title: Toll-like receptors and diabetes: a therapeutic perspective.
abstract: Diabetes is a mutifactorial metabolic disorder that leads to a number of complications. Diabetes is estimated to affect 36 million people in the U.S.A., and the prevalence of diagnosed and undiagnosed diabetes is at 9.3% and continues to rise. Evidence from experimental animal models as well as humans has indicated that systemic inflammation plays a role in the pathophysiological processes of diabetes and is facilitated by innate immune responses. TLRs (Toll-like receptors) are key innate immune receptors that recognize conserved PAMPs (pathogen-associated molecular patterns), induce inflammatory responses essential for host defences and initiate an adaptive immune response. Although TLR expression is increased in a plethora of inflammatory disorders, the effects of metabolic aberrations on TLRs and their role in diabetes and its complications is still emerging. In the present paper, we provide a systematic review on how TLRs play a detrimental role in the pathogenic processes [increased blood sugar, NEFAs (non-esterified 'free' fatty acids), cytokines and ROS (reactive oxygen species)] that manifest diabetes. Furthermore, we will highlight some of the therapeutic strategies targeted at decreasing TLRs to abrogate inflammation in diabetes that may eventually result in decreased complications.
authors: Department of Dermatology, University of California Davis, Sacramento, CA 95816, USA. ravi.dasu@ucdmc.ucdavis.edu
authors: Mohan R
authors: MR
authors: Dasu
authors: Sandra
authors: S
authors: Ramirez
authors: Roslyn R
authors: RR
authors: Isseroff
mesh_terms: D001786:Blood Glucose / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D048909:Diabetes Complications / Q000188:drug therapy; D003920:Diabetes Mellitus / Q000188:drug therapy / Q000276:immunology / Q000378:metabolism*; D005230:Fatty Acids, Nonesterified / Q000378:metabolism; D006801:Humans; D006943:Hyperglycemia / Q000150:complications / Q000188:drug therapy / Q000378:metabolism; D007113:Immunity, Innate; D007249:Inflammation / Q000276:immunology / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism; D015398:Signal Transduction / Q000276:immunology; D051193:Toll-Like Receptors / Q000378:metabolism / Q000502:physiology*
chemical_list: D001786:Blood Glucose; D016207:Cytokines; D005230:Fatty Acids, Nonesterified; D017382:Reactive Oxygen Species; D051193:Toll-Like Receptors