1 (PLIN), hormone sensitive lipase (HSL), adipose triglyceride lipase (ATGL), a/b-hydrolase domain containing 5 (ABHD5) level were analyzed, and the signal transduction pathways of CAPE such as nuclear factor-κB (NF-κB), extracellular signal- regulated kinase 1/2 (ERK1/2), and peroxisome proliferator-activated receptors gamma (PPARg) were examined by immunoblot analysis.
Results: CAPE showed an inhibitory effect on basal lipolysis in a dose- and time-dependent manner. There was a significant increase of PLIN and phosphorylated PPARg levels following CAPE treatment, based on the protein expression in western blot. However, other lipid droplet-associated proteins such as ATGL, HSL, ABHD5, and the pathways of NF-κB or ERK did not show a contribution in this study. Moreover, we used a specific PPARg inhibitor (T0070907) to elucidate the role of PPARg in CAPE treatment. Interestingly, PPARg inhibitor could partly reverse the inhibitory effect of CAPE on lipolysis.
We also checked the effect of CAPE on stimulated condition by added drug- induced lipolysis such as dibutyryl-cAMP (db-cAMP) or isoproterenol (ISO). CAPE showed an inhibitory effect on the stimulated stage of adipocytes. The lipid droplet-associated PLIN level was decreased obviously in drug-induced lipolysis group, but increased after adding CAPE.
Conclusion: Our results revealed that CAPE could inhibit basal lipolysis through activating PPARg and increase of PLIN level in mature adipocytes.
Keywords: Caffeic acid phenethyl ester; Lipolysis; Perilipin; Peroxisome proliferator-activated receptors gamma (PPARg).
Introduction: Caffeic acid phenethyl ester (CAPE), a natural compound which is extracted from honeybee hives, has been found to have a positive effect on metabolic syndrome. Abnormal lipolysis is one of the main process which strongly correlate with the change in lipid metabolism. However, it did not elucidate the effect of CAPE on lipolysis and lipid droplet-associated proteins as well as related pathway.
Methods: We separated the epididymal fat pad of male rats and isolated mature adipocytes from adipose tissues. Isolated adipocytes was incubated with CAPE or other lipolysis stimulated drugs to determine glycerol release which worked as scale for lipolysis process. Lipid droplet-associated proteins such as perilipin-1 (PLIN), hormone sensitive lipase (HSL), adipose triglyceride lipase (ATGL), a/b-hydrolase domain containing 5 (ABHD5) level were analyzed, and the signal transduction pathways of CAPE such as nuclear factor-κB (NF-κB), extracellular signal- regulated kinase 1/2 (ERK1/2), and peroxisome proliferator-activated receptors gamma (PPARg) were examined by immunoblot analysis.
Results: CAPE showed an inhibitory effect on basal lipolysis in a dose- and time-dependent manner. There was a significant increase of PLIN and phosphorylated PPARg levels following CAPE treatment, based on the protein expression in western blot. However, other lipid droplet-associated proteins such as ATGL, HSL, ABHD5, and the pathways of NF-κB or ERK did not show a contribution in this study. Moreover, we used a specific PPARg inhibitor (T0070907) to elucidate the role of PPARg in CAPE treatment. Interestingly, PPARg inhibitor could partly reverse the inhibitory effect of CAPE on lipolysis.
We also checked the effect of CAPE on stimulated condition by added drug- induced lipolysis such as dibutyryl-cAMP (db-cAMP) or isoproterenol (ISO). CAPE showed an inhibitory effect on the stimulated stage of adipocytes. The lipid droplet-associated PLIN level was decreased obviously in drug-induced lipolysis group, but increased after adding CAPE.
Conclusion: Our results revealed that CAPE could inhibit basal lipolysis through activating PPARg and increase of PLIN level in mature adipocytes.
Keywords: Caffeic acid phenethyl ester; Lipolysis; Perilipin; Peroxisome proliferator-activated receptors gamma (PPARg).