Modulation of VEGF-A and VEGF-B signaling by DDE exposure: implications in metabolic dysfunction

A. C. Guerra; R. Costa; I. Rodrigues; C. Neves; H. Vieira; S. Ferreira; S. I. Sousa; V. F. Domingues; C. Calhau; D. Pestana; R. Negrão

Modulation of VEGF-A and VEGF-B signaling by DDE exposure: implications in metabolic dysfunction

A. C. Guerra, R. Costa, I. Rodrigues, C. Neves, H. Vieira, S. Ferreira, S. I. Sousa, V. F. Domingues, C. Calhau, D. Pestana, R. Negrão

Research output: Chapter in Book/Report/Conference proceeding › Conference contribution › peer-review

Abstract

Obesity is characterized by an increase in adipose tissue (AT) mass, that should be accompanied by an increase in angiogenesis, modulated by vascular endothelial growth factor (VEGF)-A. VEGF- B signaling, increases the expression of fatty acid transport protein (FATP) 3 and FATP4, contributing to fatty acid uptake into adipose tissue (AT), liver and heart. The dichlorodiphenyldichloroethylene (DDE) is a persistent organic pollutant, accumulated in AT, that presents endocrine disruptor’s properties. It was aimed to verify if DDE exposure, can modulate Vegfb/Vegfr1 signaling, chancing tissues fatty acid uptake and Vegfa/Vegfr2 pathway, modifying the angiogenic process. Thirty Wistar rats were divided into four treatment groups during 12 weeks: Standard diet (St), St with DDE (100 μg/kg/day), High-fat diet (HFD) and HFD with DDE. At the end of the treatment the expression of Vegfb, Vegfr1, Fatp3 and Fatp4 genes was quantified by qRT-PCR in mesenteric AT (mAT), liver and heart. Tissue lipid content was also measured. In mAT the expression of Vegfa and Vegfr2 genes was analysed by qRT-PCR and blood vessels were quantified. Statistical analysis included two-way ANOVA followed by Turkey´s multiple comparison test. In mAT, HFD and DDE increased the expression of Vegfa and Vegfr2 genes, with HFD also increasing the number of blood vessels. DDE exposure and HFD also stimulated the expression of Vegfb, Vegfr1 and Fatp3 genes, in mAT. Moreover, HFD increased the adipocytes area. In liver and heart, DDE exposure increased the expression of Vegfb, Vegfr1, Fatp3 and Fatp4 genes. In liver, HFD and DDE promoted lipid accumulation, however in the heart, only rats fed with HFD increased heart triglyceride concentration. In conclusion, DDE exposure and HFD promoted angiogenesis. DDE exposure modulated Vegfb/Vegfr1 signaling and thus Fatp3 and Fatp4 genes, promoting fatty acid accumulation in several tissues. Thus, DDE exposure may contribute to metabolic disorders and obesity.

Original language	English
Title of host publication	Livro de Resumos do 10.º Encontro de Jovens Investigadores da U.PORTO
Editors	Maria João Ramos
Publisher	Universidade do Porto
Pages	140-140
Number of pages	1
ISBN (Electronic)	9789897461170
Publication status	Published - Feb 2017
Externally published	Yes
Event	10ª edição do IJUP: Encontro de Investigação Jovem da Universidade do Porto - Universidade do Porto, Porto, Portugal Duration: 8 Feb 2017 → 10 Feb 2017

Conference

Conference	10ª edição do IJUP
Abbreviated title	IJUP 2017
Country/Territory	Portugal
City	Porto
Period	8/02/17 → 10/02/17

Cite this

Guerra, A. C., Costa, R., Rodrigues, I., Neves, C., Vieira, H., Ferreira, S., Sousa, S. I., Domingues, V. F., Calhau, C., Pestana, D., & Negrão, R. (2017). Modulation of VEGF-A and VEGF-B signaling by DDE exposure: implications in metabolic dysfunction. In M. J. Ramos (Ed.), Livro de Resumos do 10.º Encontro de Jovens Investigadores da U.PORTO (pp. 140-140). Universidade do Porto.

@inproceedings{78b1d2924be14851b2bf05b28aaac0eb,

title = "Modulation of VEGF-A and VEGF-B signaling by DDE exposure: implications in metabolic dysfunction",

abstract = "Obesity is characterized by an increase in adipose tissue (AT) mass, that should be accompanied by an increase in angiogenesis, modulated by vascular endothelial growth factor (VEGF)-A. VEGF- B signaling, increases the expression of fatty acid transport protein (FATP) 3 and FATP4, contributing to fatty acid uptake into adipose tissue (AT), liver and heart. The dichlorodiphenyldichloroethylene (DDE) is a persistent organic pollutant, accumulated in AT, that presents endocrine disruptor{\textquoteright}s properties. It was aimed to verify if DDE exposure, can modulate Vegfb/Vegfr1 signaling, chancing tissues fatty acid uptake and Vegfa/Vegfr2 pathway, modifying the angiogenic process. Thirty Wistar rats were divided into four treatment groups during 12 weeks: Standard diet (St), St with DDE (100 μg/kg/day), High-fat diet (HFD) and HFD with DDE. At the end of the treatment the expression of Vegfb, Vegfr1, Fatp3 and Fatp4 genes was quantified by qRT-PCR in mesenteric AT (mAT), liver and heart. Tissue lipid content was also measured. In mAT the expression of Vegfa and Vegfr2 genes was analysed by qRT-PCR and blood vessels were quantified. Statistical analysis included two-way ANOVA followed by Turkey´s multiple comparison test. In mAT, HFD and DDE increased the expression of Vegfa and Vegfr2 genes, with HFD also increasing the number of blood vessels. DDE exposure and HFD also stimulated the expression of Vegfb, Vegfr1 and Fatp3 genes, in mAT. Moreover, HFD increased the adipocytes area. In liver and heart, DDE exposure increased the expression of Vegfb, Vegfr1, Fatp3 and Fatp4 genes. In liver, HFD and DDE promoted lipid accumulation, however in the heart, only rats fed with HFD increased heart triglyceride concentration. In conclusion, DDE exposure and HFD promoted angiogenesis. DDE exposure modulated Vegfb/Vegfr1 signaling and thus Fatp3 and Fatp4 genes, promoting fatty acid accumulation in several tissues. Thus, DDE exposure may contribute to metabolic disorders and obesity.",

author = "Guerra, \{A. C.\} and R. Costa and I. Rodrigues and C. Neves and H. Vieira and S. Ferreira and Sousa, \{S. I.\} and Domingues, \{V. F.\} and C. Calhau and D. Pestana and R. Negr{\~a}o",

year = "2017",

month = feb,

language = "English",

pages = "140--140",

editor = "Ramos, \{Maria Jo{\~a}o\}",

booktitle = "Livro de Resumos do 10.º Encontro de Jovens Investigadores da U.PORTO",

publisher = "Universidade do Porto",

address = "Portugal",

note = "10ª edi{\c c}{\~a}o do IJUP ; Conference date: 08-02-2017 Through 10-02-2017",

}

Guerra, AC, Costa, R, Rodrigues, I, Neves, C, Vieira, H, Ferreira, S, Sousa, SI, Domingues, VF, Calhau, C, Pestana, D & Negrão, R 2017, Modulation of VEGF-A and VEGF-B signaling by DDE exposure: implications in metabolic dysfunction. in MJ Ramos (ed.), Livro de Resumos do 10.º Encontro de Jovens Investigadores da U.PORTO. Universidade do Porto, pp. 140-140, 10ª edição do IJUP, Porto, Portugal, 8/02/17.

Modulation of VEGF-A and VEGF-B signaling by DDE exposure: implications in metabolic dysfunction. / Guerra, A. C.; Costa, R.; Rodrigues, I. et al.
Livro de Resumos do 10.º Encontro de Jovens Investigadores da U.PORTO. ed. / Maria João Ramos. Universidade do Porto, 2017. p. 140-140.

Research output: Chapter in Book/Report/Conference proceeding › Conference contribution › peer-review

TY - GEN

T1 - Modulation of VEGF-A and VEGF-B signaling by DDE exposure

T2 - 10ª edição do IJUP

AU - Guerra, A. C.

AU - Costa, R.

AU - Rodrigues, I.

AU - Neves, C.

AU - Vieira, H.

AU - Ferreira, S.

AU - Sousa, S. I.

AU - Domingues, V. F.

AU - Calhau, C.

AU - Pestana, D.

AU - Negrão, R.

PY - 2017/2

Y1 - 2017/2

N2 - Obesity is characterized by an increase in adipose tissue (AT) mass, that should be accompanied by an increase in angiogenesis, modulated by vascular endothelial growth factor (VEGF)-A. VEGF- B signaling, increases the expression of fatty acid transport protein (FATP) 3 and FATP4, contributing to fatty acid uptake into adipose tissue (AT), liver and heart. The dichlorodiphenyldichloroethylene (DDE) is a persistent organic pollutant, accumulated in AT, that presents endocrine disruptor’s properties. It was aimed to verify if DDE exposure, can modulate Vegfb/Vegfr1 signaling, chancing tissues fatty acid uptake and Vegfa/Vegfr2 pathway, modifying the angiogenic process. Thirty Wistar rats were divided into four treatment groups during 12 weeks: Standard diet (St), St with DDE (100 μg/kg/day), High-fat diet (HFD) and HFD with DDE. At the end of the treatment the expression of Vegfb, Vegfr1, Fatp3 and Fatp4 genes was quantified by qRT-PCR in mesenteric AT (mAT), liver and heart. Tissue lipid content was also measured. In mAT the expression of Vegfa and Vegfr2 genes was analysed by qRT-PCR and blood vessels were quantified. Statistical analysis included two-way ANOVA followed by Turkey´s multiple comparison test. In mAT, HFD and DDE increased the expression of Vegfa and Vegfr2 genes, with HFD also increasing the number of blood vessels. DDE exposure and HFD also stimulated the expression of Vegfb, Vegfr1 and Fatp3 genes, in mAT. Moreover, HFD increased the adipocytes area. In liver and heart, DDE exposure increased the expression of Vegfb, Vegfr1, Fatp3 and Fatp4 genes. In liver, HFD and DDE promoted lipid accumulation, however in the heart, only rats fed with HFD increased heart triglyceride concentration. In conclusion, DDE exposure and HFD promoted angiogenesis. DDE exposure modulated Vegfb/Vegfr1 signaling and thus Fatp3 and Fatp4 genes, promoting fatty acid accumulation in several tissues. Thus, DDE exposure may contribute to metabolic disorders and obesity.

AB - Obesity is characterized by an increase in adipose tissue (AT) mass, that should be accompanied by an increase in angiogenesis, modulated by vascular endothelial growth factor (VEGF)-A. VEGF- B signaling, increases the expression of fatty acid transport protein (FATP) 3 and FATP4, contributing to fatty acid uptake into adipose tissue (AT), liver and heart. The dichlorodiphenyldichloroethylene (DDE) is a persistent organic pollutant, accumulated in AT, that presents endocrine disruptor’s properties. It was aimed to verify if DDE exposure, can modulate Vegfb/Vegfr1 signaling, chancing tissues fatty acid uptake and Vegfa/Vegfr2 pathway, modifying the angiogenic process. Thirty Wistar rats were divided into four treatment groups during 12 weeks: Standard diet (St), St with DDE (100 μg/kg/day), High-fat diet (HFD) and HFD with DDE. At the end of the treatment the expression of Vegfb, Vegfr1, Fatp3 and Fatp4 genes was quantified by qRT-PCR in mesenteric AT (mAT), liver and heart. Tissue lipid content was also measured. In mAT the expression of Vegfa and Vegfr2 genes was analysed by qRT-PCR and blood vessels were quantified. Statistical analysis included two-way ANOVA followed by Turkey´s multiple comparison test. In mAT, HFD and DDE increased the expression of Vegfa and Vegfr2 genes, with HFD also increasing the number of blood vessels. DDE exposure and HFD also stimulated the expression of Vegfb, Vegfr1 and Fatp3 genes, in mAT. Moreover, HFD increased the adipocytes area. In liver and heart, DDE exposure increased the expression of Vegfb, Vegfr1, Fatp3 and Fatp4 genes. In liver, HFD and DDE promoted lipid accumulation, however in the heart, only rats fed with HFD increased heart triglyceride concentration. In conclusion, DDE exposure and HFD promoted angiogenesis. DDE exposure modulated Vegfb/Vegfr1 signaling and thus Fatp3 and Fatp4 genes, promoting fatty acid accumulation in several tissues. Thus, DDE exposure may contribute to metabolic disorders and obesity.

M3 - Conference contribution

SP - 140

EP - 140

BT - Livro de Resumos do 10.º Encontro de Jovens Investigadores da U.PORTO

A2 - Ramos, Maria João

PB - Universidade do Porto

Y2 - 8 February 2017 through 10 February 2017

ER -

Modulation of VEGF-A and VEGF-B signaling by DDE exposure: implications in metabolic dysfunction

Abstract

Conference

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