title: Targeting type 2 diabetes.
abstract: 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.
authors.affiliation: Molekulare Pharmakologie und Toxikologie, Technische Universität Braunschweig, Beethovenstraße 55, 38106, Braunschweig, Germany. M.Schwanstecher@tu-braunschweig.de
authors.forename: Christina
authors.initials: C
authors.lastname: Schwanstecher
authors.forename: Mathias
authors.initials: M
authors.lastname: Schwanstecher
mesh_terms: D000273:Adipose Tissue / Q000473:pathology; D031204:Caloric Restriction; D003924:Diabetes Mellitus, Type 2 / Q000188:drug therapy* / Q000473:pathology; D054873:Dipeptidyl-Peptidase IV Inhibitors / Q000627:therapeutic use; D052216:Glucagon-Like Peptide 1 / Q000037:antagonists & inhibitors; D005947:Glucose / Q000378:metabolism; D006706:Homeostasis; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use*; D007249:Inflammation / Q000473:pathology; D007333:Insulin Resistance; D050417:Insulin-Secreting Cells / Q000502:physiology; D008687:Metformin / Q000627:therapeutic use; D015398:Signal Transduction / Q000502:physiology; D053778:Thiazolidines / Q000627:therapeutic use
chemical_list: D054873:Dipeptidyl-Peptidase IV Inhibitors; D007004:Hypoglycemic Agents; D053778:Thiazolidines; D052216:Glucagon-Like Peptide 1; D008687:Metformin; D005947:Glucose