Intermittent hyperglycaemia induces macrophage dysfunction by extracellular regulated protein kinase-dependent PKM2 translocation in periodontitis.

ABSTRACT: Early fluctuations in blood glucose levels increased susceptibility to macrophage dysfunction. However, the underlying pathological mechanisms linking glucose variations and macrophage dysregulation remains elusive. In current study, we established an animal model of transient intermittent hyperglycaemia (TIH) to simulate early fluctuations in blood glucose levels. Our findings revealed that both TIH and diabetic group exhibited more severe periodontal lesions and increased secretion of pro-inflammatory cytokines compared to healthy controls. In immortalized bone marrow-derived macrophages (iBMDMs), phagocytosis and chemotaxis were impaired with transient and lasting hyperglycaemia, accompanied by enhanced glycolysis. We also found that TIH activated pyruvate kinase M2 (PKM2) through the p

SUBMITTER: Sun Y 

PROVIDER: S-EPMC11471441 | biostudies-literature | 2024 Oct

REPOSITORIES: biostudies-literature