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

Contrary to previous reports, a complete absence of glucagon signaling is not sufficient to prevent diabetes after near-total β-cell loss.

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

Hepatic TAZ coordinates the differential expression of gluconeogenic genes in the fasted and fed states by inhibiting glucocorticoid receptor.

A novel process by which counter-regulatory glucagon release is regulated in both mouse and human.

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.

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

A multi-pronged approach shows that a G_s-coupled purinergic receptor is a sensor for glucose-mediated, PKA-dependent potentiation of vascular L-type calcium channels and vasoconstriction.

Anti-asprosin monoclonal antibodies, a promising pharmacotherapy for the treatment of metabolic syndrome-associated hyperglycemia, obesity, and dyslipidemia.

The repression of HIF-1 plays a central role in mitochondrial reactive oxygen species (ROS) overproduction and subsequent tissue damage in diabetes, which is mediated by increased mitochondrial respiration, making HIF-1 signaling an attractive therapeutic target for diabetes complications.