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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2010-3-8
pubmed:abstractText
Obesity causes complex metabolic and endocrine changes that may lead to adverse outcomes, including hypogonadism. We herein studied the reproductive axis function in male rats under a high-fat diet and analyzed the impact of changes in glycosylation of pituitary LH on the bioactivity of this gonadotropin. Rats were fed with a diet enriched in saturated fat (20% of total calories) and euthanized on days 90 or 180 of diet. Long-term (180 days), high-fat feeding rats exhibited a metabolic profile compatible with insulin resistance and metabolic syndrome; they concomitantly showed decreased intrapituitary and serum LH concentrations, low serum testosterone levels, and elevated serum 17beta-estradiol concentrations. A fall in biological to immunological ratio of intrapituitary LH was detected in 180 days control diet-treated rats but not in high-fat-fed animals, as assessed by a homologous in vitro bioassay. Chromatofocusing of pituitary extracts yielded multiple LH charge isoforms; a trend towards decreased abundance of more basic isoforms (pH 9.99-9.0) was apparent in rats fed with the control diet for 180 days but not in those that were fed the diet enriched in saturated fat. It is concluded that long-term high-fat feeding alters the function of the pituitary-testicular axis, resulting in hypogonadotropic hypogonadism. The alterations in LH function found in these animals might be subserved by changes in hypothalamic GnRH output and/or sustained gonadotrope exposure to an altered sex steroid hormone milieu, representing a distinctly different regulatory mechanism whereby the pituitary attempts to counterbalance the effects of long-term obesity on reproductive function.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1095-6840
pubmed:author
pubmed:copyrightInfo
(c) 2009 Elsevier Inc. All rights reserved.
pubmed:issnType
Electronic
pubmed:day
1
pubmed:volume
166
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
356-64
pubmed:meshHeading
pubmed-meshheading:20005231-Animals, pubmed-meshheading:20005231-Blood Glucose, pubmed-meshheading:20005231-Dietary Fats, pubmed-meshheading:20005231-Disease Models, Animal, pubmed-meshheading:20005231-Estradiol, pubmed-meshheading:20005231-Glycosylation, pubmed-meshheading:20005231-Hydrogen-Ion Concentration, pubmed-meshheading:20005231-Insulin Resistance, pubmed-meshheading:20005231-Leptin, pubmed-meshheading:20005231-Luteinizing Hormone, pubmed-meshheading:20005231-Male, pubmed-meshheading:20005231-Metabolic Syndrome X, pubmed-meshheading:20005231-Obesity, pubmed-meshheading:20005231-Pituitary Gland, Anterior, pubmed-meshheading:20005231-Protein Isoforms, pubmed-meshheading:20005231-Rats, pubmed-meshheading:20005231-Rats, Wistar, pubmed-meshheading:20005231-Reproduction, pubmed-meshheading:20005231-Testosterone, pubmed-meshheading:20005231-Triglycerides
pubmed:year
2010
pubmed:articleTitle
Reproductive axis function and gonadotropin microheterogeneity in a male rat model of diet-induced obesity.
pubmed:affiliation
Research Unit in Reproductive Medicine, Hospital de Ginecobstetricia Luis Castelazo Ayala, IMSS, México D.F., Mexico. cristina.olivaress@imss.gob.mx
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't