Q3201995 (Q3201995): Difference between revisions
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(Created claim: summary (P836): Obesity dyslipemia alters lipid homeostasis and produces infertility. Objectives: 1) Identify the pathophysiological mechanisms that cause gonadal dysfunction and infertility associated with obesity in man, both those associated with adiposity, as well as gonadal and adipokin hormones; 2) To assess whether weight loss after obesity surgery improves hypogonadotrophic hypogonadism and fertility; 3) Study the pathophysiological mechanisms that caus...) |
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Obesity dyslipemia alters lipid homeostasis and produces infertility. Objectives: 1) Identify the pathophysiological mechanisms that cause gonadal dysfunction and infertility associated with obesity in man, both those associated with adiposity, as well as gonadal and adipokin hormones; 2) To assess whether weight loss after obesity surgery improves hypogonadotrophic hypogonadism and fertility; 3) Study the pathophysiological mechanisms that cause gonadal dysfunction and infertility associated with obesity dyslipemia in a preclinical mouse model fed with a diet rich in fat; 4) Analyse whether weight loss and fat mobilisation in obese mice, after diet control or treatment with polyphenols, improve lipid parameters and reverse infertility. We will analyse: (I) hormones by radioimmunoanalysis and ELISA, fertility by sperm number and mobility; and morphology by staining with hematoxylin/eosin;(ii) lipid composition by gas chromatography/mass spectrometry (GC/MS); (III) uptake of cholesterol esters (EC) from lipoproteins by class B scavenger receptors (SR-BI and SR-BII) and rLDL; hydrolysis of EC by HSL, and cholesterol efflux by ABCA1, by immunohistochemistry and western blot; (IV) gene expression of hormone and lipid synthesis pathways using RT-PCR; (V) lipid composition of lipid rafts and non-rafts of plasma membrane, isolated by density gradients, by GC/MS; and expression of SR-BI, caveolina, transferrin, MAPK, AKT and ERK, using IHQ and WB. (English) | |||||||||||||||
| Property / summary: Obesity dyslipemia alters lipid homeostasis and produces infertility. Objectives: 1) Identify the pathophysiological mechanisms that cause gonadal dysfunction and infertility associated with obesity in man, both those associated with adiposity, as well as gonadal and adipokin hormones; 2) To assess whether weight loss after obesity surgery improves hypogonadotrophic hypogonadism and fertility; 3) Study the pathophysiological mechanisms that cause gonadal dysfunction and infertility associated with obesity dyslipemia in a preclinical mouse model fed with a diet rich in fat; 4) Analyse whether weight loss and fat mobilisation in obese mice, after diet control or treatment with polyphenols, improve lipid parameters and reverse infertility. We will analyse: (I) hormones by radioimmunoanalysis and ELISA, fertility by sperm number and mobility; and morphology by staining with hematoxylin/eosin;(ii) lipid composition by gas chromatography/mass spectrometry (GC/MS); (III) uptake of cholesterol esters (EC) from lipoproteins by class B scavenger receptors (SR-BI and SR-BII) and rLDL; hydrolysis of EC by HSL, and cholesterol efflux by ABCA1, by immunohistochemistry and western blot; (IV) gene expression of hormone and lipid synthesis pathways using RT-PCR; (V) lipid composition of lipid rafts and non-rafts of plasma membrane, isolated by density gradients, by GC/MS; and expression of SR-BI, caveolina, transferrin, MAPK, AKT and ERK, using IHQ and WB. (English) / rank | |||||||||||||||
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| Property / summary: Obesity dyslipemia alters lipid homeostasis and produces infertility. Objectives: 1) Identify the pathophysiological mechanisms that cause gonadal dysfunction and infertility associated with obesity in man, both those associated with adiposity, as well as gonadal and adipokin hormones; 2) To assess whether weight loss after obesity surgery improves hypogonadotrophic hypogonadism and fertility; 3) Study the pathophysiological mechanisms that cause gonadal dysfunction and infertility associated with obesity dyslipemia in a preclinical mouse model fed with a diet rich in fat; 4) Analyse whether weight loss and fat mobilisation in obese mice, after diet control or treatment with polyphenols, improve lipid parameters and reverse infertility. We will analyse: (I) hormones by radioimmunoanalysis and ELISA, fertility by sperm number and mobility; and morphology by staining with hematoxylin/eosin;(ii) lipid composition by gas chromatography/mass spectrometry (GC/MS); (III) uptake of cholesterol esters (EC) from lipoproteins by class B scavenger receptors (SR-BI and SR-BII) and rLDL; hydrolysis of EC by HSL, and cholesterol efflux by ABCA1, by immunohistochemistry and western blot; (IV) gene expression of hormone and lipid synthesis pathways using RT-PCR; (V) lipid composition of lipid rafts and non-rafts of plasma membrane, isolated by density gradients, by GC/MS; and expression of SR-BI, caveolina, transferrin, MAPK, AKT and ERK, using IHQ and WB. (English) / qualifier | |||||||||||||||
point in time: 13 October 2021
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Revision as of 23:30, 12 October 2021
Project Q3201995 in Spain
| Language | Label | Description | Also known as |
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| English | No label defined |
Project Q3201995 in Spain |
Statements
35,750.0 Euro
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71,500.0 Euro
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50.0 percent
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1 January 2017
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31 March 2020
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FUNDACION INVESTIGACION BIOMEDICA HOSPITAL RAMON Y CAJAL
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40°25'0.12"N, 3°42'12.89"W
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28079
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La dislipemia por obesidad altera la homeostasis de lípidos y produce infertilidad. Objetivos: 1) Identificar los mecanismos fisiopatológicos que causan disfunción gonadal e infertilidad asociados a la obesidad en el hombre, tanto los asociados a la adiposidad, como a hormonas gonadales y adipoquinas; 2) Valorar si la pérdida de peso tras la cirugía de la obesidad mejora el hipogonadismo hipogonadotrófico y la fertilidad; 3) Estudiar los mecanismos fisiopatológicos que causan disfunción gonadal e infertilidad asociados a la dislipemia de la obesidad en un modelo preclínico de ratón alimentado con dieta rica en grasa; 4) Analizar si la pérdida de peso y la movilización de la grasa en los ratones obesos, tras dieta control o tratamiento con polifenoles, mejora los parámetros lipídicos y revierte la infertilidad. Analizaremos: (i) hormonas mediante radioinmunoanálisis y ELISA, fertilidad mediante el número y movilidad de espermatozoides; y morfología mediante tinción con hematoxilina/eosina;(ii) composición de lípidos mediante cromatografía de gases/espectrometría de masas (CG/EM); (iii) captación de ésteres de colesterol (EC) de las lipoproteínas por receptores scavenger clase B (SR-BI y SR-BII) y rLDL; hidrólisis de EC por HSL, y eflujo de colesterol por ABCA1, mediante inmunohistoquímica y western blot; (iv) expresión de genes de rutas de síntesis de hormonas y lípidos mediante RT-PCR; (v) composición de lípidos de lipid rafts y no rafts de membrana plasmática, aislados mediante gradientes de densidad, por CG/EM; y expresión de SR-BI, caveolina, transferrina, MAPK, AKT y ERK, mediante IHQ y WB. (Spanish)
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Obesity dyslipemia alters lipid homeostasis and produces infertility. Objectives: 1) Identify the pathophysiological mechanisms that cause gonadal dysfunction and infertility associated with obesity in man, both those associated with adiposity, as well as gonadal and adipokin hormones; 2) To assess whether weight loss after obesity surgery improves hypogonadotrophic hypogonadism and fertility; 3) Study the pathophysiological mechanisms that cause gonadal dysfunction and infertility associated with obesity dyslipemia in a preclinical mouse model fed with a diet rich in fat; 4) Analyse whether weight loss and fat mobilisation in obese mice, after diet control or treatment with polyphenols, improve lipid parameters and reverse infertility. We will analyse: (I) hormones by radioimmunoanalysis and ELISA, fertility by sperm number and mobility; and morphology by staining with hematoxylin/eosin;(ii) lipid composition by gas chromatography/mass spectrometry (GC/MS); (III) uptake of cholesterol esters (EC) from lipoproteins by class B scavenger receptors (SR-BI and SR-BII) and rLDL; hydrolysis of EC by HSL, and cholesterol efflux by ABCA1, by immunohistochemistry and western blot; (IV) gene expression of hormone and lipid synthesis pathways using RT-PCR; (V) lipid composition of lipid rafts and non-rafts of plasma membrane, isolated by density gradients, by GC/MS; and expression of SR-BI, caveolina, transferrin, MAPK, AKT and ERK, using IHQ and WB. (English)
13 October 2021
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Madrid
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Identifiers
PI16_00154
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