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Adipogenic commitment induced by green tea polyphenols remodel adipocytes to a thermogenic phenotype
Institution:1. Department of Biotechnology, Universidad Autónoma Metropolitana-Iztapalapa, 09340, México City, Mexico;2. Department of Chemical Engineering, Tecnológico de Estudios Superiores de Chimalhuacán, 56330, Estado de México, Mexico;3. Department of Food Research, Universidad Autónoma de Coahuila, 25280, Saltillo, Coahuila, Mexico;4. Research Center in Food and Development A.C., 33089, Delicias, Chihuahua, Mexico;1. Tecnológico Nacional de México/Instituto Tecnológico de Tuxtla Gutiérrez, Carretera Panamericana Km. 1080, CP 29050 Tuxtla Gutiérrez, Chiapas, Mexico;2. Centro de Investigación y Asistencia en Tecnología y Diseño del Estado de Jalisco Unidad Mérida, Parque Científico Tecnológico de Yucatán, Tablaje Catastral 31264 Km 5.5 Carretera Sierra Papacal-Chuburná Puerto, CP 97302 Mérida, Yucatán, Mexico;3. Universidad del Papaloapan, Campus Tuxtepec, Circuito Central número 200, Colonia Parque Industrial, CP 6830 Tuxtepec, Oaxaca, Mexico
Abstract:The potential contribution of green tea (GT) to the development of thermogenic/beige cells have been scarcely investigated. Here we investigated if the beneficial effects of GT in the induction of thermogenic/beige adipocytes results from an initial cell commitment during adipogenesis. Male C57Bl/6 mice (3 months) were divided into 3 groups: Control (chow diet), Obese (cafeteria diet), and Obese + GT. Mice received GT gavage (500 mg/kg of BW) over 12 weeks (5 days/week), after 4 weeks of diet, totalizing 16 weeks of experimentation. GT treatment increased energy expenditure (EE) in mice fed with cafeteria-diet leading to reduced BW gain, decreased adiposity, reduced inflammation, and improving insulin sensitivity. Those phenotypes were associated with enhanced expression of oxidative, thermogenic and beige genes. GT induced a futile cycle through de novo lipogenesis activating the thermogenic pathway. Induction of beige phenotype occurs autonomously in adipocytes and involves the PPARγ/FGF21/AMPK/UCP1 pathway. Our study identified that metabolic changes caused by GT may involve the temporal expression of PPARγ promoting the induction of thermogenic cells by reprogramming initial steps of adipocyte commitment.
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