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Biochem Biophys Res Commun. 2015 Sep 4;464(4):1171-1177. doi: 10.1016/j.bbrc.2015.07.099. Epub 2015 Jul 21.

B-cell-activating factor deficiency attenuates high-fat diet-induced glucose intolerance by potentiating adipose tissue function.

Author information

1
School of Life Science, Handong Global University, Pohang, Gyungbuk 791-708, Republic of Korea.
2
School of Life Science, Handong Global University, Pohang, Gyungbuk 791-708, Republic of Korea. Electronic address: ckhyun@handong.edu.

Abstract

B-cell-activating factor (BAFF) has recently been demonstrated to be expressed in adipocytes and up-regulated by high-fat diet feeding, indicating a possible role in metabolic regulation. Here we show that glucose tolerance was significantly improved in high-fat diet-fed BAFF knockout (BAFF(-/-)) mice. BAFF(-/-) mice revealed higher levels of glucose transporter expression and insulin-stimulated Akt phosphorylation in brown adipose tissue compared to wild type controls. Expression levels of mitochondrial ND5 and genes involved in lipid metabolism were significantly elevated in brown adipose tissue of BAFF(-/-) mice, and this enhancement was found to be mediated by FGF21 and leptin. It was also observed that expression of IL-10 and foxp3 was increased in adipose tissues, as well as PPARγ activity in white adipose tissue. Our findings suggest that suppression of BAFF could have a therapeutic potential for prevention of type 2 diabetes.

KEYWORDS:

B-cell-activating factor; Brown adipose tissue; FGF21; Glucose tolerance; IL-10; Leptin

PMID:
26208451
DOI:
10.1016/j.bbrc.2015.07.099
[Indexed for MEDLINE]

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