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Endoplasmic reticulum stress is differentially modulated in subcutaneous and visceral adipose tissue of obese mice and cultured adipocytes
Author(s) -
TorreVillalvazo Ivan,
Bunt Ana Elena,
Stern Dalia,
Torres Nimbe,
Tovar Armando R
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1103.2
Subject(s) - medicine , endocrinology , leptin , adipose tissue , adipocyte , endoplasmic reticulum , unfolded protein response , adiponectin , adipokine , fatty liver , chemistry , obesity , biology , insulin resistance , microbiology and biotechnology , disease
Obesity activates endoplasmic reticulum stress (ERS) in liver and pancreas. However it is not know whether obesity induces ERS in adipocytes. Objective To examine whether subcutaneus (SAT) or viceral (VAT) adipocytes develop ERS during obesity. Methods To asses ERS in adipocytes in vivo, mice were fed a control or a high‐fat (HF) diet for 9 weeks, followed by an ip injection of leptin. For in vitro analysis, primary SAT and VAT adipocytes were cultured with insulin, leptin or ETYA with or without tunicamicyn for 14h. Results leptin injection to control mice increased leptin receptor, SREBP1, SOCS3, ATF6 and PERK mRNA content in SAT but not in VAT. Consumption of a HF diet resulted in obesity, hyperleptinemia, fatty liver and adipocyte hypertrophy. Leptin administration did not affect the the expression of these genes in SAT but they increased in VAT of obese mice. Tunicamicyn‐induced ERS increased ATF6, BiP and SREBP1 mRNA content and reduced adiponectin mRNA in SAT but not in VAT adipocytes. Conclusion Visceral adipose tissue is probably less sensitive to leptin action but also relativelly resistant to develop obesity or tunicamicyn induced ERS. This work is supported by CONACyT(84757)