Adipsin, the oldest known adipokine, has a novel role as a a regulator of bone marrow fat and, consequently, overall bone health.

Obese Ksr2 mutant mice have increased trabecular bone but decreased marrow adiposity and are more prone to fractures, thus providing a useful model to understand how stem cells can be manipulated to produce bone at the expense of marrow fat.

OGT-mediated protein O-GlcNAcylation balances osteogenic versus adipogenic differentiation and controls hematopoietic niche function of bone marrow stromal cells.

Bone marrow adipocyte lipolysis is required for maintaining bone mass under conditions of energy deficiency and is necessary for myelopoiesis following caloric restriction and irradiation.

Diet-induced obesity in mice led to a duration of diet-dependent bone marrow adipocyte whitening, which drove monocyte expansion and skewing towards a tissue-invasive phenotype, likely contributing to ensuing tissue infiltration that accompanies obesity and diabetes.

Identification of bone marrow Adipoq-lineage progenitors as a novel and major cellular source of M-CSF in mice and humans, which controls bone marrow macrophage development, osteoclastogenesis, and bone mass in physiological and pathological conditions.

Targeted activation of Hedgehog signalling via Gli2 facilitated the reduction of high-fat-diet-induced obesity and improvement of whole-body glucose tolerance and insulin sensitivity in adult mice.

A novel secondary adipogenesis pathway is defined that is unique to the bone marrow and is activated with age and in states of metabolic stress.

Body mass index and adipose distribution have opposing and broad effects on human blood trait variation by Mendelian randomization analysis, helping to clarify the complex interplay between cardiometabolic traits and hematopoiesis at the genetic level.