Urolithin A, C, and D, but not iso-urolithin A and urolithin B, attenuate triglyceride accumulation in human cultures of adipocytes and hepatocytes

Inhae Kang, Yongeun Kim, Francisco A. Tomás-Barberán, Juan Carlos Espín, Soonkyu Chung

Research output: Contribution to journalArticle

26 Citations (Scopus)

Abstract

Scope: Urolithins (Uro) are ellagic acid (EA)-derived metabolites produced by gut microbes. There is a growing interest in the biological activities of Uro. Our aim was to evaluate the impacts of Uro on regulating triglyceride (TG) accumulation using cultures of primary human adipocytes and hepatoma Huh7 cells. Methods and results: UroA, UroB, UroC, UroD, and iso-UroA were used to determine the effect of Uro on adipogenesis and lipogenesis. Individual Uro (30 μM) were added to human adipogenic stem cells during differentiation. UroA, UroC, and UroD, but not iso-UroA and UroB, significantly inhibited new fat cell formation by decreasing TG accumulation and adipogenic protein and gene expressions. The regulation of TG synthesis by Uro was investigated via metabolic chasing with radiolabeled precursors. UroA, UroC, and UroD attenuated TG accumulation, while increasing the fatty acid (FA) oxidation in adipocytes and h/epatoma Huh7 cells. Furthermore, UroC, UroD, and UroA promoted the phosphorylation of AMP-activated protein kinase, suggesting that Uro may alter energy-sensing metabolic pathways in primary human adipocytes. Conclusions: Taken together, our results demonstrated that UroA, UroC, and UroD, but not isoUroA and UroB, reduce TG accumulation and increase FA oxidation in adipocytes as well as hepatocytes.

Original languageEnglish (US)
Pages (from-to)1129-1138
Number of pages10
JournalMolecular Nutrition and Food Research
Volume60
Issue number5
DOIs
StatePublished - May 1 2016

Fingerprint

adipocytes
Adipocytes
hepatocytes
Hepatocytes
Triglycerides
triacylglycerols
beta oxidation
Fatty Acids
Ellagic Acid
AMP-activated protein kinase
Adipogenesis
Lipogenesis
AMP-Activated Protein Kinases
ellagic acid
lipogenesis
hepatoma
Metabolic Networks and Pathways
cell differentiation
stem cells
biochemical pathways

Keywords

  • AMP-activated protein kinase
  • Adipogenesis
  • Ellagic acid
  • Lipogenesis
  • Urolithins

ASJC Scopus subject areas

  • Biotechnology
  • Food Science

Cite this

Urolithin A, C, and D, but not iso-urolithin A and urolithin B, attenuate triglyceride accumulation in human cultures of adipocytes and hepatocytes. / Kang, Inhae; Kim, Yongeun; Tomás-Barberán, Francisco A.; Espín, Juan Carlos; Chung, Soonkyu.

In: Molecular Nutrition and Food Research, Vol. 60, No. 5, 01.05.2016, p. 1129-1138.

Research output: Contribution to journalArticle

@article{5f904b248d9e4f0982fb9f59737c55f5,
title = "Urolithin A, C, and D, but not iso-urolithin A and urolithin B, attenuate triglyceride accumulation in human cultures of adipocytes and hepatocytes",
abstract = "Scope: Urolithins (Uro) are ellagic acid (EA)-derived metabolites produced by gut microbes. There is a growing interest in the biological activities of Uro. Our aim was to evaluate the impacts of Uro on regulating triglyceride (TG) accumulation using cultures of primary human adipocytes and hepatoma Huh7 cells. Methods and results: UroA, UroB, UroC, UroD, and iso-UroA were used to determine the effect of Uro on adipogenesis and lipogenesis. Individual Uro (30 μM) were added to human adipogenic stem cells during differentiation. UroA, UroC, and UroD, but not iso-UroA and UroB, significantly inhibited new fat cell formation by decreasing TG accumulation and adipogenic protein and gene expressions. The regulation of TG synthesis by Uro was investigated via metabolic chasing with radiolabeled precursors. UroA, UroC, and UroD attenuated TG accumulation, while increasing the fatty acid (FA) oxidation in adipocytes and h/epatoma Huh7 cells. Furthermore, UroC, UroD, and UroA promoted the phosphorylation of AMP-activated protein kinase, suggesting that Uro may alter energy-sensing metabolic pathways in primary human adipocytes. Conclusions: Taken together, our results demonstrated that UroA, UroC, and UroD, but not isoUroA and UroB, reduce TG accumulation and increase FA oxidation in adipocytes as well as hepatocytes.",
keywords = "AMP-activated protein kinase, Adipogenesis, Ellagic acid, Lipogenesis, Urolithins",
author = "Inhae Kang and Yongeun Kim and Tom{\'a}s-Barber{\'a}n, {Francisco A.} and Esp{\'i}n, {Juan Carlos} and Soonkyu Chung",
year = "2016",
month = "5",
day = "1",
doi = "10.1002/mnfr.201500796",
language = "English (US)",
volume = "60",
pages = "1129--1138",
journal = "Molecular Nutrition and Food Research",
issn = "1613-4125",
publisher = "Wiley-VCH Verlag",
number = "5",

}

TY - JOUR

T1 - Urolithin A, C, and D, but not iso-urolithin A and urolithin B, attenuate triglyceride accumulation in human cultures of adipocytes and hepatocytes

AU - Kang, Inhae

AU - Kim, Yongeun

AU - Tomás-Barberán, Francisco A.

AU - Espín, Juan Carlos

AU - Chung, Soonkyu

PY - 2016/5/1

Y1 - 2016/5/1

N2 - Scope: Urolithins (Uro) are ellagic acid (EA)-derived metabolites produced by gut microbes. There is a growing interest in the biological activities of Uro. Our aim was to evaluate the impacts of Uro on regulating triglyceride (TG) accumulation using cultures of primary human adipocytes and hepatoma Huh7 cells. Methods and results: UroA, UroB, UroC, UroD, and iso-UroA were used to determine the effect of Uro on adipogenesis and lipogenesis. Individual Uro (30 μM) were added to human adipogenic stem cells during differentiation. UroA, UroC, and UroD, but not iso-UroA and UroB, significantly inhibited new fat cell formation by decreasing TG accumulation and adipogenic protein and gene expressions. The regulation of TG synthesis by Uro was investigated via metabolic chasing with radiolabeled precursors. UroA, UroC, and UroD attenuated TG accumulation, while increasing the fatty acid (FA) oxidation in adipocytes and h/epatoma Huh7 cells. Furthermore, UroC, UroD, and UroA promoted the phosphorylation of AMP-activated protein kinase, suggesting that Uro may alter energy-sensing metabolic pathways in primary human adipocytes. Conclusions: Taken together, our results demonstrated that UroA, UroC, and UroD, but not isoUroA and UroB, reduce TG accumulation and increase FA oxidation in adipocytes as well as hepatocytes.

AB - Scope: Urolithins (Uro) are ellagic acid (EA)-derived metabolites produced by gut microbes. There is a growing interest in the biological activities of Uro. Our aim was to evaluate the impacts of Uro on regulating triglyceride (TG) accumulation using cultures of primary human adipocytes and hepatoma Huh7 cells. Methods and results: UroA, UroB, UroC, UroD, and iso-UroA were used to determine the effect of Uro on adipogenesis and lipogenesis. Individual Uro (30 μM) were added to human adipogenic stem cells during differentiation. UroA, UroC, and UroD, but not iso-UroA and UroB, significantly inhibited new fat cell formation by decreasing TG accumulation and adipogenic protein and gene expressions. The regulation of TG synthesis by Uro was investigated via metabolic chasing with radiolabeled precursors. UroA, UroC, and UroD attenuated TG accumulation, while increasing the fatty acid (FA) oxidation in adipocytes and h/epatoma Huh7 cells. Furthermore, UroC, UroD, and UroA promoted the phosphorylation of AMP-activated protein kinase, suggesting that Uro may alter energy-sensing metabolic pathways in primary human adipocytes. Conclusions: Taken together, our results demonstrated that UroA, UroC, and UroD, but not isoUroA and UroB, reduce TG accumulation and increase FA oxidation in adipocytes as well as hepatocytes.

KW - AMP-activated protein kinase

KW - Adipogenesis

KW - Ellagic acid

KW - Lipogenesis

KW - Urolithins

UR - http://www.scopus.com/inward/record.url?scp=84963647506&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84963647506&partnerID=8YFLogxK

U2 - 10.1002/mnfr.201500796

DO - 10.1002/mnfr.201500796

M3 - Article

C2 - 26872561

AN - SCOPUS:84963647506

VL - 60

SP - 1129

EP - 1138

JO - Molecular Nutrition and Food Research

JF - Molecular Nutrition and Food Research

SN - 1613-4125

IS - 5

ER -