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Review
. 2012 Dec;61(12):3037-45.
doi: 10.2337/db12-0190.

Air pollution and type 2 diabetes: mechanistic insights

Sanjay Rajagopalan  1 , Robert D Brook
Affiliations
Review

Air pollution and type 2 diabetes: mechanistic insights

Sanjay Rajagopalan et al. Diabetes. 2012 Dec.
No abstract available

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Figures

FIG. 1.
FIG. 1.
A model for development of cardiometabolic disease highlighting importance of gene–environment interactions. (A high-quality digital representation of this figure is available in the online issue.)
FIG. 2.
FIG. 2.
Hypothesized mechanisms of air pollution–mediated cardiometabolic disease wherein inhalational or nutritional signals either directly or via the generation of signals such as DAMPs may serve to activate innate immune mechanisms such as the TLR and NLR. AP1, activator protein 1; CARD, caspase activation and recruitment domain; IKKb, IκB kinase b; IRAK, interleukin receptor-associated kinase; IRF3, interferon regulatory factor 3; MAPK, mitogen-activated protein kinase; MyD88, myeloid differentiation primary response gene 88; NAFLD, nonalcoholic fatty liver disease; PAMP, pathogen-associated molecular pattern; PAPC, palmitoyl-arachidonyl phosphocholine; RNS, reactive nitrogen species; ROS, reactive oxygen species; TAK, transforming growth factor-β–activated kinase; TBK, TANK-binding kinase 1; TRAF, TNF receptor-associated factor; TRIF, Toll/IL-1 receptor-domain-containing adapter-inducing interferon-β; UCP-1, uncoupling protein-1; WAT, white adipose tissue. (A high-quality digital representation of this figure is available in the online issue.)
See this image and copyright information in PMC

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