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Green tea extract improves high fat diet-induced hypothalamic inflammation,without affecting the serotoninergic system
Affiliation:1. Departamento de Química Inorgánica, Universidad de Granada, Avda Fuentenueva s/n, 18071 Granada, Spain;2. Instituto de Parasitología y Biomedicina López-Neyra, CSIC, Avenida del Conocimiento S.N., Armilla, Granada, Spain;3. Instituto de Nutrición y Tecnología de los Alimentos y Departamento de Fisiología, Campus Cartuja, Universidad de Granada, 18071 Granada, Spain;1. Food Science Research Institute, Fuji Oil Co, Ltd, 1 Sumiyoshi-cho, Izumisano 598-8540, Japan;2. Laboratory of Biochemistry Frontiers, Graduate School of Agricultural Sciences, Kobe University, Kobe 657-8501, Japan;3. Department of Molecular Biosciences, Graduate School of Bioagricultural Sciences, Nagoya University, Nagoya 464-8601, Japan
Abstract:To investigate possible mechanisms of green tea’s anti-obesity and anti-diabetic effects in the hypothalamus, the central regulator of metabolism, of mice fed with high-fat diet (HFD), we analyzed proteins of the toll-like receptor 4 (TLR4) pathway and serotoninergic proteins involved in energy homeostasis. Thirty-day-old male Swiss mice were fed with HFD rich in saturated fat and green tea extract (GTE) for 8 weeks. After that, body weight and mass of fat depots were evaluated. Oral glucose tolerance test was performed 3 days prior to euthanasia; serum glucose, insulin and adiponectin were measured in fasted mice. Hypothalamic TLR4 pathway proteins, serotonin receptors 1B and 2C and serotonin transporter were analyzed by Western blotting or enzyme-linked immunosorbent assay. A second set of animals was used to measure food intake in response to fluoxetine, a selective serotonin reuptake inhibitor. Mice fed with HFD had increased body weight and mass of fat depots, impaired oral glucose tolerance, elevated glucose and insulin and decreased adiponectin serum levels. TLR4, IκB-α, nuclear factor κB p50 and interleukin 6 were increased by HFD. Concomitant GTE treatment ameliorated these parameters. The serotoninergic system remained functional after HFD treatment despite a few alterations in protein content of serotonin receptors 1B and 2C and serotonin transporter. In summary, the GTE attenuated the deleterious effects of the HFD investigated in this study, partially due to reduced hypothalamic inflammation.
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