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1.
Biosci Rep ; 25(3-4): 251-69, 2005.
Artigo em Inglês | MEDLINE | ID: mdl-16283556

RESUMO

Programming is an epigenetic phenomena by which nutritional, hormonal, physical psychological and other stressful events acting in a critical period of life, such as gestation and lactation, modifies in a prolonged way certain physiological functions. This process was preserved by natural selection as an important adaptive tool for survival of organisms living in nutritional impaired areas. So, malnutrition during gestation and lactation turns on different genes that provide the organism with a thrifty phenotype. In the case of an abundant supply of nutrients after this period, those organisms that were adapted to a low metabolic waste and higher energy utilization will be in a higher risk of developing metabolic diseases, such as obesity, hyperlipidemia, diabetes mellitus and hypertension. The kind of malnutrition, duration and intensity are important for the type of programming obtained. We discuss some of the hormonal and metabolic changes that occur in gestation or lactation, when malnutrition is applied to the mothers and their offspring. Some of these changes, such as an increase of maternal triiodothyronine (T(3)), leptin and glucocorticoids (GC) and decrease in prolactin are by itself potential programming factors. Most of these hormones can be transfer through the milk that has other important macronutrients composition changes in malnourished dams. We discuss 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.


Assuntos
Animais Recém-Nascidos , Peso Corporal , Metabolismo Energético , Glândulas Suprarrenais/fisiologia , Animais , Diabetes Mellitus Tipo 2/fisiopatologia , Epigênese Genética , Feminino , Sistema Hipotálamo-Hipofisário/fisiologia , Leptina/metabolismo , Estado Nutricional , Hipófise/citologia , Hipófise/fisiologia , Gravidez , Sistema Nervoso Simpático/fisiologia , Glândula Tireoide/fisiologia , Hormônios Tireóideos/metabolismo
2.
Nutrition ; 20(10): 924-8, 2004 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-15474883

RESUMO

OBJECTIVE: Recent studies have shown that leptin receptor is expressed in human and rat pituitary glands. The expression of leptin receptor in rats whose dams were malnourished during lactation has not been previously reported. METHODS: We examined leptin receptor expression in the pituitary gland of adult rats whose dams were assigned to one of the following groups during lactation: control diet, protein-restricted diet (8% protein), or energy-restricted diet (the control diet fed in restricted quantities that were calculated according to the mean ingestion of the protein-restricted group). After weaning, all pups had free access to the control diet until they reached adult age, at which time leptin receptor expression in the pituitary was analyzed by immunohistochemistry. RESULTS: Adult animals from protein- and energy-restricted dams had a higher expression of leptin receptor in pituitary tissue, normal serum leptin concentrations, higher serum tri-iodothyronine concentrations, and lower thyroid-stimulating hormone concentrations than did the control rats. CONCLUSIONS: In the fed state, leptin has a stimulatory effect on release of thyroid-stimulating hormone. The higher expression of leptin receptor in the pituitary of animals from protein- and energy-restricted dams may suggest a postreceptor failure in leptin action. This higher receptor expression may have allowed a greater inhibition of release of thyroid-stimulating hormone.


Assuntos
Lactação/metabolismo , Leptina/sangue , Hipófise/metabolismo , Desnutrição Proteico-Calórica/metabolismo , Receptores de Superfície Celular/metabolismo , Tireotropina/metabolismo , Animais , Animais Lactentes , Dieta com Restrição de Proteínas , Dieta Redutora , Feminino , Imuno-Histoquímica , Desnutrição Proteico-Calórica/fisiopatologia , Distribuição Aleatória , Ratos , Ratos Wistar , Receptores de Superfície Celular/imunologia , Receptores para Leptina
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