glycogen has been researched along with Ascorbic-Acid-Deficiency* in 5 studies
1 review(s) available for glycogen and Ascorbic-Acid-Deficiency
Article | Year |
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[Participation of vitamins in the control of structural integrity of the cell and intracellular organelles: results of the release of enzymes].
Topics: Acidosis; Animals; Ascorbic Acid; Ascorbic Acid Deficiency; Deoxyribonucleases; Glycogen; Guinea Pigs; Hydrogen-Ion Concentration; Iron; Lysosomes; Male; Membranes; Mitochondria; Muscles; Oxidation-Reduction; Testis | 1969 |
4 other study(ies) available for glycogen and Ascorbic-Acid-Deficiency
Article | Year |
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Vitamin C deficiency induces hypoglycemia and cognitive disorder through S-nitrosylation-mediated activation of glycogen synthase kinase 3β.
Vitamin C (VC, l-ascorbic acid) is an essential nutrient that plays a key role in metabolism and functions as a potent antioxidant in regulating the S-nitrosylation and denitrosylation of target proteins. The precise function of VC deprivation in glucose homeostasis is still unknown. In the absence of L-gulono-1,4-lactone oxidoreductase, an essential enzyme for the last step of VC synthesis, VC deprivation resulted in persistent hypoglycemia and subsequent impairment of cognitive functions in female but not male mouse pups. The cognitive disorders caused by VC deprivation were largely reversed when these female pups were given glucose. VC deprivation-induced S-nitrosylation of glycogen synthase kinase 3β (GSK3β) at Cys14, which activated GSK3β and inactivated glycogen synthase to decrease glycogen synthesis and storage under the feeding condition, while VC deprivation inactivated glycogen phosphorylase to decrease glycogenolysis under the fasting condition, ultimately leading to hypoglycemia and cognitive disorders. Treatment with Nω-Nitro-l-arginine methyl ester (l-NAME), a specific inhibitor of nitric oxide synthase, on the other hand, effectively prevented S-nitrosylation and activation of GSK3β in female pups in response to the VC deprivation and reversed hypoglycemia and cognitive disorders. Overall, this research identifies S-nitrosylation of GSK3β and subsequent GSK3β activation as a previously unknown mechanism controlling glucose homeostasis in female pups in response to VC deprivation, implying that VC supplementation in the prevention of hypoglycemia and cognitive disorders should be considered in the certain groups of people, particularly young females. Topics: Animals; Antioxidants; Ascorbic Acid; Ascorbic Acid Deficiency; Cognition; Female; Glucose; Glycogen; Glycogen Phosphorylase; Glycogen Synthase; Glycogen Synthase Kinase 3 beta; Humans; Hypoglycemia; Lactones; Mice; Neurocognitive Disorders; NG-Nitroarginine Methyl Ester; Nitric Oxide Synthase | 2022 |
ENA-A actimineral resource A extends lifespan associated with antioxidant mechanism in SMP30 knockout mice.
ENA-actimineral resource A (ENA-A) is an alkaline mineral water and has a few biological activities such as antioxidant activity. The aim of this study was to examine the effects of ENA-A on lifespan in mice using senescence marker protein-30 knockout mice. The present study had groups of 18-week-old mice (n = 24), 26-week-old mice (n = 12), and 46-week-old mice (n = 20). Each differently aged mice group was divided into three subgroups: a control group, a 5 % ENA-A-treated group, and a 10 % ENA-A-treated group. Mice in the 18-week-old group were treated with vitamin C drinking water 1.5 g/L. However, the mice in the 26-week-old and 46-week-old groups were not treated with vitamin C. The experiments were done for 18 weeks. All vitamin C-treated mice were alive at week 18 (100% survival rate). In the non-vitamin C group, the 10% ENA-A-treated mice were alive at week 18. The control and 5% ENA-A-treated mice died by week 15. As expected, vitamin C was not detected in the non-vitamin C-treated group. However, vitamin C levels were increased in an ENA-A dose-dependent manner in the vitamin C-treated group. In the TUNEL assay, a number of positive hepatocytes significantly decreased in an ENA-A dose-dependent manner. Periodic acid Schiff positive hepatocytes were significantly increased in an ENA-A dose-dependent manner. In addition, the expression level of CuZnSOD was increased by the ENA-A treatment. These data suggest that the intake of ENA-A has a critical role in the anti-aging mechanism and could be applied toward the lifespans of humans. Topics: Animals; Antioxidants; Apoptosis; Ascorbic Acid; Ascorbic Acid Deficiency; Body Weight; Bone and Bones; Calcium-Binding Proteins; Glycogen; Hepatocytes; Immunoblotting; Intracellular Signaling Peptides and Proteins; Liver; Longevity; Mice, Knockout; Minerals; Plant Preparations; Staining and Labeling; Superoxide Dismutase; Survival Analysis | 2014 |
Influence of quercetin and epicatechin on biochemical changes in guinea-pigs during an experimental C-hypovitaminosis.
Topics: Adrenal Glands; Alanine Transaminase; Alkaline Phosphatase; Animals; Ascorbic Acid; Ascorbic Acid Deficiency; Aspartate Aminotransferases; Body Weight; Brain; Catechols; Ceruloplasmin; Cholesterol; Flavonoids; Glycogen; Guinea Pigs; Kidney; Lipoproteins; Liver; Liver Glycogen; Male; Myocardium; Spleen | 1969 |
Studies on hepatic glycolytic enzymes of normal and scorbutic guinea pigs administered acetoacetate.
Topics: Acetoacetates; Animals; Ascorbic Acid Deficiency; Blood Glucose; Body Weight; Glucose-6-Phosphatase; Glucosyltransferases; Glycogen; Glycolysis; Guinea Pigs; Liver; Male; Organ Size; Phosphoglucomutase | 1968 |