Feng Li1, Chunjun Sheng2, Kexiu Song2, Manna Zhang2, Le Bu2, Peng Yang2, Hui Sheng2, Hong Li2, Shen Qu3. 1. Department of Endocrinology and Metabolism, Shanghai Tenth People's Hospital, Tong-Ji University, 301 Middle Yan-Chang Road, ShangHai, 200072, China. med193@126.com. 2. Department of Endocrinology and Metabolism, Shanghai Tenth People's Hospital, Tong-Ji University, 301 Middle Yan-Chang Road, ShangHai, 200072, China. 3. Department of Endocrinology and Metabolism, Shanghai Tenth People's Hospital, Tong-Ji University, 301 Middle Yan-Chang Road, ShangHai, 200072, China. qushencn@hotmail.com.
Abstract
BACKGROUND: We used the leptin-receptor (LPR)-deficient mice model (db/db), a spontaneous model of type 2 diabetes with early β cell dysfunction to determine whether a preventative sleeve gastrectomy (SG) is an effective technique for the treatment of β cell failure. METHODS: The animals operated at an early stage of life, prior to metabolic alterations, were used to study the molecular mechanisms of β cell function improvement after a SG. RESULTS: β cell function was significantly increased, and islet morphology remained normal, after the SG. The expression of Glut2, Pdx1, MafA, and Nkx6.1 were significantly increased after the SG. The expression of GLP-1 in the colonic tissue, as well as GLP-1R and PKC in islets, was significantly increased after the SG. CONCLUSIONS: β cell dysfunction can be ameliorated by a preventative SG for db/db mice. Maintaining the GLP-1 pathway and key transcript factor (TF) activation contributes to the improvement of β cell function after a preventative SG.
BACKGROUND: We used the leptin-receptor (LPR)-deficient mice model (db/db), a spontaneous model of type 2 diabetes with early β cell dysfunction to determine whether a preventative sleeve gastrectomy (SG) is an effective technique for the treatment of β cell failure. METHODS: The animals operated at an early stage of life, prior to metabolic alterations, were used to study the molecular mechanisms of β cell function improvement after a SG. RESULTS: β cell function was significantly increased, and islet morphology remained normal, after the SG. The expression of Glut2, Pdx1, MafA, and Nkx6.1 were significantly increased after the SG. The expression of GLP-1 in the colonic tissue, as well as GLP-1R and PKC in islets, was significantly increased after the SG. CONCLUSIONS: β cell dysfunction can be ameliorated by a preventative SG for db/db mice. Maintaining the GLP-1 pathway and key transcript factor (TF) activation contributes to the improvement of β cell function after a preventative SG.
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