Negative legacy of obesity

Kosuke Shirakawa, Jin Endo, Yoshinori Katsumata, Tsunehisa Yamamoto, Masaharu Kataoka, Sarasa Isobe, Naohiro Yoshida, Keiichi Fukuda, Motoaki Sano

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

Obesity promotes excessive inflammation, which is associated with senescence-like changes in visceral adipose tissue (VAT) and the development of type 2 diabetes (T2DM) and cardiovascular diseases. We have reported that a unique population of CD44hi CD62Llo CD4+ T cells that constitutively express PD-1 and CD153 exhibit cellular senescence and cause VAT inflammation by producing large amounts of osteopontin. Weight loss improves glycemic control and reduces cardiovascular disease risk factors, but its long-term effects on cardiovascular events and longevity in obese individuals with T2DM are somewhat disappointing and not well understood. High-fat diet (HFD)-fed obese mice were subjected to weight reduction through a switch to a control diet. They lost body weight and visceral fat mass, reaching the same levels as lean mice fed a control diet. However, the VAT of weight reduction mice exhibited denser infiltration of macrophages, which formed more crown-like structures compared to the VAT of obese mice kept on the HFD. Mechanistically, CD153+ PD-1+ CD4+ T cells are long-lived and not easily eliminated, even after weight reduction. Their continued presence maintains a self-sustaining chronic inflammatory loop via production of large amounts of osteopontin. Thus, we concluded that T-cell senescence is essentially a negative legacy effect of obesity.

Original languageEnglish
Article numbere0186303
JournalPLoS One
Volume12
Issue number10
DOIs
Publication statusPublished - 2017 Oct 1

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Intra-Abdominal Fat
Nutrition
adipose tissue
T-cells
obesity
weight loss
Obesity
Tissue
Weight Loss
osteopontin
Osteopontin
T-lymphocytes
Fats
mice
high fat diet
Obese Mice
cardiovascular diseases
Cell Aging
High Fat Diet
T-Lymphocytes

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Agricultural and Biological Sciences(all)

Cite this

Shirakawa, K., Endo, J., Katsumata, Y., Yamamoto, T., Kataoka, M., Isobe, S., ... Sano, M. (2017). Negative legacy of obesity. PLoS One, 12(10), [e0186303]. https://doi.org/10.1371/journal.pone.0186303

Negative legacy of obesity. / Shirakawa, Kosuke; Endo, Jin; Katsumata, Yoshinori; Yamamoto, Tsunehisa; Kataoka, Masaharu; Isobe, Sarasa; Yoshida, Naohiro; Fukuda, Keiichi; Sano, Motoaki.

In: PLoS One, Vol. 12, No. 10, e0186303, 01.10.2017.

Research output: Contribution to journalArticle

Shirakawa, K, Endo, J, Katsumata, Y, Yamamoto, T, Kataoka, M, Isobe, S, Yoshida, N, Fukuda, K & Sano, M 2017, 'Negative legacy of obesity', PLoS One, vol. 12, no. 10, e0186303. https://doi.org/10.1371/journal.pone.0186303
Shirakawa K, Endo J, Katsumata Y, Yamamoto T, Kataoka M, Isobe S et al. Negative legacy of obesity. PLoS One. 2017 Oct 1;12(10). e0186303. https://doi.org/10.1371/journal.pone.0186303
Shirakawa, Kosuke ; Endo, Jin ; Katsumata, Yoshinori ; Yamamoto, Tsunehisa ; Kataoka, Masaharu ; Isobe, Sarasa ; Yoshida, Naohiro ; Fukuda, Keiichi ; Sano, Motoaki. / Negative legacy of obesity. In: PLoS One. 2017 ; Vol. 12, No. 10.
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