Endoplasmic reticulum stress in adipose tissue augments lipolysis

The endoplasmic reticulum (ER) is an organelle important for protein synthesis and folding, lipid synthesis and Ca2+ homoeostasis. Consequently, ER stress or dysfunction affects numerous cellular processes and has been implicated as a contributing factor in several pathophysiological conditions. Tun...

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Main Authors:	Bogdanovic, Elena, Kraus, Nicole, Patsouris, David, Diao, Li, Wang, Vivian, Abdullahi, Abdikarim, Jeschke, Marc G
Format:	Online
Language:	English
Published:	Blackwell Publishing Ltd 2015
Online Access:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4288352/

id	pubmed-4288352
recordtype	oai_dc
spelling	pubmed-42883522015-01-21 Endoplasmic reticulum stress in adipose tissue augments lipolysis Bogdanovic, Elena Kraus, Nicole Patsouris, David Diao, Li Wang, Vivian Abdullahi, Abdikarim Jeschke, Marc G Original Articles The endoplasmic reticulum (ER) is an organelle important for protein synthesis and folding, lipid synthesis and Ca2+ homoeostasis. Consequently, ER stress or dysfunction affects numerous cellular processes and has been implicated as a contributing factor in several pathophysiological conditions. Tunicamycin induces ER stress in various cell types in vitro as well as in vivo. In mice, a hallmark of tunicamycin administration is the development of fatty livers within 24–48 hrs accompanied by hepatic ER stress. We hypothesized that tunicamycin would induce ER stress in adipose tissue that would lead to increased lipolysis and subsequently to fatty infiltration of the liver and hepatomegaly. Our results show that intraperitoneal administration of tunicamycin rapidly induced an ER stress response in adipose tissue that correlated with increased circulating free fatty acids (FFAs) and glycerol along with decreased adipose tissue mass and lipid droplet size. Furthermore, we found that in addition to fatty infiltration of the liver as well as hepatomegaly, lipid accumulation was also present in the heart, skeletal muscle and kidney. To corroborate our findings to a clinical setting, we examined adipose tissue from burned patients where increases in lipolysis and the development of fatty livers have been well documented. We found that burned patients displayed significant ER stress within adipose tissue and that ER stress augments lipolysis in cultured human adipocytes. Our results indicate a possible role for ER stress induced lipolysis in adipose tissue as an underlying mechanism contributing to increases in circulating FFAs and fatty infiltration into other organs. Blackwell Publishing Ltd 2015-01 2014-11-08 /pmc/articles/PMC4288352/ /pubmed/25381905 http://dx.doi.org/10.1111/jcmm.12384 Text en © 2014 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine. http://creativecommons.org/licenses/by/3.0/ This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
repository_type	Open Access Journal
institution_category	Foreign Institution
institution	US National Center for Biotechnology Information
building	NCBI PubMed
collection	Online Access
language	English
format	Online
author	Bogdanovic, Elena Kraus, Nicole Patsouris, David Diao, Li Wang, Vivian Abdullahi, Abdikarim Jeschke, Marc G
spellingShingle	Bogdanovic, Elena Kraus, Nicole Patsouris, David Diao, Li Wang, Vivian Abdullahi, Abdikarim Jeschke, Marc G Endoplasmic reticulum stress in adipose tissue augments lipolysis
author_facet	Bogdanovic, Elena Kraus, Nicole Patsouris, David Diao, Li Wang, Vivian Abdullahi, Abdikarim Jeschke, Marc G
author_sort	Bogdanovic, Elena
title	Endoplasmic reticulum stress in adipose tissue augments lipolysis
title_short	Endoplasmic reticulum stress in adipose tissue augments lipolysis
title_full	Endoplasmic reticulum stress in adipose tissue augments lipolysis
title_fullStr	Endoplasmic reticulum stress in adipose tissue augments lipolysis
title_full_unstemmed	Endoplasmic reticulum stress in adipose tissue augments lipolysis
title_sort	endoplasmic reticulum stress in adipose tissue augments lipolysis
description	The endoplasmic reticulum (ER) is an organelle important for protein synthesis and folding, lipid synthesis and Ca2+ homoeostasis. Consequently, ER stress or dysfunction affects numerous cellular processes and has been implicated as a contributing factor in several pathophysiological conditions. Tunicamycin induces ER stress in various cell types in vitro as well as in vivo. In mice, a hallmark of tunicamycin administration is the development of fatty livers within 24–48 hrs accompanied by hepatic ER stress. We hypothesized that tunicamycin would induce ER stress in adipose tissue that would lead to increased lipolysis and subsequently to fatty infiltration of the liver and hepatomegaly. Our results show that intraperitoneal administration of tunicamycin rapidly induced an ER stress response in adipose tissue that correlated with increased circulating free fatty acids (FFAs) and glycerol along with decreased adipose tissue mass and lipid droplet size. Furthermore, we found that in addition to fatty infiltration of the liver as well as hepatomegaly, lipid accumulation was also present in the heart, skeletal muscle and kidney. To corroborate our findings to a clinical setting, we examined adipose tissue from burned patients where increases in lipolysis and the development of fatty livers have been well documented. We found that burned patients displayed significant ER stress within adipose tissue and that ER stress augments lipolysis in cultured human adipocytes. Our results indicate a possible role for ER stress induced lipolysis in adipose tissue as an underlying mechanism contributing to increases in circulating FFAs and fatty infiltration into other organs.
publisher	Blackwell Publishing Ltd
publishDate	2015
url	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4288352/
_version_	1613174711802396672

Endoplasmic reticulum stress in adipose tissue augments lipolysis

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