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B-cell-activating factor deficiency attenuates high-fat diet-induced glucose intolerance by potentiating adipose tissue function
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...
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Published in: | Biochemical and biophysical research communications 2015-09, Vol.464 (4), p.1171-1177 |
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Main Authors: | , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | 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.
•BAFF deficient mice show improved glucose tolerance under HFD feeding condition.•Akt phosphorylation was increased in brown adipose tissue (BAT).•Expression of genes involved in thermogenesis and lipid metabolism was enhanced in BAT.•Expression of IL-10, foxp3, FGF21 and leptin was enhanced in adipose tissues.•Inhibitory phosphorylation of PPARγ was reduced in adipose tissue. |
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ISSN: | 0006-291X 1090-2104 |
DOI: | 10.1016/j.bbrc.2015.07.099 |