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Article

Social Stress Increases Vulnerability to High-Fat Diet-Induced Insulin Resistance by Enhancing Neutrophil Elastase Activity in Adipose Tissue

1
Department of Cardiovascular Medicine, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan
2
Department of Regenerative Medicine, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan
3
Department of Pathology and Cell Regulation, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan
4
Department of Pharmacology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan
*
Author to whom correspondence should be addressed.
Cells 2020, 9(4), 996; https://doi.org/10.3390/cells9040996
Received: 9 February 2020 / Revised: 11 April 2020 / Accepted: 15 April 2020 / Published: 16 April 2020
Social stress (SS) has been linked to the development of cardiovascular disease (CVD), which is closely associated with insulin resistance (IR); however, the causal effect of SS on IR remains unclear. The 8-week-old male C57BL/6 mice were exposed to SS by housing with a larger CD-1 mouse in a shared home cage without physical contact for 10 consecutive days followed by high-fat diet (HFD) feeding. Control mice were housed in the same cage without a CD-1 mouse. After 6 weeks of HFD, insulin sensitivity was significantly impaired in stressed mice. While the percentage of classically activated macrophages in epididymal white adipose tissue (eWAT) was equivalent between the two groups, the percentage of lymphocyte antigen 6 complex locus G6D (Ly-6G)/neutrophil elastase (NE)-double positive cells markedly increased in stressed mice, accompanied by augmented NE activity assessed by ex vivo eWAT fluorescent imaging. Treatment with an NE inhibitor completely abrogated the insulin sensitivity impairment of stressed mice. In vitro NE release upon stimulation with a formyl peptide receptor 1 agonist was significantly higher in bone marrow neutrophils of stressed mice. Our findings show that SS-exposed mice are susceptible to the development of HFD-induced IR accompanied by augmented NE activity. Modulation of neutrophil function may represent a potential therapeutic target for SS-associated IR. View Full-Text
Keywords: social stress; insulin resistance; neutrophil; neutrophil elastase; adipose tissue; heat-shock protein 72 social stress; insulin resistance; neutrophil; neutrophil elastase; adipose tissue; heat-shock protein 72
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MDPI and ACS Style

Motoyama, S.; Yamada, H.; Yamamoto, K.; Wakana, N.; Terada, K.; Kikai, M.; Wada, N.; Saburi, M.; Sugimoto, T.; Kubota, H.; Miyawaki, D.; Kami, D.; Ogata, T.; Ibi, M.; Yabe-Nishimura, C.; Matoba, S. Social Stress Increases Vulnerability to High-Fat Diet-Induced Insulin Resistance by Enhancing Neutrophil Elastase Activity in Adipose Tissue. Cells 2020, 9, 996. https://doi.org/10.3390/cells9040996

AMA Style

Motoyama S, Yamada H, Yamamoto K, Wakana N, Terada K, Kikai M, Wada N, Saburi M, Sugimoto T, Kubota H, Miyawaki D, Kami D, Ogata T, Ibi M, Yabe-Nishimura C, Matoba S. Social Stress Increases Vulnerability to High-Fat Diet-Induced Insulin Resistance by Enhancing Neutrophil Elastase Activity in Adipose Tissue. Cells. 2020; 9(4):996. https://doi.org/10.3390/cells9040996

Chicago/Turabian Style

Motoyama, Shinichiro, Hiroyuki Yamada, Keita Yamamoto, Noriyuki Wakana, Kensuke Terada, Masakazu Kikai, Naotoshi Wada, Makoto Saburi, Takeshi Sugimoto, Hiroshi Kubota, Daisuke Miyawaki, Daisuke Kami, Takehiro Ogata, Masakazu Ibi, Chihiro Yabe-Nishimura, and Satoaki Matoba. 2020. "Social Stress Increases Vulnerability to High-Fat Diet-Induced Insulin Resistance by Enhancing Neutrophil Elastase Activity in Adipose Tissue" Cells 9, no. 4: 996. https://doi.org/10.3390/cells9040996

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