Nitric oxide accounts for an increased glycolytic rate in activated astrocytes through a glycogenolysis-independent mechanism.
The possible interference of nitric oxide (NO) in glucose metabolism was studied in activated astrocytes. Lipopolysaccharide (LPS) treatment triggered a NO-mediated increase in glucose consumption and lactate production, suggesting an enhanced rate of glycolysis. Active glycogen synthesis was also observed after LPS treatment, but NO synthase inhibition was unable to prevent this effect. These results strongly suggest that endogenously-formed NO stimulates glycolysis through a glycogenolysis-independent mechanism in astrocytes.
Almeida
Angeles
A
Departamento de Bioquímica y Biología Molecular, Universidad de Salamanca, Salamanca, Spain.
Cidad
Pilar
P
Bolaños
Juan P
JP
D000818:Animals; D000831:Animals, Newborn; D001253:Astrocytes / Q000187:drug effects / Q000502:physiology*; D002478:Cells, Cultured; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005947:Glucose / Q000378:metabolism; D006003:Glycogen / Q000378:metabolism*; D006019:Glycolysis; D007773:Lactates / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D051381:Rats; D017208:Rats, Wistar
D004791:Enzyme Inhibitors; D007773:Lactates; D008070:Lipopolysaccharides; D009569:Nitric Oxide; D006003:Glycogen; D019001:Nitric Oxide Synthase; D005947:Glucose; D019331:NG-Nitroarginine Methyl Ester