Altered glycolysis triggers impaired mitochondrial metabolism and mTORC1 activation in diabetic β-cells.

Chronic hyperglycaemia causes a dramatic decrease in mitochondrial metabolism and insulin content in pancreatic β-cells. This underlies the progressive decline in β-cell function in diabetes. However, the molecular mechanisms by which hyperglycaemia produces these effects remain unresolved.

Phenotype of a transient neonatal diabetes point mutation (SUR1-R1183W) in mice.

The K channel plays a key role in glucose homeostasis by coupling metabolically generated changes in ATP to insulin secretion from pancreatic beta-cells.  Gain-of-function mutations in either the pore-forming (Kir6.2) or regulatory (SUR1) subunit of this channel are a common cause of transient neonatal diabetes mellitus (TNDM), in which diabetes presents shortly after birth but remits within the first few years of life, only to return in later life.

Wintertime Nitrous Oxide Emissions in the San Joaquin Valley of California Estimated from Aircraft Observations.

Nitrous oxide (NO) is a long-lived greenhouse gas that also destroys stratospheric ozone. NO emissions are uncertain and characterized by high spatiotemporal variability, making individual observations difficult to upscale, especially in mixed land use source regions like the San Joaquin Valley (SJV) of California. Here, we calculate spatially integrated NO emission rates using nocturnal and convective boundary-layer budgeting methods.

The Gene Variant Hastens Diabetes Progression by Impairing Glucose-Induced Insulin Secretion.

The ATP-sensitive K (K) channel controls blood glucose levels by coupling glucose metabolism to insulin secretion in pancreatic β-cells. E23K, a common polymorphism in the pore-forming K channel subunit () gene, has been linked to increased risk of type 2 diabetes. Understanding the risk-allele-specific pathogenesis has the potential to improve personalized diabetes treatment, but the underlying mechanism has remained elusive.