Obesity alters the ovarian glucidic homeostasis disrupting the reproductive outcome of female rats

Obesity constitutes a health problem of increasing worldwide prevalence related to many reproductive problems such as infertility, ovulation dysfunction, preterm delivery, fetal growth disorders, etc. The mechanisms linking obesity to these pathologies are not fully understood. Cafeteria diet (CAF)...

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Autor principal: Bazzano, M.V
Otros Autores: Paz, D.A, Elia, E.M
Formato: Capítulo de libro
Lenguaje:Inglés
Publicado: Elsevier Inc. 2017
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024 7 |2 cas  |a glucose, 50-99-7, 84778-64-3; glucose transporter 4, 188071-24-1; insulin, 9004-10-8; nitric oxide synthase, 125978-95-2; Glucose Transporter Type 4; Nitric Oxide Synthase; Receptor, Insulin; Slc2a4 protein, rat 
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100 1 |a Bazzano, M.V. 
245 1 0 |a Obesity alters the ovarian glucidic homeostasis disrupting the reproductive outcome of female rats 
260 |b Elsevier Inc.  |c 2017 
270 1 0 |m Elia, E.M.; Laboratorio de Biología del Desarrollo, IFIBYNE-CONICET –UBA, Facultad de Ciencias Exactas y Naturales, Ciudad Universitaria, Pabellón II, 4 (C1428EHA), Argentina; email: evelinmariel@gmail.com.ar 
506 |2 openaire  |e Política editorial 
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520 3 |a Obesity constitutes a health problem of increasing worldwide prevalence related to many reproductive problems such as infertility, ovulation dysfunction, preterm delivery, fetal growth disorders, etc. The mechanisms linking obesity to these pathologies are not fully understood. Cafeteria diet (CAF) is the animal model used for the study of obesity that more closely reflects western diet habits. Previously we described that CAF induces obesity associated to hyperglycemia, reduced ovarian reserve, presence of follicular cysts and ovulatory impairments. The aim of the present study was to contribute in the understanding of the physiological mechanisms altered as consequence of obesity. For that purpose, female Wistar rats were fed ad libitum with a standard diet (control group) or CAF (Obese group). We found that CAF fed-rats developed obesity, glucose intolerance and insulin resistance. Ovaries from obese rats showed decreased glucose uptake and became insulin resistant, showing decreased ovarian expression of glucotransporter type 4 and insulin receptor gene expression respect to controls. These animals showed an increased follicular nitric oxyde synthase expression that may be responsible for the ovulatory disruptions and for inflammation, a common feature in obesity. Obese rats resulted subfertile and their pups were macrosomic. We conclude that obesity alters the systemic and the ovarian glucidic homeostasis impairing the reproductive outcome. Since macrosomia is a risk factor for metabolic and obstetric disorders in adult life, we suggest that obesity is impacting not only on health and reproduction but it is also impacting on health and reproduction of the offspring. © 2017  |l eng 
593 |a Laboratorio de Biología del Desarrollo, Instituto de Fisiología, Biología Molecular y Neurociencias (IFIBYNE-CONICET-UBA), Pabellón 2, Cdad. Universitaria, Buenos Aires, Argentina 
593 |a Departamento de Biodiversidad y Biología Experimental, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Pabellón 2. Cdad. Universitaria, Buenos Aires, Argentina 
690 1 0 |a FERTILITY 
690 1 0 |a GLUCOSE 
690 1 0 |a GLUT-4 
690 1 0 |a INSULIN 
690 1 0 |a OBESITY 
690 1 0 |a OVARY 
690 1 0 |a REPRODUCTIVE OUTCOME 
690 1 0 |a GLUCOSE 
690 1 0 |a GLUCOSE TRANSPORTER 4 
690 1 0 |a INSULIN 
690 1 0 |a INSULIN RECEPTOR 
690 1 0 |a GLUCOSE TRANSPORTER 4 
690 1 0 |a INSULIN RECEPTOR 
690 1 0 |a NITRIC OXIDE SYNTHASE 
690 1 0 |a SLC2A4 PROTEIN, RAT 
690 1 0 |a ANIMAL EXPERIMENT 
690 1 0 |a ANIMAL TISSUE 
690 1 0 |a ARTICLE 
690 1 0 |a BODY FAT DISTRIBUTION 
690 1 0 |a CAFETERIA DIET 
690 1 0 |a CONTROLLED STUDY 
690 1 0 |a DIET 
690 1 0 |a DIET INDUCED OBESITY 
690 1 0 |a FEMALE 
690 1 0 |a GENE EXPRESSION 
690 1 0 |a GLUCOSE INTOLERANCE 
690 1 0 |a GLUCOSE TOLERANCE TEST 
690 1 0 |a GLUCOSE TRANSPORT 
690 1 0 |a HYPERGLYCEMIA 
690 1 0 |a IMMUNOHISTOCHEMISTRY 
690 1 0 |a INSULIN RESISTANCE 
690 1 0 |a INSULIN TOLERANCE TEST 
690 1 0 |a MACROSOMIA 
690 1 0 |a NONHUMAN 
690 1 0 |a OBESITY 
690 1 0 |a OVARIAN GLUCIDIC HOMEOSTASIS 
690 1 0 |a OVARY 
690 1 0 |a RAT 
690 1 0 |a REPRODUCTION 
690 1 0 |a REPRODUCTIVE SUCCESS 
690 1 0 |a ANIMAL 
690 1 0 |a COMPLICATION 
690 1 0 |a GENETICS 
690 1 0 |a METABOLISM 
690 1 0 |a OBESITY 
690 1 0 |a OVARY FOLLICLE 
690 1 0 |a PATHOLOGY 
690 1 0 |a PATHOPHYSIOLOGY 
690 1 0 |a PREGNANCY 
690 1 0 |a WISTAR RAT 
690 1 0 |a ANIMALS 
690 1 0 |a BODY FAT DISTRIBUTION 
690 1 0 |a DIET 
690 1 0 |a FEMALE 
690 1 0 |a GLUCOSE TOLERANCE TEST 
690 1 0 |a GLUCOSE TRANSPORTER TYPE 4 
690 1 0 |a INSULIN RESISTANCE 
690 1 0 |a NITRIC OXIDE SYNTHASE 
690 1 0 |a OBESITY 
690 1 0 |a OVARIAN FOLLICLE 
690 1 0 |a OVARY 
690 1 0 |a PREGNANCY 
690 1 0 |a RATS, WISTAR 
690 1 0 |a RECEPTOR, INSULIN 
650 1 7 |2 spines  |a HOMEOSTASIS 
650 1 7 |2 spines  |a HOMEOSTASIS 
650 1 7 |2 spines  |a HOMEOSTASIS 
700 1 |a Paz, D.A. 
700 1 |a Elia, E.M. 
773 0 |d Elsevier Inc., 2017  |g v. 42  |h pp. 194-202  |p J. Nutr. Biochem.  |x 09552863  |w (AR-BaUEN)CENRE-5723  |t Journal of Nutritional Biochemistry 
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856 4 0 |u https://doi.org/10.1016/j.jnutbio.2017.01.003  |y DOI 
856 4 0 |u https://hdl.handle.net/20.500.12110/paper_09552863_v42_n_p194_Bazzano  |y Handle 
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