Article1 min read·Published May 2021Older

A BAFF/APRIL axis regulates obesogenic diet-driven weight gain

Part of Inflammatory & Immune-Mediated GI Disease 9 items

pubmed.ncbi.nlm.nih.gov

Michael Helmrath

The impact of immune mediators on weight homeostasis remains underdefined. Interrogation of resistance to diet-induced obesity in mice lacking a negative regulator of Toll-like receptor signaling serendipitously uncovered a role for B cell activating factor (BAFF). Here we show that overexpression of BAFF in multiple mouse models associates with protection from weight gain, approximating a log-linear dose response relation to BAFF concentrations. Gene expression analysis of BAFF-stimulated subcutaneous white adipocytes unveils upregulation of lipid metabolism pathways, with BAFF inducing white adipose tissue (WAT) lipolysis. Brown adipose tissue (BAT) from BAFF-overexpressing mice exhibits increased Ucp1 expression and BAFF promotes brown adipocyte respiration and in vivo energy expenditure. A proliferation-inducing ligand (APRIL), a BAFF homolog, similarly modulates WAT and BAT lipid handling. Genetic deletion of both BAFF and APRIL augments diet-induced obesity. Lastly, BAFF/APRIL effects are conserved in human adipocytes and higher BAFF/APRIL levels correlate with greater BMI decrease after bariatric surgery. Together, the BAFF/APRIL axis is a multifaceted immune regulator of weight gain and adipose tissue function.

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Article · May 2021 · 1 min read

In brief

This study reveals that immune cytokines BAFF and APRIL regulate weight gain by modulating adipose tissue metabolism. BAFF overexpression protects against diet-induced obesity through enhanced lipolysis in white fat and increased thermogenesis in brown fat, with effects conserved in human adipocytes and correlating with bariatric surgery outcomes.

Written by the GCMD Library team from the article.

Michael Helmrath

Statements in this article

Overexpression of BAFF in multiple mouse models associates with protection from weight gain, approximating a log-linear dose response relation to BAFF concentrations.
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BAFF stimulation of subcutaneous white adipocytes upregulates lipid metabolism pathways.
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BAFF induces white adipose tissue lipolysis.
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Brown adipose tissue from BAFF-overexpressing mice exhibits increased Ucp1 expression.
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BAFF promotes brown adipocyte respiration and in vivo energy expenditure.
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APRIL similarly modulates white adipose tissue and brown adipose tissue lipid handling.
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Genetic deletion of both BAFF and APRIL augments diet-induced obesity.
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BAFF and APRIL effects are conserved in human adipocytes.
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Higher BAFF and APRIL levels correlate with greater BMI decrease after bariatric surgery.
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