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Significance Adipose tissue dysfunction such as impaired insulin action in adipocytes is causally implicated in obesity-related metabolic disorders. However, molecular mechanisms underlying obesity-related adipocyte insulin resistance remain unclear. Here we identify a mechanism in the regulation of adipocyte insulin signaling by Fam13a, which is impaired in obesity. We revealed that Fam13a protects IRS1 from proteasomal degradation by recruiting PP2A and consequently accentuates adipocyte insulin signal cascade. We further demonstrated that genetic loss of Fam13a exacerbated obesity-related metabolic disorders, while targeted activation of Fam13a in adipocytes improved it by altering adipose tissue insulin sensitivity. Our data unveiled a previously unknown mechanism underlying obesity-related adipocyte insulin resistance through Fam13a, highlighting Fam13a as a vital player in the pathogenesis of obesity-related metabolic disorders.

Family with sequence similarity 13, member A modulates adipocyte insulin signaling and preserves systemic metabolic homeostasis