Skeletal muscle mitochondrial pyruvate carrier disruption increases muscle fatty acid oxidation and systemic glucose turnover that drive whole-body leanness.

In vivo imaging reveals that gradually increased amount of glucose mediates the heterogeneous functional development of individual β-cells by activating its major downstream calcineurin/NFAT signaling pathway.

Feeding and fasting associated alterations in proopiomelanocortin neuronal responses to insulin coordinate glucose metabolism.

Zebrafish insulin mutants serve as an innovative platform to identify novel mechanisms regulating glucose homeostasis.

Loss miRNA maturation in proopiomelanocortin (POMC) neurons causes metabolic dysregulation and favors the differentiation of Pomc progenitors into neuropeptide Y neurons, a developmental process that appears to specifically involve miR-103/107.

Selection bias, also known as collider bias, likely explains the apparent protective effect of G6PD deficiency against cerebral falciparum malaria.

Hyperglycaemia increases influenza severity by damaging the pulmonary epithelial-endothelial barrier and increasing pulmonary oedema during Influenza A virus infection.

During cardiogenesis, the major role of glucose is not the catabolic extraction of energy but the anabolic biosynthesis of nucleotides.

A quantitative analysis of glucose-dependent transport regulation indicates that mitochondrial accumulation in regions of high nutrient availability can enhance metabolism in neuronal axons under physiologically relevant conditions.

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.