β-Arrestin1 mediates nicotinic acid–induced flushing, but not its antilipolytic effect, in mice
J. Clin. Invest. 119:5 doi:10.1172/JCI36806
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Figure 2
Adipocytes, macrophages, and Langerhans cells express β-arrestins, and β-arrestin1 is recruited to the cell membrane with stimulation of GPR109A in Langerhans cells.

(A) Cell lysates from differentiated 3T3-L1 adipocytes, differentiated THP-1 macrophages, and Langerhans cells (LHC) expressed both β-arrestin1 (Barr1) and β-arrestin2 (Barr2). (B) After stimulation with 10 μM nicotinic acid for 10 minutes, Langerhans cells were harvested, and membranes were separated from the cytosol, as demonstrated by presence of tubulin only in the cytosolic fractions. Increased β-arrestin1 was detected in the membranes after nicotinic acid stimulation, in contrast to control-treated samples. (C) Recruitment of β-arrestin1 to the membrane after nicotinic acid stimulation. *P = 0.0014 versus nicotinic acid. Data are mean ± SEM of 3 independent experiments.