Biliverdinuria Caused by Exonic Deletions in Two Dogs with Green Urine.

In heme degradation, biliverdin reductase catalyzes the conversion of biliverdin to bilirubin. Defects in the biliverdin reductase A gene () causing biliverdinuria are extraordinarily rare in humans, and this inborn error of metabolism has not been reported in other mammals. The objective of this study was to diagnose biliverdinuria and identify the causal variants in two adult mixed-breed dogs with life-long green urine.

Plasma membrane remodeling determines adipocyte expansion and mechanical adaptability.

Adipocytes expand massively to accommodate excess energy stores and protect the organism from lipotoxicity. Adipose tissue expandability is at the center of disorders such as obesity and lipodystrophy; however, little is known about the relevance of adipocyte biomechanics on the etiology of these conditions. Here, we show in male mice in vivo that the adipocyte plasma membrane undergoes caveolar domain reorganization upon lipid droplet expansion.

Enzymatic production of rare sugars with a new mutant of cellobiose 2-epimerase from Caldicellulosiruptor saccharolyticus.

Cellobiose 2-epimerase from Caldicellulosiruptor saccharolyticus (CsCE) can epimerize and isomerize lactose into epilactose and lactulose respectively. Competition between these reactions reactions has prompted the search for new enzymes to drive the reaction in one direction or the other. The isomerization and epimerization capacity of a novel mutant CsCE (CsCE H356N) was evaluated, obtaining a maximum lactulose yield of 64.

Ferroptosis Inhibition Combats Metabolic Derangements and Improves Cardiac Function in Pulmonary Artery Banded Pigs.

Right heart failure (RHF) is a leading cause of mortality in multiple cardiovascular diseases and preclinical and human data suggest impaired metabolism is a significant contributor to right-sided cardiac dysfunction. Ferroptosis is a nonapopotic form of cell death driven by impaired metabolism. Rodent data suggests ferroptosis inhibition can restore mitochondrial electron transport chain function and enhance cardiac contractility in left heart failure models, but the effects of ferroptosis inhibition in translational large animal models of RHF are unknown.