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Modulation of gastric nesfatin by rapamycin
Author(s) -
Li Ziru,
xu geyang,
Li yin,
Zhao Jin,
zhang weizhen
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.lb762
Subject(s) - pi3k/akt/mtor pathway , endocrinology , medicine , leptin , rptor , p70 s6 kinase 1 , chemistry , signal transduction , biology , microbiology and biotechnology , obesity
Nesfatin‐1, an 82 amino acid peptide mainly found in the hypothalamus and stomach, is a novel satiety hormone acting through a leptin‐independent mechanism in the hypothalamus. Mechanism by which production of nesfatin‐1 is regulated remains unknown. Here we showed the co‐localization of pS6K, the downstream target of the mammalian target of rapamycin (mTOR) in the gastric X/A like cells. Reciprocal relationship of gastric mTOR signaling and nesfatin‐1 was observed during changes in energy status. Both mTOR activity and gastric nesfatin‐1 were down‐regulated by fasting, and returned to near basal level by re‐feeding. In high fat diet induced obese mice, gastric mTOR signaling and nesfatin‐1 were enhanced. Inhibition of the gastric mTOR signaling by rapamycin attenuated the expression of gastric nesfatin‐1 mRNA and protein in both lean and obese mice. Attenuation of mTOR activity by rapamycin or over‐expression of TSC1 or TSC2 reduced the expression of nesfatin in Min‐6 cells, suggesting a direct effect of mTOR signaling. In conclusion, gastric mTOR is a gastric sensor whose activity is linked to the regulation of gastric nesfatin‐1.