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. 2020 Dec 29;162(2):bqaa235. doi: 10.1210/endocr/bqaa235

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© The Author(s) 2020. Published by Oxford University Press on behalf of the Endocrine Society.

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs licence (http://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial reproduction and distribution of the work, in any medium, provided the original work is not altered or transformed in any way, and that the work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

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Figure 3. — Direct engagement of pattern recognition receptors by microbial-associated molecular patterns play a role in T2DM. (A) Microbial-associated molecular patterns (MAMPs) can contribute to T2DM via the direct engagement of host pattern recognition receptors (PRRs), promoting chronic low-grade inflammation in insulin producing and insulin sensitive tissues. In the context of T2DM, gut microbial communities are significantly altered and associated gut hyperpermeability can elicit local direct MAMP-PRR signaling within key tissue microenvironments (gut, liver, pancreas, adipose, kidney, etc.). This MAMP-PRR signaling can promote tissue inflammation, which can contribute to the complications of T2DM. (B) Conversely, some MAMPS and PRRs are implicated in protecting against T2DM. Abbreviations: CD14, cluster of differentiation 14; CpG ODNs, CpG oligodeoxynucleotides; LPS, lipopolysaccharide; MAMPs, microbial-associated molecular patterns; MI, myocardial infarction; NOD1, nucleotide oligomerization domain-containing 1; NOD2, nucleotide oligomerization domain-containing 2; T2DM, type II diabetes mellitus; TLR, toll-like receptor.