Open AccessThe dipeptidyl peptidase‐4 ( DPP ‐4) inhibitor teneligliptin enhances brown adipose tissue function, thereby preventing obesity in mice
Author(s) -
Takeda Kenichiro,
Sawazaki Honami,
Takahashi Haruya,
Yeh YuSheng,
Jheng HueiFen,
Nomura Wataru,
Ara Takeshi,
Takahashi Nobuyuki,
Seno Shigeto,
Osato Naoki,
Matsuda Hideo,
Kawada Teruo,
Goto Tsuyoshi
Publication year - 2018
Publication title -
febs open bio
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.718
H-Index - 31
ISSN - 2211-5463
DOI - 10.1002/2211-5463.12498
Subject(s) - brown adipose tissue , endocrinology , adipose tissue , medicine , dipeptidyl peptidase 4 , white adipose tissue , chemistry , thermogenin , dipeptidyl peptidase , dipeptidyl peptidase 4 inhibitor , downregulation and upregulation , pharmacology , biology , biochemistry , enzyme , type 2 diabetes , diabetes mellitus , gene
To clarify the effects of a dipeptidyl peptidase‐4 ( DPP ‐4) inhibitor on whole‐body energy metabolism, we treated mice fed a high‐fat diet ( HFD ) with teneligliptin, a clinically available DPP ‐4 inhibitor. Teneligliptin significantly prevented HFD ‐induced obesity and obesity‐associated metabolic disorders. It also increased oxygen consumption rate and upregulated uncoupling protein 1 ( UCP 1) expression in both brown adipose tissue ( BAT ) and inguinal white adipose tissue ( iWAT ), suggesting that it enhances BAT function. Soluble DPP ‐4 inhibited β‐adrenoreceptor‐stimulated UCP 1 expression in primary adipocytes, and this inhibition was prevented in the presence of teneligliptin, or an extracellular signal‐related kinase inhibitor. These results indicate that soluble DPP ‐4 inhibits β‐adrenoreceptor‐stimulated UCP 1 induction and that chronic DPP ‐4 inhibitor treatment may prevent obesity through the activation of BAT function.