ER stress induces GATA3 expression in visceral adipocytes and leads to TRIP-Br2 upregulation. qPCR analysis of GATA1, GATA2 or GATA3 gene expression in ( a ) 3T3-L1 differentiated adipocytes ( n =3 per group replicated twice); ( b ) WT1 differentiated adipocytes ( n =3 per group replicated twice) after 6 h of vehicle or tunicamycin (Tuni; 1 μg ml −1 ) treatment; ( c ) WT gWAT or iWAT ( n =5 per group replicated twice) 18 h after vehicle or Tuni (2.5 mg kg −1 , i.p.) injection; ( d ) WT gWAT or iWAT adipocytes ( n =3 per group) after vehicle or Tuni (1 μg ml −1 ) treatment for 6 h; ( e ) gWAT and iWAT SVF or mature adipocytes after 12 weeks of CD or HFD ( n =5 per group replicated twice); ( f ) gWAT and iWAT from lean or obese ob/ob mice ( n =6 per group); ( g ) human adipocytes from immortalized human preadipocytes or SGBS cells after vehicle or Tuni (1 μg ml −1 ) treatment for 24 h ( n =3–4 per group replicated twice). ( h ) Gene expression of human TRIP-Br2 and GATA3 in visceral adipose tissue from human subjects ( n =24 per group). qPCR analysis of TRIP-Br2 in ( i ) gWAT adipocytes treated with Tuni (1 μg ml −1 ) and/or GATA inhibitor K7174 (1, 5 μM) for 24 h ( n =3 per group replicated twice); ( j ) gWAT adipocytes infected with control (Ctrl) or DN-GATA3 retrovirus ( n =3 per group); ( k ) gWAT adipocytes infected with Ctrl or GATA3 retrovirus ( n =3 per group replicated twice); ( l ) gWAT adipocytes differentiated from GATA3fl/fl-CreERT2 primary SVF with or without tamoxifen (0.5 μM) treatment to induce GATA3 KO ( n =5 per group). ( m ) qPCR analysis of proximal or distal genomic region of TRIP-Br2 transcript 3 promoter after GATA3 chromatin immunoprecipitation ( n =3 per group replicated twice). All qPCR data are normalized to TATA box-binding protein (TBP) and presented as mean±s.e.m. Two-tailed Student's t -test or ANOVA, * P