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.

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Record number 551153
Title Toll-like receptors TLR2 and TLR4 block the replication of pancreatic β cells 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, 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 Nature Immunology 20 (2019)6. - ISSN 1529-2908 - p. 677 - 686.
DOI https://doi.org/10.1038/s41590-019-0396-z
Department(s) VLAG
Nutrition, Metabolism and Genomics
Publication type Refereed Article in a scientific journal
Publication year 2019
Abstract

Consumption of a high-energy Western diet triggers mild adaptive β cell proliferation to compensate for peripheral insulin resistance; however, the underlying molecular mechanism remains unclear. In the present study we show that the toll-like receptors TLR2 and TLR4 inhibited the diet-induced replication of β cells in mice and humans. The combined, but not the individual, loss of TLR2 and TLR4 increased the replication of β cells, but not that of α cells, leading to enlarged β cell area and hyperinsulinemia in diet-induced obesity. Loss of TLR2 and TLR4 increased the nuclear abundance of the cell cycle regulators cyclin D2 and Cdk4 in a manner dependent on the signaling mediator Erk. These data reveal a regulatory mechanism controlling the proliferation of β cells in diet-induced obesity and suggest that selective targeting of the TLR2/TLR4 pathways may reverse β cell failure in patients with diabetes.

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