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高脂饮食喂养和糖尿病中肠道神经病变的分子机制

Molecular mechanisms of enteric neuropathies in high-fat diet feeding and diabetes.

作者信息

Cingolani Francesca, Balasubramaniam Arun, Srinivasan Shanthi

机构信息

Division of Digestive Diseases, Emory University School of Medicine, Atlanta, Georgia, USA.

Atlanta Veterans Affairs Health Care System, Decatur, Georgia, USA.

出版信息

Neurogastroenterol Motil. 2024 Aug 9:e14897. doi: 10.1111/nmo.14897.

Abstract

BACKGROUND

Obesity and diabetes are associated with altered gastrointestinal function and with the development of abdominal pain, nausea, diarrhea, and constipation among other symptoms. The enteric nervous system (ENS) regulates gastrointestinal motility. Enteric neuropathies defined as damage or loss of enteric neurons can lead to motility disorders.

PURPOSE

Here, we review the molecular mechanisms that drive enteric neurodegeneration in diabetes and obesity, including signaling pathways leading to neuronal cell death, oxidative stress, and microbiota alteration. We also highlight potential approaches to treat enteric neuropathies including antioxidant therapy to prevent oxidative stress-induced damage and the use of stem cells.

摘要

背景

肥胖和糖尿病与胃肠功能改变以及腹痛、恶心、腹泻和便秘等症状的发生有关。肠神经系统(ENS)调节胃肠蠕动。定义为肠神经元损伤或丧失的肠神经病变可导致蠕动障碍。

目的

在此,我们综述了驱动糖尿病和肥胖中肠神经变性的分子机制,包括导致神经元细胞死亡、氧化应激和微生物群改变的信号通路。我们还强调了治疗肠神经病变的潜在方法,包括预防氧化应激诱导损伤的抗氧化治疗和干细胞的应用。

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