<t>GPR43</t> suppresses insulin signalling via G(i/o)βγ-PLC–PKC–PTEN signalling. ( a ) Inhibitory effects of GPR43 agonists (10 mM acetate and 10 μM PA) and a GPR41 agonist (10 μM cyclopropanecarboxylic acid (CPC)) on insulin-induced <t>Akt</t> phosphorylation ( n =3). PA, phenylacetamide. ( b ) Effects of Gi/o signalling inhibition on suppression of insulin-induced Akt phosphorylation by acetate ( n =3). ( c ) Effects of Gq signalling inhibition using siRNA (no. 1) on suppression of insulin-induced Akt phosphorylation by acetate ( n =3). ( d ) Effects of Gβγ signalling inhibition on suppression of insulin-induced Akt phosphorylation by acetate ( n =3). ( e ) Effects of GPR43 stimulation on PTEN phosphorylation ( n =3). ( f ) Effects of PTEN signalling inhibition on suppression of insulin-induced Akt phosphorylation by acetate ( n =3). Cells were stimulated with insulin (3 μg ml −1 ) in the presence of acetate (10 mM) and bpV(pic) (1 μM) for 5 min after pretreatment with acetate for 2 h. ( g ) Effect of GPR43 agonists (10 mM acetate and 10 μM PA) on insulin-induced glucose uptake ( n =4). ( h ) Effect of acetate on insulin-induced LPL activity ( n =4). Cells were stimulated with insulin (3 μg ml −1 ) in the presence of acetate (10 mM) and inhibitor for 30 min after pretreatment with acetate for 2 h and PTX (1 μg ml −1 ) for 4 h. In all experiments, cells were stimulated with insulin (3 μg ml −1 ) in the presence of GPR43 agonist (10 mM acetate, 10 μM PA, or 10 μM CPC) for 5 min after pretreatment with GPR43 agonists for 2 h, Gallein (10 μM), NF023 (10 μM), PTX (1 μg ml −1 ), U73122 (1 μM), Go6983 (10 μM),or U0126 (10 μM) for 4 h. All experiments were performed by using 3T3-L1-derived adipocytes ( a – f , h ) and MEF-derived adipocytes ( g ). All data are presented as mean±s.e.m. analysis of variance followed by Tukey–Kramer's post hoc test; * P
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