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Egberto Gaspar de Moura

Researcher at Rio de Janeiro State University

Publications -  230
Citations -  5382

Egberto Gaspar de Moura is an academic researcher from Rio de Janeiro State University. The author has contributed to research in topics: Offspring & Lactation. The author has an hindex of 39, co-authored 219 publications receiving 4833 citations. Previous affiliations of Egberto Gaspar de Moura include University of Texas Southwestern Medical Center & Federal University of Rio de Janeiro.

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Divergent roles for thyroid hormone receptor β isoforms in the endocrine axis and auditory system

TL;DR: Mice with targeted disruption of the entire TR beta locus develop a similar degree of central resistance to thyroid hormone as TR beta-null mice, indicating the important role of TR beta 2 in the regulation of the hypothalamic-pituitary-thyroid axis.
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Short and long term effects of malnutrition in rats during lactation on the body weight of offspring

TL;DR: The short and long term effects of maternal protein or energy malnutrition during lactation on offspring body weight were determined using lactating rats fed a 8% protein-restricted diet, a control 23% protein diet (C), and an energy-restricted pair-fed to PR group (PF).
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Maternal high-fat diet induces obesity and adrenal and thyroid dysfunction in male rat offspring at weaning.

TL;DR: Maternal high‐fat diet increased adrenal catecholamines in offspring but reduced liver and adipose tissue adrenoreceptors, thereby contributing to increased adiposity in these animals and contributing to the development of hypertension.
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Neonatal programming of body weight regulation and energetic metabolism.

TL;DR: The programming effects of some of these hormones upon body weight and composition, leptin, thyroid and adrenal functions, and their effects on liver, muscle and adipose tissue metabolism and the consequences on thermogenesis are discussed.
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Neonatal leptin treatment programmes leptin hypothalamic resistance and intermediary metabolic parameters in adult rats.

TL;DR: It is concluded that neonatal leptin treatment programmes both hyperleptinaemia and hyperinsulinaemia in adulthood, which leads to leptin resistance by reducing the expression of the hypothalamic leptin receptor.