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.

Patients with a-PBC showing lack of biochemical response to UDCA by 6 months after treatment commencement should be considered for further treatments.

Nonalcoholic steatohepatitis patients had higher levels of serum BAFF than patients with SS, and higher levels were associated with the presence of hepatocyte ballooning and advanced fibrosis. The serum BAFF level may be a useful tool for distinguishing NASH from SS.

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We treated a 66-year-old woman with hepatic encephalopathy secondarily induced by an intrahepatic portosystemic venous shunt (IPSVS). In serial observations, the volume of the liver became smaller and encephalopathy could not be controlled with conservative therapy. We occluded the IPSVS successfully using percutaneous transcatheter embolization with micro coils. Following embolization, encephalopathy disappeared and blood flow of all branches of portal vein improved. In cases with an IPSVS without liver cirrhosis, blood flow in the portal vein and liver volume must be followed carefully, and interventional radiology may be considered effective in those who do not show a satisfactory response to conservative therapy.