Osteoblast-derived intraflagellar transport 140 suppresses insulin sensitivity I

Hyperglycemia-induced damage to bone formations and function has been recognized.However, as the largest connective tissue organ, whether bone and osteocytes in turn regulate blood sugar and insulin sensitivity has not been addressed. Here we identified a novel protein termed intraflagellar transport 140 with functional importance in regulating osteogenesis, which is also related to the osteoblastic insulin sensitivity. We established Ift140 osteoblastic conditional knockout mice model, and found that blood glucose metabolism could be regulated through osteoblastic IFT140 interacting with O-GlcNAc transferase to regulate insulin signaling. The discovery provides new insight for two-way regulation between bone and glucose metabolism, and also exploring potential new target for blood glucose interventions. Overall design: MRNA profiles of 2-week old wild type (ctrl) and Ift140-/-(cko) mouse bone marrow deriived progenitor cells.The experimental group and the control group each had three biological replicates.