Methylglyoxal attenuates isoproterenol-induced increase in uncoupling protein 1 expression through activation of JNK signaling pathway in beige adipocytes.
BBGC, S-p-bromobenzylglutathione cyclopentyl diester
Beige adipocytes
CREB, cAMP response element-binding protein
ERK, extracellular receptor kinase
HSL, hormone-sensitive lipase
JNK
JNK, c-Jun N-terminal kinase
MG, methylglyoxal
Methylglyoxal
NAC, N-acetyl-l-cysteine
NEFA, non-esterified fatty acids
PKA, protein kinase A
SEM, standard error of the mean
Ucp1
iWAT, inguinal white adipose tissue
Journal
Biochemistry and biophysics reports
ISSN: 2405-5808
Titre abrégé: Biochem Biophys Rep
Pays: Netherlands
ID NLM: 101660999
Informations de publication
Date de publication:
Dec 2021
Dec 2021
Historique:
received:
14
07
2021
revised:
27
08
2021
accepted:
01
09
2021
entrez:
16
9
2021
pubmed:
17
9
2021
medline:
17
9
2021
Statut:
epublish
Résumé
Methylglyoxal (MG) is a metabolite derived from glycolysis whose levels in the blood and tissues of patients with diabetes are higher than those of healthy individuals, suggesting that MG is associated with the development of diabetic complications. However, it remains unknown whether high levels of MG are a cause or consequence of diabetes. Here, we show that MG negatively affects the expression of uncoupling protein 1 (UCP1), which is involved in thermogenesis and the regulation of systemic metabolism. Decreased
Identifiants
pubmed: 34527816
doi: 10.1016/j.bbrep.2021.101127
pii: S2405-5808(21)00221-1
pmc: PMC8430270
doi:
Types de publication
Journal Article
Langues
eng
Pagination
101127Informations de copyright
© 2021 The Authors. Published by Elsevier B.V.
Déclaration de conflit d'intérêts
The authors declare that they have no known competing financial interests or personal relationships that could have influenced the work reported in this paper.
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