Structured Review

U73122 PLC insulin induced akt phosphorylation
<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
Insulin Induced Akt Phosphorylation, supplied by U73122 PLC, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/insulin induced akt phosphorylation/product/U73122 PLC
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Article Title: The gut microbiota suppresses insulin-mediated fat accumulation via the short-chain fatty acid receptor GPR43

Journal: Nature Communications

doi: 10.1038/ncomms2852

GPR43 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 Akt 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
Figure Legend Snippet: GPR43 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 Akt 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

Techniques Used: Planar Chromatography, Inhibition, Activity Assay, Derivative Assay

GPR43 suppresses insulin signalling in the adipose tissues but not in muscles or liver. Insulin-stimulated Akt phosphorylation of Ser473 in the WAT ( a , n =3), muscles ( b , n =4) and liver ( c , n =3) of aP2-Gpr43TG mice fed an HFD after 6 h of fasting. ( d – f ) Inhibitory effects of acetate on insulin signalling (1 g kg −1 , i.p.). After pretreatment with acetate for 40 min, a bolus of insulin (0.15 U kg −1 ) with or without acetate (1 g kg −1 ) was administered intraperitoneally. Akt phosphorylation of Ser473 in the WAT ( d , n =3), muscles ( e , n =3) and liver ( f , n =3) of Gpr43 −/− mice after 6 h of fasting. ( g , h ) Effect of acetate on glucose uptake in MEF-derived adipocytes from Gpr43−/− or aP2-Gpr43TG mice ( n =4, respectively). ( i , j ) Effect of acetate on the fatty acid uptake in MEF-derived adipocytes from Gpr43−/− or aP2-Gpr43TG mice ( n =8–15). LPL activity in the WAT ( k , n =4–5) and the muscles ( l , n =3–5) of Gpr43−/− or aP2-Gpr43TG mice ( n =3–4). ( m ) LPL activity of Gpr43−/− mice fed an HFD under GF conditions ( n =4, 6) or aP2-Gpr43TG mice treated with antibiotics ( n =7, 6). All mice were analysed at 15–16 weeks of age. All data are presented as mean±s.e.m. analysis of variance followed by Tukey–Kramer’s post hoc test ( a – j ) and Student’s t -test ( k – m ); * P
Figure Legend Snippet: GPR43 suppresses insulin signalling in the adipose tissues but not in muscles or liver. Insulin-stimulated Akt phosphorylation of Ser473 in the WAT ( a , n =3), muscles ( b , n =4) and liver ( c , n =3) of aP2-Gpr43TG mice fed an HFD after 6 h of fasting. ( d – f ) Inhibitory effects of acetate on insulin signalling (1 g kg −1 , i.p.). After pretreatment with acetate for 40 min, a bolus of insulin (0.15 U kg −1 ) with or without acetate (1 g kg −1 ) was administered intraperitoneally. Akt phosphorylation of Ser473 in the WAT ( d , n =3), muscles ( e , n =3) and liver ( f , n =3) of Gpr43 −/− mice after 6 h of fasting. ( g , h ) Effect of acetate on glucose uptake in MEF-derived adipocytes from Gpr43−/− or aP2-Gpr43TG mice ( n =4, respectively). ( i , j ) Effect of acetate on the fatty acid uptake in MEF-derived adipocytes from Gpr43−/− or aP2-Gpr43TG mice ( n =8–15). LPL activity in the WAT ( k , n =4–5) and the muscles ( l , n =3–5) of Gpr43−/− or aP2-Gpr43TG mice ( n =3–4). ( m ) LPL activity of Gpr43−/− mice fed an HFD under GF conditions ( n =4, 6) or aP2-Gpr43TG mice treated with antibiotics ( n =7, 6). All mice were analysed at 15–16 weeks of age. All data are presented as mean±s.e.m. analysis of variance followed by Tukey–Kramer’s post hoc test ( a – j ) and Student’s t -test ( k – m ); * P

Techniques Used: Mouse Assay, Derivative Assay, Activity Assay

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    U73122 PLC insulin induced akt phosphorylation
    <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
    Insulin Induced Akt Phosphorylation, supplied by U73122 PLC, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/insulin induced akt phosphorylation/product/U73122 PLC
    Average 85 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    insulin induced akt phosphorylation - by Bioz Stars, 2020-11
    85/100 stars
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    GPR43 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 Akt 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

    Journal: Nature Communications

    Article Title: The gut microbiota suppresses insulin-mediated fat accumulation via the short-chain fatty acid receptor GPR43

    doi: 10.1038/ncomms2852

    Figure Lengend Snippet: GPR43 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 Akt 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

    Article Snippet: GPR43-mediated suppression of insulin-induced Akt phosphorylation was effectively blocked by the treatment with U73122 (PLC inhibitor) and Go6983 (PKC inhibitor), but not U0126 (MEK inhibitor) ( ).

    Techniques: Planar Chromatography, Inhibition, Activity Assay, Derivative Assay

    GPR43 suppresses insulin signalling in the adipose tissues but not in muscles or liver. Insulin-stimulated Akt phosphorylation of Ser473 in the WAT ( a , n =3), muscles ( b , n =4) and liver ( c , n =3) of aP2-Gpr43TG mice fed an HFD after 6 h of fasting. ( d – f ) Inhibitory effects of acetate on insulin signalling (1 g kg −1 , i.p.). After pretreatment with acetate for 40 min, a bolus of insulin (0.15 U kg −1 ) with or without acetate (1 g kg −1 ) was administered intraperitoneally. Akt phosphorylation of Ser473 in the WAT ( d , n =3), muscles ( e , n =3) and liver ( f , n =3) of Gpr43 −/− mice after 6 h of fasting. ( g , h ) Effect of acetate on glucose uptake in MEF-derived adipocytes from Gpr43−/− or aP2-Gpr43TG mice ( n =4, respectively). ( i , j ) Effect of acetate on the fatty acid uptake in MEF-derived adipocytes from Gpr43−/− or aP2-Gpr43TG mice ( n =8–15). LPL activity in the WAT ( k , n =4–5) and the muscles ( l , n =3–5) of Gpr43−/− or aP2-Gpr43TG mice ( n =3–4). ( m ) LPL activity of Gpr43−/− mice fed an HFD under GF conditions ( n =4, 6) or aP2-Gpr43TG mice treated with antibiotics ( n =7, 6). All mice were analysed at 15–16 weeks of age. All data are presented as mean±s.e.m. analysis of variance followed by Tukey–Kramer’s post hoc test ( a – j ) and Student’s t -test ( k – m ); * P

    Journal: Nature Communications

    Article Title: The gut microbiota suppresses insulin-mediated fat accumulation via the short-chain fatty acid receptor GPR43

    doi: 10.1038/ncomms2852

    Figure Lengend Snippet: GPR43 suppresses insulin signalling in the adipose tissues but not in muscles or liver. Insulin-stimulated Akt phosphorylation of Ser473 in the WAT ( a , n =3), muscles ( b , n =4) and liver ( c , n =3) of aP2-Gpr43TG mice fed an HFD after 6 h of fasting. ( d – f ) Inhibitory effects of acetate on insulin signalling (1 g kg −1 , i.p.). After pretreatment with acetate for 40 min, a bolus of insulin (0.15 U kg −1 ) with or without acetate (1 g kg −1 ) was administered intraperitoneally. Akt phosphorylation of Ser473 in the WAT ( d , n =3), muscles ( e , n =3) and liver ( f , n =3) of Gpr43 −/− mice after 6 h of fasting. ( g , h ) Effect of acetate on glucose uptake in MEF-derived adipocytes from Gpr43−/− or aP2-Gpr43TG mice ( n =4, respectively). ( i , j ) Effect of acetate on the fatty acid uptake in MEF-derived adipocytes from Gpr43−/− or aP2-Gpr43TG mice ( n =8–15). LPL activity in the WAT ( k , n =4–5) and the muscles ( l , n =3–5) of Gpr43−/− or aP2-Gpr43TG mice ( n =3–4). ( m ) LPL activity of Gpr43−/− mice fed an HFD under GF conditions ( n =4, 6) or aP2-Gpr43TG mice treated with antibiotics ( n =7, 6). All mice were analysed at 15–16 weeks of age. All data are presented as mean±s.e.m. analysis of variance followed by Tukey–Kramer’s post hoc test ( a – j ) and Student’s t -test ( k – m ); * P

    Article Snippet: GPR43-mediated suppression of insulin-induced Akt phosphorylation was effectively blocked by the treatment with U73122 (PLC inhibitor) and Go6983 (PKC inhibitor), but not U0126 (MEK inhibitor) ( ).

    Techniques: Mouse Assay, Derivative Assay, Activity Assay