Regulation of Metabolic Disease-Associated Inflammation by Nutrient Sensors

Alex S. Yamashita; Thiago Belchior; Fábio S. Lira; Nicolette C. Bishop; Barbara Wessner; José C. Rosa; William T. Festuccia

doi:10.1155/2018/8261432

Regulation of Metabolic Disease-Associated Inflammation by Nutrient Sensors

Alex S. Yamashita, Thiago Belchior, Fábio S. Lira, Nicolette C. Bishop, Barbara Wessner, José C. Rosa, William T. Festuccia

Research output: Contribution to journal › Review article › peer-review

12 Scopus citations

Abstract

Visceral obesity is frequently associated with the development of type 2 diabetes (T2D), a highly prevalent chronic disease that features insulin resistance and pancreatic β-cell dysfunction as important hallmarks. Recent evidence indicates that the chronic, low-grade inflammation commonly associated with visceral obesity plays a major role connecting the excessive visceral fat deposition with the development of insulin resistance and pancreatic β-cell dysfunction. Herein, we review the mechanisms by which nutrients modulate obesity-associated inflammation.

Original language	English (US)
Article number	8261432
Journal	Mediators of inflammation
Volume	2018
DOIs	https://doi.org/10.1155/2018/8261432
State	Published - 2018
Externally published	Yes

ASJC Scopus subject areas

Immunology
Cell Biology

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10.1155/2018/8261432

Cite this

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title = "Regulation of Metabolic Disease-Associated Inflammation by Nutrient Sensors",

abstract = "Visceral obesity is frequently associated with the development of type 2 diabetes (T2D), a highly prevalent chronic disease that features insulin resistance and pancreatic β-cell dysfunction as important hallmarks. Recent evidence indicates that the chronic, low-grade inflammation commonly associated with visceral obesity plays a major role connecting the excessive visceral fat deposition with the development of insulin resistance and pancreatic β-cell dysfunction. Herein, we review the mechanisms by which nutrients modulate obesity-associated inflammation.",

author = "Yamashita, {Alex S.} and Thiago Belchior and Lira, {F{\'a}bio S.} and Bishop, {Nicolette C.} and Barbara Wessner and Rosa, {Jos{\'e} C.} and Festuccia, {William T.}",

note = "Funding Information: Funding was provided by Funda{\c c}{\~a}o de Amparo {\`a} Pesquisa do Estado de S{\~a}o Paulo (FAPESP) to Alex S. Yamashita (no. 13/15825-5), Thiago Belchior (no. 15/22983-1), and William T. Festuccia (nos. 10/52191-6 and 15/19530-5). The authors thank Marina da Costa Rosa for the fruitful discussion during the development of this article. Publisher Copyright: {\textcopyright} 2018 Alex S. Yamashita et al.",

year = "2018",

doi = "10.1155/2018/8261432",

language = "English (US)",

volume = "2018",

journal = "Mediators of Inflammation",

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AU - Yamashita, Alex S.

AU - Belchior, Thiago

AU - Lira, Fábio S.

AU - Bishop, Nicolette C.

AU - Wessner, Barbara

AU - Rosa, José C.

AU - Festuccia, William T.

N1 - Funding Information: Funding was provided by Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) to Alex S. Yamashita (no. 13/15825-5), Thiago Belchior (no. 15/22983-1), and William T. Festuccia (nos. 10/52191-6 and 15/19530-5). The authors thank Marina da Costa Rosa for the fruitful discussion during the development of this article. Publisher Copyright: © 2018 Alex S. Yamashita et al.

PY - 2018

Y1 - 2018

N2 - Visceral obesity is frequently associated with the development of type 2 diabetes (T2D), a highly prevalent chronic disease that features insulin resistance and pancreatic β-cell dysfunction as important hallmarks. Recent evidence indicates that the chronic, low-grade inflammation commonly associated with visceral obesity plays a major role connecting the excessive visceral fat deposition with the development of insulin resistance and pancreatic β-cell dysfunction. Herein, we review the mechanisms by which nutrients modulate obesity-associated inflammation.

AB - Visceral obesity is frequently associated with the development of type 2 diabetes (T2D), a highly prevalent chronic disease that features insulin resistance and pancreatic β-cell dysfunction as important hallmarks. Recent evidence indicates that the chronic, low-grade inflammation commonly associated with visceral obesity plays a major role connecting the excessive visceral fat deposition with the development of insulin resistance and pancreatic β-cell dysfunction. Herein, we review the mechanisms by which nutrients modulate obesity-associated inflammation.

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Regulation of Metabolic Disease-Associated Inflammation by Nutrient Sensors

Abstract

ASJC Scopus subject areas

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