These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Adipocyte IRE1α promotes PGC1α mRNA decay and restrains adaptive thermogenesis.
    Author: Chen Y, Wu Z, Huang S, Wang X, He S, Liu L, Hu Y, Chen L, Chen P, Liu S, He S, Shan B, Zheng L, Duan SZ, Song Z, Jiang L, Wang QA, Gan Z, Song BL, Liu J, Rui L, Shao M, Liu Y.
    Journal: Nat Metab; 2022 Sep; 4(9):1166-1184. PubMed ID: 36123394.
    Abstract:
    Adipose tissue undergoes thermogenic remodeling in response to thermal stress and metabolic cues, playing a crucial role in regulating energy expenditure and metabolic homeostasis. Endoplasmic reticulum (ER) stress is associated with adipose dysfunction in obesity and metabolic disease. It remains unclear, however, if ER stress-signaling in adipocytes mechanistically mediates dysregulation of thermogenic fat. Here we show that inositol-requiring enzyme 1α (IRE1α), a key ER stress sensor and signal transducer, acts in both white and beige adipocytes to impede beige fat activation. Ablation of adipocyte IRE1α promotes browning/beiging of subcutaneous white adipose tissue following cold exposure or β3-adrenergic stimulation. Loss of IRE1α alleviates diet-induced obesity and augments the anti-obesity effect of pharmacologic β3-adrenergic stimulation. Notably, IRE1α suppresses stimulated lipolysis and degrades Ppargc1a messenger RNA through its RNase activity to downregulate the thermogenic gene program. Hence, blocking IRE1α bears therapeutic potential in unlocking adipocytes' thermogenic capacity to combat obesity and metabolic disorders.
    [Abstract] [Full Text] [Related] [New Search]