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1.
Cell Mol Neurobiol ; 30(7): 1025-33, 2010 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-20526668

RESUMO

Hypothalamic serotonin inhibits food intake and stimulates energy expenditure. High-fat feeding is obesogenic, but the role of polyunsaturated fats is not well understood. This study examined the influence of different high-PUFA diets on serotonin-induced hypophagia, hypothalamic serotonin turnover, and hypothalamic protein levels of serotonin transporter (ST), and SR-1B and SR-2C receptors. Male Wistar rats received for 9 weeks from weaning a diet high in either soy oil or fish oil or low fat (control diet). Throughout 9 weeks, daily intake of fat diets decreased such that energy intake was similar to that of the control diet. However, the fish group developed heavier retroperitoneal and epididymal fat depots. After 12 h of either 200 or 300 µg intracerebroventricular serotonin, food intake was significantly inhibited in control group (21-25%) and soy group (37-39%) but not in the fish group. Serotonin turnover was significantly lower in the fish group than in both the control group (-13%) and the soy group (-18%). SR-2C levels of fish group were lower than those of control group (50%, P = 0.02) and soy group (37%, P = 0.09). ST levels tended to decrease in the fish group in comparison to the control group (16%, P = 0.339) and the soy group (21%, P = 0.161). Thus, unlike the soy-oil diet, the fish-oil diet decreased hypothalamic serotonin turnover and SR-2C levels and abolished serotonin-induced hypophagia. Fish-diet rats were potentially hypophagic, suggesting that, at least up to this point in its course, the serotonergic impairment was either compensated by other factors or not of a sufficient extent to affect feeding. That fat pad weight increased in the absence of hyperphagia indicates that energy expenditure was affected by the serotonergic hypofunction.


Assuntos
Gorduras Insaturadas na Dieta/farmacologia , Ingestão de Alimentos/efeitos dos fármacos , Óleos de Peixe/farmacologia , Serotonina/metabolismo , Tecido Adiposo/anatomia & histologia , Animais , Dieta , Óleos de Peixe/administração & dosagem , Humanos , Ácido Hidroxi-Indolacético/química , Ácido Hidroxi-Indolacético/metabolismo , Hipotálamo/química , Hipotálamo/metabolismo , Infusões Intraventriculares , Masculino , Tamanho do Órgão , Distribuição Aleatória , Ratos , Ratos Wistar , Receptor 5-HT1B de Serotonina/metabolismo , Receptor 5-HT2C de Serotonina/metabolismo , Serotonina/administração & dosagem , Serotonina/química , Proteínas da Membrana Plasmática de Transporte de Serotonina/metabolismo , Óleo de Soja/administração & dosagem , Óleo de Soja/farmacologia
2.
Nutr Neurosci ; 12(6): 242-8, 2009 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-19925717

RESUMO

We used c-Fos immunoreactivity to estimate neuronal activation in hypothalamic feeding-regulatory areas of 3-month-old rats fed control or oil-enriched diets (soy or fish) since weaning. While no diet effect was observed in c-Fos immunoreactivity of 24-h fasted animals, the acute response to refeeding was modified by both hyperlipidic diets but with different patterns. Upon refeeding, control-diet rats had significantly increased c-Fos immunoreactivity only in the paraventricular hypothalamic nucleus (PVH, 142%). In soy-diet rats, refeeding with the soy diet increased c-Fos immunoreactivity in dorsomedial hypothalamic nucleus (DMH, 271%) and lateral hypothalamic area (LH, 303%). Refeeding fish-diet rats with the fish diet increased c-Fos immunoreactivity in PVH (161%), DMH (177%), VMH (81%), and ARC (127%). Compared to the fish-diet, c-Fos immunoreactivity was increased in LH by the soy-diet while it was decreased in ventromedial hypothalamic nucleus (VMH) and arcuate hypothalamic nucleus (ARC). Based on the known roles of the activated nuclei, it is suggested that, unlike the fish-diet, the soy-diet induced a potentially obesogenic profile, with high LH and low VMH/PVH activation after refeeding.


Assuntos
Dieta , Ingestão de Alimentos/fisiologia , Jejum/fisiologia , Óleos de Peixe , Hipotálamo/fisiologia , Neurônios/fisiologia , Óleo de Soja , Animais , Peso Corporal , Ingestão de Energia , Ácidos Graxos/análise , Óleos de Peixe/química , Hipotálamo/química , Hipotálamo/citologia , Imuno-Histoquímica , Masculino , Neurônios/metabolismo , Especificidade de Órgãos , Proteínas Proto-Oncogênicas c-fos/metabolismo , Distribuição Aleatória , Ratos , Ratos Wistar , Óleo de Soja/química
3.
Nutrition ; 24(3): 255-61, 2008 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-18178060

RESUMO

OBJECTIVE: We examined whether feeding pregnant and lactating rats hydrogenated fats rich in trans-fatty acids modifies the plasma lipid profiles and the expression of adipokines involved with insulin resistance and cardiovascular disease in their 21-d-old offspring. METHODS: Pregnant and lactating Wistar rats were fed with a control diet (C group) or one enriched with hydrogenated vegetable fat (T group). After delivery, male offspring were weighed weekly and killed at day 21 of life by decapitation. Blood and retroperitoneal, epididymal, and subcutaneous white adipose tissues were collected. RESULTS: Offspring of T-group rats had increased serum triacylglycerols and cholesterol, white adipose tissue plasminogen activator inhibitor-1, and tumor necrosis factor-alpha gene expression, and carcass lipid content and decreased blood leptin and adiponectin and adiponectin gene expression. CONCLUSION: Ingestion of hydrogenated vegetable fat by the mother during gestation and lactation alters the blood lipid profiles and the expression of proinflammatory adipokynes by the adipose tissue of offspring aged 21 d.


Assuntos
Adipocinas/metabolismo , Tecido Adiposo/metabolismo , Gorduras na Dieta/administração & dosagem , Resistência à Insulina , Lactação , Lipídeos/sangue , Animais , Colesterol/sangue , Feminino , Hidrogenação , Masculino , Inibidor 1 de Ativador de Plasminogênio/metabolismo , Gravidez , Efeitos Tardios da Exposição Pré-Natal , RNA Mensageiro/análise , RNA Mensageiro/metabolismo , Ratos , Ratos Wistar , Ácidos Graxos trans/administração & dosagem , Ácidos Graxos trans/metabolismo , Triglicerídeos/sangue , Fator de Necrose Tumoral alfa/metabolismo
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