BTK targeting suppresses inflammatory genes and ameliorates insulin resistance (notice n° 236461)

détails MARC
000 -LEADER
fixed length control field 02609cam a2200289 4500500
005 - DATE AND TIME OF LATEST TRANSACTION
control field 20250112064114.0
041 ## - LANGUAGE CODE
Language code of text/sound track or separate title fre
042 ## - AUTHENTICATION CODE
Authentication code dc
100 10 - MAIN ENTRY--PERSONAL NAME
Personal name Althubiti, Mohammad
Relator term author
245 00 - TITLE STATEMENT
Title BTK targeting suppresses inflammatory genes and ameliorates insulin resistance
260 ## - PUBLICATION, DISTRIBUTION, ETC.
Date of publication, distribution, etc. 2020.<br/>
500 ## - GENERAL NOTE
General note 24
520 ## - SUMMARY, ETC.
Summary, etc. Type 2 diabetes (T2D) causes profound psychological and physical distress to patients and burdens the health-care system. Although several antidiabetic drugs have been approved, none of them are adequately effective in the long-term management of T2D. Therefore, novel treatment options are needed for disease prevention or delaying disease progression. Bruton's tyrosine kinase (BTK) is a cytoplasmic enzyme that plays a role in B-cell differentiation and proliferation, and therapeutic targeting of BTK offers protection against chronic diseases. In this study, we analyzed BTK expression and its correlation with inflammatory mediators in patients with diabetes and obesity. The levels of BTK were significantly high in visceral adipose tissues of patients (p &lt; 0.01) with diabetes and obesity compared with healthy controls. Additionally, a positive correlation was noted between the expression of BTK and the inflammatory cytokine genes TNF-α, INF-γ, IL-6, and IL-1 (p &lt; 0.01) in adipose tissue. In insulin-resistant HepG2 cells (IR-HepG2), ibrutinib inhibited BTK expression in parallel with inflammatory genes, and increased insulin signaling and activity compared with untreated IR-HepG2 cells. Additionally, ibrutinib-treated IR-HepG2 cells showed increased glucose uptake compared with untreated IR-HepG2 cells. These results provide evidence that BTK inhibition may serve as a novel therapeutic strategy for the treatment of T2D. These findings also uncover the novel role of BTK in diabetes and insulin resistance; however, further in vivo studies are required prior to translating the findings into clinical settings.
690 ## - LOCAL SUBJECT ADDED ENTRY--TOPICAL TERM (OCLC, RLIN)
Topical term or geographic name as entry element Bruton's tyrosine kinase
690 ## - LOCAL SUBJECT ADDED ENTRY--TOPICAL TERM (OCLC, RLIN)
Topical term or geographic name as entry element diabetes mellitus
690 ## - LOCAL SUBJECT ADDED ENTRY--TOPICAL TERM (OCLC, RLIN)
Topical term or geographic name as entry element inflammation
690 ## - LOCAL SUBJECT ADDED ENTRY--TOPICAL TERM (OCLC, RLIN)
Topical term or geographic name as entry element insulin resistance
700 10 - ADDED ENTRY--PERSONAL NAME
Personal name Almaimani, Riyad
Relator term author
700 10 - ADDED ENTRY--PERSONAL NAME
Personal name Yehia Eid, Safaa
Relator term author
700 10 - ADDED ENTRY--PERSONAL NAME
Personal name Elzubaier, Mohammad
Relator term author
700 10 - ADDED ENTRY--PERSONAL NAME
Personal name Refaat, Bassem
Relator term author
700 10 - ADDED ENTRY--PERSONAL NAME
Personal name Idris, Shakir
Relator term author
700 10 - ADDED ENTRY--PERSONAL NAME
Personal name Atia Alqurashi, Turki
Relator term author
700 10 - ADDED ENTRY--PERSONAL NAME
Personal name Zaki El-Readi, Mahmoud
Relator term author
786 0# - DATA SOURCE ENTRY
Note European Cytokine Network | Volume 31 | 4 | 2020-12-01 | p. 168-179 | 1148-5493
856 41 - ELECTRONIC LOCATION AND ACCESS
Uniform Resource Identifier <a href="https://shs.cairn.info/revue-european-cytokine-network-2020-4-page-168?lang=en">https://shs.cairn.info/revue-european-cytokine-network-2020-4-page-168?lang=en</a>

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