NOD1: An Interface Between Innate Immunity and Insulin Resistance

Endocrinology
Sydney L RiversAdria Giacca

Abstract

Insulin resistance is driven, in part, by activation of the innate immune system. We have discussed the evidence linking nucleotide-binding oligomerization domain (NOD)1, an intracellular pattern recognition receptor, to the onset and progression of obesity-induced insulin resistance. On a molecular level, crosstalk between downstream NOD1 effectors and the insulin receptor pathway inhibits insulin signaling, potentially through reduced insulin receptor substrate action. In vivo studies have demonstrated that NOD1 activation induces peripheral, hepatic, and whole-body insulin resistance. Also, NOD1-deficient models are protected from high-fat diet (HFD)-induced insulin resistance. Moreover, hematopoietic NOD1 deficiency prevented HFD-induced changes in proinflammatory macrophage polarization status, thus protecting against the development of metabolic inflammation and insulin resistance. Serum from HFD-fed mice activated NOD1 signaling ex vivo; however, the molecular identity of the activating factors remains unclear. Many have proposed that an HFD changes the gut permeability, resulting in increased translocation of bacterial fragments and increased circulating NOD1 ligands. In contrast, others have suggested that NOD1 ligands...Continue Reading

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Citations

Nov 6, 2020·Endocrine Reviews·Sandra PereiraTimothy J Kieffer
Feb 3, 2021·Placenta·Johanne Johnsen RaknerAnn-Charlotte Iversen
Jun 3, 2021·Biomedicines·Victoria Fernández-GarcíaLisardo Boscá

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