We studied the effect of hypoxia (days 9-15 of pregnancy) on phosphate-dependent glutaminase activity in the brain of rat offspring aging 18 days and 1, 3, and 6 months. Activity of glutaminase significantly increased in mitochondria from the orbital, visual, and limbic cortex, hypothalamus, and midbrain of 17-day-old offspring. Activity of this enzyme in all brain regions increased at the age of 1 month, but significantly decreased in animals aging 3 and 6 months and prenatally exposed to hypoxia (during organogenesis). Changes in glutaminase activity in various structures of the brain are probably associated with activation of the glutamatergic and GABAergic systems and serve as an adaptive and compensatory reaction of the brain.
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http://dx.doi.org/10.1007/s10517-015-3123-2 | DOI Listing |
Anim Nutr
September 2024
Poultry Research Foundation within the University of Sydney, Camden, NSW 2570, Australia.
This review explores the potential of including glutamine, a so-called non-essential amino acid, in the formulation of reduced-crude protein (CP) diets for broiler chickens. There is a precedent for benefits when including glycine and serine in reduced-CP diets. Fundamentally this is due to decreases in non-essential amino acid concentrations in reduced-CP diets - an unavoidable consequence of reducing CP without amino acid supplementation.
View Article and Find Full Text PDFAm J Physiol Renal Physiol
February 2022
Division of Nephrology, Hypertension, and Renal Transplantation, University of Florida College of Medicine, Gainesville, Florida.
The molecular mechanisms regulating ammonia metabolism are fundamental to acid-base homeostasis. Deletion of the A splice variant of Na-bicarbonate cotransporter, electrogenic, isoform 1 (NBCe1-A) partially blocks the effect of acidosis to increase urinary ammonia excretion, and this appears to involve the dysregulated expression of ammoniagenic enzymes in the proximal tubule (PT) in the cortex but not in the outer medulla (OM). A second NBCe1 splice variant, NBCe1-B, is present throughout the PT, including the OM, where NBCe1-A is not present.
View Article and Find Full Text PDFKidney Int
February 2020
Centre de Recherche des Cordeliers, INSERM, Sorbonne Université, Université Sorbonne Paris Cité (USPC), Université Paris Descartes, Université Paris Diderot, Paris, France; Centre National de la Recherche Scientifique (CNRS), ERL 8228, Paris, France. Electronic address:
The kidneys excrete the daily acid load mainly by generating and excreting ammonia but the underlying molecular mechanisms are not fully understood. Here we evaluated the role of the inwardly rectifying potassium channel subunit Kir4.2 (Kcnj15 gene product) in this process.
View Article and Find Full Text PDFJ Am Soc Nephrol
May 2018
Division of Nephrology, Hypertension and Renal Transplantation, University of Florida College of Medicine, Gainesville, Florida;
Hyperkalemia in association with metabolic acidosis that are out of proportion to changes in glomerular filtration rate defines type 4 renal tubular acidosis (RTA), the most common RTA observed, but the molecular mechanisms underlying the associated metabolic acidosis are incompletely understood. We sought to determine whether hyperkalemia directly causes metabolic acidosis and, if so, the mechanisms through which this occurs. We studied a genetic model of hyperkalemia that results from early distal convoluted tubule (DCT)-specific overexpression of constitutively active Ste20/SPS1-related proline-alanine-rich kinase (DCT-CA-SPAK).
View Article and Find Full Text PDFJ Am Soc Nephrol
April 2018
Division of Nephrology, Hypertension and Transplantation, University of Florida College of Medicine, Gainesville, Florida;
Renal ammonia metabolism is the primary mechanism through which the kidneys maintain acid-base homeostasis, but the molecular mechanisms regulating renal ammonia generation are unclear. In these studies, we evaluated the role of the proximal tubule basolateral plasma membrane electrogenic sodium bicarbonate cotransporter 1 variant A (NBCe1-A) in this process. Deletion of the NBCe1-A gene caused severe spontaneous metabolic acidosis in mice.
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