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B Cell‐Activating Factor Controls the Production of Adipokines and Induces Insulin Resistance
Author(s) -
Hamada Maho,
Abe Masanori,
Miyake Teruki,
Kawasaki Keitarou,
Tada Fujimasa,
Furukawa Shinya,
Matsuura Bunzo,
Hiasa Yoichi,
Onji Morikazu
Publication year - 2011
Publication title -
obesity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.438
H-Index - 199
eISSN - 1930-739X
pISSN - 1930-7381
DOI - 10.1038/oby.2011.165
Subject(s) - b cell activating factor , insulin resistance , adipokine , endocrinology , medicine , autocrine signalling , insulin , adipose tissue , insulin receptor , paracrine signalling , insulin receptor substrate , receptor , immunology , b cell , antibody
Visceral adipose tissue (VAT) inflammation has been linked to the pathogenesis of insulin resistance and metabolic syndrome. VAT has recently been established as a new component of the immune system and is involved in the production of various adipokines and cytokines. These molecules contribute to inducing and accelerating systemic insulin resistance. In this report, we investigated the role of B cell‐activating factor (BAFF) in the induction of insulin resistance. We investigated BAFF levels in the sera and VAT of obese mice. In obese mice, the BAFF levels were preferentially increased in VAT and sera compared to these levels in normal control mice. Next, we treated mice with BAFF to analyze its influence on insulin sensitivity. BAFF impaired insulin sensitivity in normal mice. Finally, we investigated the mechanisms underlying insulin resistance induced by BAFF in adipocytes. BAFF also induced alterations in the expression levels of genes related to insulin resistance in adipocytes. In addition, BAFF directly affected the glucose uptake and phosphorylation of insulin receptor substrate‐1 in adipocytes. We propose that autocrine or paracrine BAFF and BAFF‐receptor (BAFF‐R) interaction in VAT leads to impaired insulin sensitivity via inhibition of insulin signaling pathways and alterations in adipokine production.