Small heterodimer partner (SHP) contributes to insulin resistance in cardiomyocytes

Ricardo Rodriguez-Calvo; Dipanjan Chanda; Yvonne Oligschlaeger; Marie Miglianico; Will A. Coumans; Emma Barroso; Marta Tajes; Joost J. F. P. Luiken; Jan F. C. Glatz; Manuel Vazquez-Carrera; Dietbert Neumann

doi:10.1016/j.bbalip.2017.02.006

Small heterodimer partner (SHP) contributes to insulin resistance in cardiomyocytes

Ricardo Rodriguez-Calvo^*, Dipanjan Chanda, Yvonne Oligschlaeger, Marie Miglianico, Will A. Coumans, Emma Barroso, Marta Tajes, Joost J. F. P. Luiken, Jan F. C. Glatz, Manuel Vazquez-Carrera, Dietbert Neumann

^*Corresponding author for this work

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Abstract

Small heterodimer partner (SHP) is an atypical nuclear receptor expressed in heart that has been shown to inhibit the hypertrophic response. Here, we assessed the role of SHP in cardiac metabolism and inflammation. Mice fed a high-fat diet (HFD) displayed glucose intolerance accompanied by increased cardiac mRNA levels of Shp. In HL-1 cardiomyocytes, SHP overexpression inhibited both basal and insulin-stimulated glucose uptake and impaired the insulin signalling pathway (evidenced by reduced ART and AS160 phosphorylation), similar to insulin resistant cells generated by high palmitate/high insulin treatment (HP/HI; 500 mu M/100 nM). In addition, SHP overexpression increased Socs3 mRNA and reduced IRS-1 protein levels. SHP overexpression also induced Cd36 expression (similar to 6.2 fold; p

Original language	English
Pages (from-to)	541-551
Number of pages	11
Journal	Biochimica et Biophysica Acta-Molecular and Cell Biology of Lipids
Volume	1862
Issue number	5
DOIs	https://doi.org/10.1016/j.bbalip.2017.02.006
Publication status	Published - May 2017

Keywords

Insulin resistance
Diabetic cardiomyopathy
Nuclear receptors
Small heterodimer partner
ORPHAN NUCLEAR RECEPTOR
FATTY-ACID TRANSPORT
FACTOR-KAPPA-B
ACTIVATED RECEPTOR
CARDIAC-HYPERTROPHY
HEPATIC GLUCONEOGENESIS
DOWN-REGULATION
HEART-DISEASE
MOUSE MODELS
MUSCLE-CELLS

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10.1016/j.bbalip.2017.02.006

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Cite this

Rodriguez-Calvo, R., Chanda, D., Oligschlaeger, Y., Miglianico, M., Coumans, W. A., Barroso, E., Tajes, M., Luiken, J. J. F. P., Glatz, J. F. C., Vazquez-Carrera, M., & Neumann, D. (2017). Small heterodimer partner (SHP) contributes to insulin resistance in cardiomyocytes. Biochimica et Biophysica Acta-Molecular and Cell Biology of Lipids, 1862(5), 541-551. https://doi.org/10.1016/j.bbalip.2017.02.006

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title = "Small heterodimer partner (SHP) contributes to insulin resistance in cardiomyocytes",

abstract = "Small heterodimer partner (SHP) is an atypical nuclear receptor expressed in heart that has been shown to inhibit the hypertrophic response. Here, we assessed the role of SHP in cardiac metabolism and inflammation. Mice fed a high-fat diet (HFD) displayed glucose intolerance accompanied by increased cardiac mRNA levels of Shp. In HL-1 cardiomyocytes, SHP overexpression inhibited both basal and insulin-stimulated glucose uptake and impaired the insulin signalling pathway (evidenced by reduced ART and AS160 phosphorylation), similar to insulin resistant cells generated by high palmitate/high insulin treatment (HP/HI; 500 mu M/100 nM). In addition, SHP overexpression increased Socs3 mRNA and reduced IRS-1 protein levels. SHP overexpression also induced Cd36 expression (similar to 6.2 fold; p",

keywords = "Insulin resistance, Diabetic cardiomyopathy, Nuclear receptors, Small heterodimer partner, ORPHAN NUCLEAR RECEPTOR, FATTY-ACID TRANSPORT, FACTOR-KAPPA-B, ACTIVATED RECEPTOR, CARDIAC-HYPERTROPHY, HEPATIC GLUCONEOGENESIS, DOWN-REGULATION, HEART-DISEASE, MOUSE MODELS, MUSCLE-CELLS",

author = "Ricardo Rodriguez-Calvo and Dipanjan Chanda and Yvonne Oligschlaeger and Marie Miglianico and Coumans, {Will A.} and Emma Barroso and Marta Tajes and Luiken, {Joost J. F. P.} and Glatz, {Jan F. C.} and Manuel Vazquez-Carrera and Dietbert Neumann",

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doi = "10.1016/j.bbalip.2017.02.006",

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Rodriguez-Calvo, R, Chanda, D, Oligschlaeger, Y, Miglianico, M, Coumans, WA, Barroso, E, Tajes, M, Luiken, JJFP, Glatz, JFC, Vazquez-Carrera, M & Neumann, D 2017, 'Small heterodimer partner (SHP) contributes to insulin resistance in cardiomyocytes', Biochimica et Biophysica Acta-Molecular and Cell Biology of Lipids, vol. 1862, no. 5, pp. 541-551. https://doi.org/10.1016/j.bbalip.2017.02.006

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AU - Oligschlaeger, Yvonne

AU - Miglianico, Marie

AU - Coumans, Will A.

AU - Barroso, Emma

AU - Tajes, Marta

AU - Luiken, Joost J. F. P.

AU - Glatz, Jan F. C.

AU - Vazquez-Carrera, Manuel

AU - Neumann, Dietbert

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AB - Small heterodimer partner (SHP) is an atypical nuclear receptor expressed in heart that has been shown to inhibit the hypertrophic response. Here, we assessed the role of SHP in cardiac metabolism and inflammation. Mice fed a high-fat diet (HFD) displayed glucose intolerance accompanied by increased cardiac mRNA levels of Shp. In HL-1 cardiomyocytes, SHP overexpression inhibited both basal and insulin-stimulated glucose uptake and impaired the insulin signalling pathway (evidenced by reduced ART and AS160 phosphorylation), similar to insulin resistant cells generated by high palmitate/high insulin treatment (HP/HI; 500 mu M/100 nM). In addition, SHP overexpression increased Socs3 mRNA and reduced IRS-1 protein levels. SHP overexpression also induced Cd36 expression (similar to 6.2 fold; p

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KW - DOWN-REGULATION

KW - HEART-DISEASE

KW - MOUSE MODELS

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DO - 10.1016/j.bbalip.2017.02.006

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