Angiotensin II Type 1 Receptor-associated Protein Inhibits Angiotensin II-induced Insulin Resistance with Suppression of Oxidative Stress in Skeletal Muscle Tissue

• DOI: 10.1038/s41598-018-21270-8
• Publication Date: 2018-02-06T15:01:14Z
• Authors: Kohji Ohki; Hiromichi Wakui; Nozomu Kishio; Kengo Azushima; Kazushi Uneda; Sona Haku; Ryu Kobayashi; Kotaro Haruhara; Sho Kinguchi; Takahiro Yamaji; Takayuki Yamada; Shintaro Minegishi; Tomoaki Ishigami; Yoshiyuki Toya; Akio Yamashita; Kento Imajo; Atsushi Nakajima; Ikuma Kato; Kenichi Ohashi; Kouichi Tamura
• Keywords: Male; 0301 basic medicine; Glucose Transporter Type 4; Angiotensin II; Mice, Transgenic; Lipid Metabolism; p38 Mitogen-Activated Protein Kinases; Article; 3. Good health; Mice; Oxidative Stress; 03 medical and health sciences; Glucose; Adipose Tissue; Animals; Insulin Resistance; Infusions, Intravenous; Muscle, Skeletal; Adaptor Proteins, Signal Transducing

Abstract Enhancement of AT1 receptor-associated protein (ATRAP) in adipose tissue improves high fat diet (HFD)-induced visceral obesity and insulin resistance, suppresses oxidative stress. However, HFD loading is not a direct stimulatory factor for receptor. In the present study, we investigated effect chronic, low-dose angiotensin II (Ang II) stimulation on glucose lipid metabolism mice functional role ATRAP. ATRAP expression was higher (5–10-fold) skeletal muscle (approximately 1.6-fold) transgenic (TG) compared with wild-type (WT) mice. After Ang infusion, sensitivity impaired WT mice, but this response suppressed TG Unexpectedly, infusion did affect profile or tissue, stimulus caused an increase stress activation p38 MAPK, resulting decrease transporter type 4 These responses were Our study suggests that II-induced resistance by increased tissue. Hyperactivity receptor could be related to formation metabolic syndrome.