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

NUTRIM - Liver and digestive health

Research output: Contribution to journal › Article › Academic › peer-review

168 Downloads (Pure)

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

Access to Document

10.1016/j.bbalip.2017.02.006

Full TextFinal published version, 948 KBLicence: Taverne

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

@article{f779b74208344faf80c1cdc672d67a61,

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",

year = "2017",

month = may,

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

language = "English",

volume = "1862",

pages = "541--551",

journal = "Biochimica et Biophysica Acta-Molecular and Cell Biology of Lipids",

issn = "1388-1981",

publisher = "Elsevier B.V.",

number = "5",

}

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

TY - JOUR

T1 - Small heterodimer partner (SHP) contributes to insulin resistance in cardiomyocytes

AU - Rodriguez-Calvo, Ricardo

AU - Chanda, Dipanjan

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

PY - 2017/5

Y1 - 2017/5

N2 - 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

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

KW - Insulin resistance

KW - Diabetic cardiomyopathy

KW - Nuclear receptors

KW - Small heterodimer partner

KW - ORPHAN NUCLEAR RECEPTOR

KW - FATTY-ACID TRANSPORT

KW - FACTOR-KAPPA-B

KW - ACTIVATED RECEPTOR

KW - CARDIAC-HYPERTROPHY

KW - HEPATIC GLUCONEOGENESIS

KW - DOWN-REGULATION

KW - HEART-DISEASE

KW - MOUSE MODELS

KW - MUSCLE-CELLS

U2 - 10.1016/j.bbalip.2017.02.006

DO - 10.1016/j.bbalip.2017.02.006

M3 - Article

C2 - 28214558

SN - 1388-1981

VL - 1862

SP - 541

EP - 551

JO - Biochimica et Biophysica Acta-Molecular and Cell Biology of Lipids

JF - Biochimica et Biophysica Acta-Molecular and Cell Biology of Lipids

IS - 5

ER -

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

Abstract

Keywords

Access to Document

Fingerprint

Cite this