Staff Publications

Staff Publications

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    'Staff publications' is the digital repository of Wageningen University & Research

    'Staff publications' contains references to publications authored by Wageningen University staff from 1976 onward.

    Publications authored by the staff of the Research Institutes are available from 1995 onwards.

    Full text documents are added when available. The database is updated daily and currently holds about 240,000 items, of which 72,000 in open access.

    We have a manual that explains all the features 

Record number 561023
Title Toll-like receptors 2 and 4 control adaptive β-cell expansion in diet-induced obesity
Author(s) Ji, Yewei; Sun, Shengyi; Shrestha, Neha; Darragh, Laurel B.; Shirakawa, Jun; Xing, Yuan; He, Yi; Carboneau, Bethany A.; Kim, G.; Kim, Hana; An, Duo; Ma, Minglin; Oberholzer, Jose; Soleimanpour, Scott A.; Gannon, Maureen; Liu, Chengyang; Naji, Ali; Kulkarni, Rohit N.; Wang, Yong; Kersten, Sander; Qi, Ling
Source Wageningen University
Department(s) VLAG
Nutrition, Metabolism and Genomics
Publication type Dataset
Publication year 2019
Keyword(s) GSE101392 - Mus musculus - PRJNA394076
Abstract Adult pancreatic β cells are refractory to proliferation, a roadblock for the treatment of insulin-deficient diabetes. Consumption of energy-dense Western or high-fat diet (HFD) triggers mild adaptive β cell mass expansion to compensate for peripheral insulin resistance; however, the underlying molecular mechanism remains unclear. Here we show that Toll-like receptors (TLR) 2/TLR4 act as molecular “brakes” for diet-induced β cell replication in both mice and humans. The combined loss of TLR2/TLR4, but not individually, dramatically increases facultative β, not α, cell replication, leading to progressively enlarged islet mass and hyperinsulinemia in diet-induced obesity. Mechanistically, loss of TLR2/TLR4 increases β cell proliferation and nuclear abundance of Cyclin D2 and CDK4 in an extracellular signal-regulated kinase (ERK)-dependent manner. These data reveal a novel mechanism governing adaptive β cell mass expansion in diet-induced obesity and suggest that selective targeting of TLR2/TLR4 pathways may hold promise for reversing β cell failure in diabetic patients.
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