Calcium-driven protein changes, causing glycogenolysis, poor synthesis, and diminished content of glycogen, along with diminished glucose transporters, lead to hyperglycemia in patients prone to calcium leaks from intracellular muscle stores.

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

Under metabolic syndrome, joint subchondral preosteoclasts acquire a senescence-associated secretome, which causes a rapid structural alteration of subchondral bone and contributes to the development of osteoarthritis.

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.

Intracellular and interorgan skeletal crosstalk highlights integrative skeletal physiology.

Osteoblast glucose metabolism is impaired in a mouse model for type II diabetes and can be boosted pharmacologically or genetically to alleviate diabetic osteopenia.

Metformin selectively improves bone healing of three types of bone injuries in hyperglycemic but not in normoglycemic mice.

In individuals with type 2 diabetes, downregulation of bone canonical Wnt signaling is linked to higher levels of advanced glycation end-products within the bone, contributing to lower bone strength.