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DOI 10.1016/j.bbrc.2017.11.069

Медицинская библиотека · Biochemical and biophysical research communications · 2017

Adipose tissue complement factor B promotes adipocyte maturation.

Matsunaga Hiroaki, Iwashita Misaki, Shinjo Takanori, Yamashita Akiko, Tsuruta Mitsudai, Nagasaka Shoichiro, Taniguchi Ataru, Fukushima Mitsuo, Watanabe Naoya, Nishimura Fusanori

СтатьяПоддержка исследования: вне правительства СШАПеревод в очереди

Аннотация

OBJECTIVES

It is well-known that the complement system plays an essential role in host immunity. Observational studies have indicated that complement system-related molecules such as complement factor B (CfB) and other components are correlated with obesity and/or insulin resistance parameters. In this study, we investigated the role of adipocyte-derived CfB in adipose tissue metabolism.

METHODS

We investigated the expression level of complement system-related genes in adipocytes. To understand the role of CfB in adipocyte, we performed Cfb overexpression in 3T3-L1 preadipocytes and generated adipocyte-specific Cfb transgenic mice.

RESULTS

Cfb expression was markedly enhanced in 3T3-L1 adipocytes co-cultured with macrophages following endotoxin stimulation. In Cfb-overexpressing cells, the expression of adipocyte differentiation/maturation-related genes encoding peroxisome proliferator-activated receptor γ (Pparγ), adipocyte Protein 2 and perilipin was significantly enhanced. Cfb transgenic mice showed a marked increase in the expression of genes encoding Pparγ, perilipin, sterol regulatory element-binding protein 1 c, and Cd36 in the subcutaneous adipose tissue.

CONCLUSIONS

CfB plays a crucial role in late-phase of adipocyte differentiation and subsequent lipid droplet formation.

Для цитирования: Matsunaga Hiroaki, Iwashita Misaki, Shinjo Takanori, Yamashita Akiko, Tsuruta Mitsudai, Nagasaka Shoichiro, Taniguchi Ataru, Fukushima Mitsuo, Watanabe Naoya, Nishimura Fusanori. Adipose tissue complement factor B promotes adipocyte maturation.. Biochemical and biophysical research communications. 2017. DOI: 10.1016/j.bbrc.2017.11.069.

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