Effects of epigallocatechin-3-gallate on autophagic lipolysis in adipocytes

Sang Nam Kim, Hyun Jung Kwon, Seun Akindehin, Hyun Woo Jeong, Yun Hee Lee

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

Previous studies demonstrated effects of green tea on weight loss; however, green tea-induced modulation of adipocyte function is not fully understood. Here, we investigated effects of the major green tea phytochemical, epigallocatechin-3-gallate (EGCG) on triglyceride contents, lipolysis, mitochondrial function, and autophagy, in adipocytes differentiated from C3H10T1/2 cells and immortalized pre-adipocytes in vitro. EGCG reduced the triglycerol content significantly in adipocytes by 25%, comparable to the nutrient starvation state. EGCG did not affect protein kinase A signaling or brown adipocyte marker expression in adipocytes; however, EGCG increased autophagy, as measured by autophagy flux analysis and immunoblot analysis of LC3B, ATG7, and Beclin1. EGCG treatment reduced mitochondrial membrane potential by 56.8% and intracellular ATP levels by 49.1% compared to controls. Although mammalian target of rapamycin signaling was not upregulated by EGCG treatment, EGCG treatment induced AMP-activated protein kinase phosphorylation, indicating an energy-depleted state. In addition, EGCG increased the association between RAB7 and lipid droplets, suggesting that lipophagy was activated. Finally, knockdown of Rab7 attenuated the EGCG-dependent reduction in lipid contents. Collectively, these results indicated that EGCG upregulated autophagic lipolysis in adipocytes, supporting the therapeutic potential of EGCG as a caloric restriction mimetic to prevent obesity and obesity-related metabolic diseases.

Original languageEnglish
Article number680
JournalNutrients
Volume9
Issue number7
DOIs
Publication statusPublished - 2017 Jul

Fingerprint

Lipolysis
epigallocatechin
lipolysis
adipocytes
Adipocytes
autophagy
Autophagy
green tea
Tea
obesity
epigallocatechin gallate
Obesity
Brown Adipocytes
AMP-activated protein kinase
Caloric Restriction
AMP-Activated Protein Kinases
cAMP-dependent protein kinase
Mitochondrial Membrane Potential
Metabolic Diseases
metabolic diseases

All Science Journal Classification (ASJC) codes

  • Food Science
  • Nutrition and Dietetics

Cite this

Kim, S. N., Kwon, H. J., Akindehin, S., Jeong, H. W., & Lee, Y. H. (2017). Effects of epigallocatechin-3-gallate on autophagic lipolysis in adipocytes. Nutrients, 9(7), [680]. https://doi.org/10.3390/nu9070680
Kim, Sang Nam ; Kwon, Hyun Jung ; Akindehin, Seun ; Jeong, Hyun Woo ; Lee, Yun Hee. / Effects of epigallocatechin-3-gallate on autophagic lipolysis in adipocytes. In: Nutrients. 2017 ; Vol. 9, No. 7.
@article{95a2e03354294bbca0e7f4328a941c34,
title = "Effects of epigallocatechin-3-gallate on autophagic lipolysis in adipocytes",
abstract = "Previous studies demonstrated effects of green tea on weight loss; however, green tea-induced modulation of adipocyte function is not fully understood. Here, we investigated effects of the major green tea phytochemical, epigallocatechin-3-gallate (EGCG) on triglyceride contents, lipolysis, mitochondrial function, and autophagy, in adipocytes differentiated from C3H10T1/2 cells and immortalized pre-adipocytes in vitro. EGCG reduced the triglycerol content significantly in adipocytes by 25{\%}, comparable to the nutrient starvation state. EGCG did not affect protein kinase A signaling or brown adipocyte marker expression in adipocytes; however, EGCG increased autophagy, as measured by autophagy flux analysis and immunoblot analysis of LC3B, ATG7, and Beclin1. EGCG treatment reduced mitochondrial membrane potential by 56.8{\%} and intracellular ATP levels by 49.1{\%} compared to controls. Although mammalian target of rapamycin signaling was not upregulated by EGCG treatment, EGCG treatment induced AMP-activated protein kinase phosphorylation, indicating an energy-depleted state. In addition, EGCG increased the association between RAB7 and lipid droplets, suggesting that lipophagy was activated. Finally, knockdown of Rab7 attenuated the EGCG-dependent reduction in lipid contents. Collectively, these results indicated that EGCG upregulated autophagic lipolysis in adipocytes, supporting the therapeutic potential of EGCG as a caloric restriction mimetic to prevent obesity and obesity-related metabolic diseases.",
author = "Kim, {Sang Nam} and Kwon, {Hyun Jung} and Seun Akindehin and Jeong, {Hyun Woo} and Lee, {Yun Hee}",
year = "2017",
month = "7",
doi = "10.3390/nu9070680",
language = "English",
volume = "9",
journal = "Nutrients",
issn = "2072-6643",
publisher = "Multidisciplinary Digital Publishing Institute (MDPI)",
number = "7",

}

Kim, SN, Kwon, HJ, Akindehin, S, Jeong, HW & Lee, YH 2017, 'Effects of epigallocatechin-3-gallate on autophagic lipolysis in adipocytes', Nutrients, vol. 9, no. 7, 680. https://doi.org/10.3390/nu9070680

Effects of epigallocatechin-3-gallate on autophagic lipolysis in adipocytes. / Kim, Sang Nam; Kwon, Hyun Jung; Akindehin, Seun; Jeong, Hyun Woo; Lee, Yun Hee.

In: Nutrients, Vol. 9, No. 7, 680, 07.2017.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Effects of epigallocatechin-3-gallate on autophagic lipolysis in adipocytes

AU - Kim, Sang Nam

AU - Kwon, Hyun Jung

AU - Akindehin, Seun

AU - Jeong, Hyun Woo

AU - Lee, Yun Hee

PY - 2017/7

Y1 - 2017/7

N2 - Previous studies demonstrated effects of green tea on weight loss; however, green tea-induced modulation of adipocyte function is not fully understood. Here, we investigated effects of the major green tea phytochemical, epigallocatechin-3-gallate (EGCG) on triglyceride contents, lipolysis, mitochondrial function, and autophagy, in adipocytes differentiated from C3H10T1/2 cells and immortalized pre-adipocytes in vitro. EGCG reduced the triglycerol content significantly in adipocytes by 25%, comparable to the nutrient starvation state. EGCG did not affect protein kinase A signaling or brown adipocyte marker expression in adipocytes; however, EGCG increased autophagy, as measured by autophagy flux analysis and immunoblot analysis of LC3B, ATG7, and Beclin1. EGCG treatment reduced mitochondrial membrane potential by 56.8% and intracellular ATP levels by 49.1% compared to controls. Although mammalian target of rapamycin signaling was not upregulated by EGCG treatment, EGCG treatment induced AMP-activated protein kinase phosphorylation, indicating an energy-depleted state. In addition, EGCG increased the association between RAB7 and lipid droplets, suggesting that lipophagy was activated. Finally, knockdown of Rab7 attenuated the EGCG-dependent reduction in lipid contents. Collectively, these results indicated that EGCG upregulated autophagic lipolysis in adipocytes, supporting the therapeutic potential of EGCG as a caloric restriction mimetic to prevent obesity and obesity-related metabolic diseases.

AB - Previous studies demonstrated effects of green tea on weight loss; however, green tea-induced modulation of adipocyte function is not fully understood. Here, we investigated effects of the major green tea phytochemical, epigallocatechin-3-gallate (EGCG) on triglyceride contents, lipolysis, mitochondrial function, and autophagy, in adipocytes differentiated from C3H10T1/2 cells and immortalized pre-adipocytes in vitro. EGCG reduced the triglycerol content significantly in adipocytes by 25%, comparable to the nutrient starvation state. EGCG did not affect protein kinase A signaling or brown adipocyte marker expression in adipocytes; however, EGCG increased autophagy, as measured by autophagy flux analysis and immunoblot analysis of LC3B, ATG7, and Beclin1. EGCG treatment reduced mitochondrial membrane potential by 56.8% and intracellular ATP levels by 49.1% compared to controls. Although mammalian target of rapamycin signaling was not upregulated by EGCG treatment, EGCG treatment induced AMP-activated protein kinase phosphorylation, indicating an energy-depleted state. In addition, EGCG increased the association between RAB7 and lipid droplets, suggesting that lipophagy was activated. Finally, knockdown of Rab7 attenuated the EGCG-dependent reduction in lipid contents. Collectively, these results indicated that EGCG upregulated autophagic lipolysis in adipocytes, supporting the therapeutic potential of EGCG as a caloric restriction mimetic to prevent obesity and obesity-related metabolic diseases.

UR - http://www.scopus.com/inward/record.url?scp=85022089499&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85022089499&partnerID=8YFLogxK

U2 - 10.3390/nu9070680

DO - 10.3390/nu9070680

M3 - Article

C2 - 28665330

AN - SCOPUS:85022089499

VL - 9

JO - Nutrients

JF - Nutrients

SN - 2072-6643

IS - 7

M1 - 680

ER -