Postbiotics for NOD2 require non-hematopoietic RIPK2 to improve blood glucose and metabolic inflammation in mice.

Postbiotics for NOD2 require non-hematopoietic RIPK2 to improve blood glucose and metabolic inflammation in mice. Am J Physiol Endocrinol Metab. 2020 Feb 26;: Authors: Cavallari JF, Barra NG, Foley KP, Lee A, Duggan BM, Henriksbo BD, Anhê FF, Ashkar AA, Schertzer JD Abstract Defining the host receptors and metabolic consequences of bacterial components can help explain how the microbiome influences metabolic diseases. Bacterial peptidoglycans that activate nucleotide-binding oligomerization domain-containing (NOD)1 worsen glucose control, whereas NOD2 activation improves glycemia. Receptor-interacting serine/threonine-protein kinase 2 (RIPK2) is required for innate immunity instigated by NOD1 and NOD2. The role of RIPK2 in the divergent effects of NOD1 versus NOD2 on blood glucose was unknown. We found that whole body deletion of RIPK2 negated all effects of NOD1 or NOD2 activation on blood glucose during an acute, low level endotoxin challenge in mice. It was known that NOD1 in hematopoietic cells participates in insulin resistance and metabolic inflammation in obese mice. It was unknown if RIPK2 in hematopoietic cells is required for the glucose lowering and anti-inflammatory effects of NOD2 activation. We hypothesized that RIPK2 in non-hematopoietic cells dictated the glycemic effects of NOD2 activation. We found that whole-body deletion of RIPK2 prevented the glucose-lowering effects of repeated NOD2 activation that was evident ...
Source: Am J Physiol Endocri... - Category: Endocrinology Authors: Tags: Am J Physiol Endocrinol Metab Source Type: research