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.
The major protein disulfide isomerase family member, PDIA1, is essential in beta cells of mice fed a high-fat diet to maintain glucose homeostasis, proinsulin maturation and organelle integrity.
β2-adrenergic receptors control glucose metabolism by regulating cross-talk between pancreatic islet endocrine cells and vasculature during development.
Use of a newly developed experimental model in fruit flies reveals that death following traumatic brain injury is largely due to a mechanism by which brain damage triggers disruption of the intestinal barrier, leading to elevated levels of glucose in the circulatory system with deleterious consequences.
Rhythmic transcriptome analyses of human skeletal muscle tissue and cultured primary myotubes reveal an essential role for the circadian coordination of glucose homeostasis and lipid metabolism in human skeletal muscle.
A subset of hypothalamic POMC neurons that express leptin receptors control metabolic responses to changing energy availability including regulating blood glucose and leptin levels.
Stimulation of endothelial glucose metabolism and vascular growth by genetic depletion of endothelial Foxo1 improves the whole-body response to a high-fat diet, by preserving adipose tissue functions and glucose homeostasis.
Primary cilia on endothelial cells are required for VEGF-A/ VEGFR2-dependent signaling, islet vascularization and, consequently, nutrient delivery and insulin disposal.
