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.

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.

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

Distinct phosphorylations of Akt determine the regulation of glucose uptake into fat and epithelial cells, revealing unexpected specialization in both Akt activation and its downstream control of glucose metabolism.

Upon AMPK activation by acute glucose restriction, Atg14p shifts its distribution from ER exit sites to liquid-ordered membrane domains on the vacuolar surface where, together with Atg6p, it facilitates LD-specific autophagy (i.e., microautophagy of lipid droplets) for energy production and long-term survival of starved cells.