ascorbate-2-phosphate and Ascorbic-Acid-Deficiency

Pancreatic islets from young normal and scorbutic male guinea pigs were examined for their ability to release insulin when stimulated with elevated D-glucose. Islets from normal guinea pigs released insulin in a D-glucose-dependent manner showing a rapid initial secretion phase and three secondary secretion waves during a 120-min period. Islets from scorbutic guinea pigs failed to release insulin during the immediate period, and only delayed and decreased responses were observed over the 40-60 min after D-glucose elevation. Insulin release from scorbutic islets was greatly elevated if 5 mM L-ascorbic acid 2-phosphate was supplemented in the perifusion medium during the last 60 min of perifusion. When 5 mM L-ascorbic acid 2-phosphate was added to the perifusion medium concurrently with elevation of medium D-glucose, islets from scorbutic guinea pigs released insulin as rapidly as control guinea pig islets and to a somewhat greater extent. L-Ascorbic acid 2-phosphate without elevated D-glucose had no effect on insulin release by islets from normal or scorbutic guinea pigs. The pancreas from scorbutic guinea pigs contained 2.4 times more insulin than that from control guinea pigs, suggesting that the decreased insulin release from the scorbutic islets was not due to decreased insulin synthesis but due to abnormal insulin secretion.

Topics: Animals; Ascorbic Acid; Ascorbic Acid Deficiency; Biological Transport; Glucose; Glutathione; Glutathione Disulfide; Guinea Pigs; In Vitro Techniques; Insulin; Insulin Secretion; Islets of Langerhans; Male; Perfusion

Channel catfish (Ictalurus punctatus) fingerlings (13 g average initial weight) were fed semipurified diets supplemented with 0, 0.06, 0.12, 0.24 and 0.72 mmol/kg (0, 11, 22, 44 or 132 mg/kg) of ascorbic acid molar equivalent supplied by either L-ascorbic acid, L-ascorbyl-2-monophosphate (Mg salt) (AAP), or L-ascorbyl-2-sulfate (K salt) (AAS). After 14 wk, weight gains were equal for all fish fed diets containing L-ascorbic acid or AAP; however, growth rates were less for fish fed AAS at all dietary levels and for fish fed the ascorbic acid-free diet (control). There were no gross signs of vitamin C deficiency in any of the fish fed L-ascorbic acid or AAP, whereas spinal deformities were found in the controls and in fish fed all but the highest concentration of AAS. The percentage of spinal deformities decreased as dietary levels of AAS increased. Reduced bone collagen content and histopathology in liver and gill tissues also indicated ascorbic acid deficiency in the controls and in fish fed all but the highest concentration of AAS. Limited histopathology was found in fish fed the lowest level of L-ascorbic acid but not in those fed the lowest level of AAP. Regression analysis of weight gain data showed that the vitamin activity of ascorbic acid from AAS was only 5.2% of that from L-ascorbic acid for growth. This study indicates that AAP has equimolar activity to L-ascorbic acid as a vitamin C source for channel catfish and that AAS has vitamin activity for this species but at a much lower level than the other compounds.

Topics: Administration, Oral; Animals; Anticholesteremic Agents; Ascorbic Acid; Ascorbic Acid Deficiency; Ictaluridae; Liver