Schwanstecher Christina, Schwanstecher Mathias
Molekulare Pharmakologie und Toxikologie, Technische Universität Braunschweig, Beethovenstraße 55, 38106, Braunschweig, Germany.
Handb Exp Pharmacol. 2011(203):1-33. doi: 10.1007/978-3-642-17214-4_1.
The evolving concept of how nutrient excess and inflammation modulate metabolism provides new opportunities for strategies to correct the detrimental health consequences of obesity. In this review, we focus on the complex interplay among lipid overload, immune response, proinflammatory pathways and organelle dysfunction through which excess adiposity might lead to type 2 diabetes. We then consider evidence linking dysregulated CNS circuits to insulin resistance and results on nutrient-sensing pathways emerging from studies with calorie restriction. Subsequently, recent recommendations for the management of type 2 diabetes are discussed with emphasis on prevailing current therapeutic classes of biguanides, thiazolidinediones and incretin-based approaches.
营养素过剩和炎症如何调节新陈代谢这一不断演变的概念，为纠正肥胖对健康造成的有害后果的策略提供了新机遇。在本综述中，我们聚焦于脂质超载、免疫反应、促炎途径和细胞器功能障碍之间的复杂相互作用，肥胖可能通过这些相互作用导致2型糖尿病。然后，我们考虑将失调的中枢神经系统回路与胰岛素抵抗联系起来的证据，以及热量限制研究中出现的营养感应途径的结果。随后，将讨论2型糖尿病管理的最新建议，重点是目前流行的双胍类、噻唑烷二酮类和基于肠促胰岛素的治疗类别。
