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

The centipede peptide toxin SpTx1 blocks the pore of ATP-sensitive potassium channels in pancreatic β cells to markedly enhance insulin secretion and mitigate hyperglycemia in diabetic mice insensitive to the anti-diabetic sulfonylurea glibenclamide.

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

Cardiac intercellular communication plays a critical role in diabetic myocardial fibrosis and specific targeting of Hrc^hi fibroblasts may be a potential therapeutic target for diabetic cardiomyopathy.

After an injury to the skin, murine wounds upregulate apoptosis and efferocytosis pathways, which are required for effective healing and may similarly impact wound healing in diabetic patients.

High glucose levels promote CTSL maturation and translocation from the endoplasmic reticulum to the lysosome via the ER-Golgi-lysosome axis.

Therapeutic potential of CCL3 for the treatment of diabetic foot ulcers if it is applied topically after the surgical debridement.

Monounsaturated fatty acids protect against DKD by enhancing membrane fluidity and decreasing ER lipid bilayer stress in renal proximal tubules.

Loss of mature β cell identity in diabetes can be prevented and rescued by small molecule inhibitors of the TGFβ pathway.

A proteomics screening in mouse adipose tissue shows that loss of adipose Hexokinase 2 is a mechanism of obesity-induced insulin insensitivity.