Toll-like receptors and diabetes

A therapeutic perspective

Mohan R. Dasu, Sandra Ramirez, Roslyn Rivkah Isseroff

Research output: Contribution to journalArticle

56 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)203-214
Number of pages12
JournalClinical Science
Volume122
Issue number5
DOIs
StatePublished - Mar 2012

Fingerprint

Toll-Like Receptors
Inflammation
Therapeutics
Adaptive Immunity
Diabetes Complications
Nonesterified Fatty Acids
Innate Immunity
Blood Glucose
Reactive Oxygen Species
Animal Models
Cytokines

Keywords

  • Hyperglycaemia
  • Inflammation
  • Insulin resistance
  • Oxidative stress
  • Toll-like receptor
  • Type 2 diabetes

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Toll-like receptors and diabetes : A therapeutic perspective. / Dasu, Mohan R.; Ramirez, Sandra; Isseroff, Roslyn Rivkah.

In: Clinical Science, Vol. 122, No. 5, 03.2012, p. 203-214.

Research output: Contribution to journalArticle

Dasu, Mohan R. ; Ramirez, Sandra ; Isseroff, Roslyn Rivkah. / Toll-like receptors and diabetes : A therapeutic perspective. In: Clinical Science. 2012 ; Vol. 122, No. 5. pp. 203-214.
@article{702b1e850613441dbd854351963c74bd,
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.",
keywords = "Hyperglycaemia, Inflammation, Insulin resistance, Oxidative stress, Toll-like receptor, Type 2 diabetes",
author = "Dasu, {Mohan R.} and Sandra Ramirez and Isseroff, {Roslyn Rivkah}",
year = "2012",
month = "3",
doi = "10.1042/CS20110357",
language = "English (US)",
volume = "122",
pages = "203--214",
journal = "Clinical Science",
issn = "0143-5221",
publisher = "Portland Press Ltd.",
number = "5",

}

TY - JOUR

T1 - Toll-like receptors and diabetes

T2 - A therapeutic perspective

AU - Dasu, Mohan R.

AU - Ramirez, Sandra

AU - Isseroff, Roslyn Rivkah

PY - 2012/3

Y1 - 2012/3

N2 - 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.

AB - 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.

KW - Hyperglycaemia

KW - Inflammation

KW - Insulin resistance

KW - Oxidative stress

KW - Toll-like receptor

KW - Type 2 diabetes

UR - http://www.scopus.com/inward/record.url?scp=84855481978&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84855481978&partnerID=8YFLogxK

U2 - 10.1042/CS20110357

DO - 10.1042/CS20110357

M3 - Article

VL - 122

SP - 203

EP - 214

JO - Clinical Science

JF - Clinical Science

SN - 0143-5221

IS - 5

ER -