Autophagy participants in the dedifferentiation of mouse 3T3-L1 adipocytes triggered by hypofunction of insulin signaling |
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| Institution: | 1. Department of Food Science and Nutrition, and Research Institute of Ecology for the Elderly, Pusan National University, Busan 609-735, Republic of Korea;2. Department of Food and Nutrition, College of Medical and Life Science, Silla University, Busan 616-735, Republic of Korea;1. Physics Program, Faculty of Science and Technology, Muban Chombueng Rajabhat University, Ratchaburi, 70150, Thailand;2. Physics Program, Faculty of Science and Technology, Nakhon Pathom Rajabhat University, Nakhon Pathom, 73000, Thailand;3. Center of Excellence in Glass Technology and Materials Science (CEGM), Nakhon Pathom Rajabhat University, Nakhon Pathom, 73000, Thailand;4. Department of Physics, Kyungpook National University, Daegu 702-701, Republic of Korea;1. Center of Radiation Research and Medical Imaging, Department of Radiologic Technology, Faculty of Associated Medical Sciences, Chiang Mai University, Chiang Mai, 50200, Thailand;2. Physics Program, Faculty of Science and Technology, Nakhon Pathom Rajabhat University, Nakhon Pathom, 73000, Thailand;3. Center of Excellence in Glass Technology and Materials Science (CEGM), Nakhon Pathom Rajabhat University, Nakhon Pathom, 73000, Thailand;4. Department of Physics, Kyungpook National University, Daegu 41566, South Korea;1. Department of Genetics, Albert Einstein College of Medicine, Bronx, NY, 10461, USA;2. The Scripps Research Institute, La Jolla, CA 92037, USA;3. J. Craig Venter Institute, La Jolla, CA, 92037, USA;4. Department of Medicine, Albert Einstein College of Medicine, Bronx, NY, 10461, USA;5. Department of Ophthalmology and Visual Sciences, Albert Einstein College of Medicine, Bronx, NY, 10461, USA |
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| Abstract: | Our previous data indicate that both insulin and IGF-1 signallings dysfunction promotes the dedifferentiation of primary human and mouse white adipocytes. Based on the fact that insulin activates mTOR and inhibits autophagy, and autophagy deficiency can inhibit the differentiation of white adipocytes, we speculate that autophagy may be related to the dedifferentiation of white adipocytes. We investigated the underlying mechanism of autophagy during dedifferentiation of mouse 3T3-L1 adipocytes. After incomplete inhibition of insulin and IGF-1 signallings, 3T3-L1 adipocytes manifest dedifferentiation accompanied with an increase of autophagy level. If induction only of autophagy in the adipocytes, then the cells also occur somewhat dedifferentiation, and with a slight decrease of insulin signal, while its degree was weaker than insulin signal inhibited cells. Notably, after inhibition of the insulin and IGF-1 signallings and simultaneously inducing autophagy, the dedifferentiation of 3T3-L1 adipocytes was the most obvious compared with other groups, and the insulin and IGF-1 signallings decreases was greater than the cells with inhibition only of insulin signalling. If inhibition of both insulin signal and autophagy simultaneously, the dedifferentiation of the adipocytes reveals similar tendencies to the cells that insulin signal was inhibited. No significant dedifferentiation occurs of 3T3-L1 cells if only inhibition of autophagy. Taken all together, in this study, we proved that autophagy is positively related to the dedifferentiation of 3T3-L1 adipocytes and is regulated through the insulin-PI3K-AKT-mTOCR1-autophagy pathway. Autophagy may also has a certain degree of negative feedback affect on the insulin signalling of 3T3-L1 cells. Our work may help to better understand the biological properties of mature adipocytes and may help formulate anti-obesity strategies by regulating insulin and insulin signaling level. |
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