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Objective  A genomic region near the CDKN2A locus, encoding p16 INK4a , has been associated to type 2 diabetes and atherosclerotic vascular disease, conditions in which inflammation plays an important role. Recently, we found that deficiency of p16 INK4a  results in decreased inflammatory signaling in murine macrophages and that p16 INK4a  influences the phenotype of human adipose tissue macrophages. Therefore, we investigated the influence of immune cell p16 INK4a  on glucose tolerance and atherosclerosis in mice.    Methods and Results  Bone marrow p16 INK4a -deficiency in C57Bl6 mice did not influence high fat diet-induced obesity nor plasma glucose and lipid levels. Glucose tolerance tests showed no alterations in high fat diet-induced glucose intolerance. While bone marrow p16 INK4a -deficiency did not affect the gene expression profile of adipose tissue, hepatic expression of the alternative markers Chi3l3, Mgl2 and IL10 was increased and the induction of pro-inflammatory Nos2 was restrained on the high fat diet. Bone marrow p16 INK4a -deficiency in low density lipoprotein receptor-deficient mice did not affect western diet-induced atherosclerotic plaque size or morphology. In line, plasma lipid levels remained unaffected and p16 INK4a -deficient macrophages displayed equal cholesterol uptake and efflux compared to wild type macrophages.    Conclusion  Bone marrow p16 INK4a -deficiency does not affect plasma lipids, obesity, glucose tolerance or atherosclerosis in mice.

Bone Marrow p16INK4a-Deficiency Does Not Modulate Obesity, Glucose Homeostasis or Atherosclerosis Development