Thyroid-Hormone-Induced Browning of White Adipose Tissue Does Not Contribute to Thermogenesis and Glucose Consumption.

Adipose Tissue, Beige / metabolism Adipose Tissue, Brown / metabolism Adipose Tissue, White / metabolism Animals Glucose / metabolism Male Mice Mice, Inbred C57BL Muscle, Skeletal / metabolism Receptors, Adrenergic, beta-3 / metabolism Thermogenesis Thyroid Hormones / metabolism Uncoupling Protein 1 / genetics

beige adipose tissue beta3-adrenergic receptor body temperature brown adipose tissue glucose tolerance hyperthermia metabolism norepinephrine pyrexia sympathetic nervous system thyroid hormone receptor uncoupling protein 1

Journal

Cell reports

ISSN: 2211-1247

Titre abrégé: Cell Rep

Pays: United States

ID NLM: 101573691

Informations de publication

Date de publication:
11 06 2019

Historique:

received: 26 09 2018

revised: 07 05 2019

accepted: 15 05 2019

entrez: 13 6 2019

pubmed: 13 6 2019

medline: 4 8 2020

Statut: ppublish

Résumé

Regulation of body temperature critically depends on thyroid hormone (TH). Recent studies revealed that TH induces browning of white adipose tissue, possibly contributing to the observed hyperthermia in hyperthyroid patients and potentially providing metabolic benefits. Here, we show that browning by TH requires TH-receptor β and occurs independently of the sympathetic nervous system. The beige fat, however, lacks sufficient adrenergic stimulation and is not metabolically activated despite high levels of uncoupling protein 1 (UCP1). Studies at different environmental temperatures reveal that TH instead causes hyperthermia by actions in skeletal muscle combined with a central body temperature set-point elevation. Consequently, the metabolic and thermogenic effects of systemic hyperthyroidism were maintained in UCP1 knockout mice, demonstrating that neither beige nor brown fat contributes to the TH-induced hyperthermia and elevated glucose consumption, and underlining that the mere presence of UCP1 is insufficient to draw conclusions on the therapeutic potential of browning agents.

Identifiants

DOI: 10.1016/j.celrep.2019.05.054 PMID: 31189119

pubmed: 31189119

pii: S2211-1247(19)30683-7

doi: 10.1016/j.celrep.2019.05.054

pii:

doi:

Substances chimiques

Receptors, Adrenergic, beta-3 0

Thyroid Hormones 0

Ucp1 protein, mouse 0

Uncoupling Protein 1 0

Glucose IY9XDZ35W2

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng