Related Experiment Video
Updated: Jul 21, 2026
11:56
A Rapid and Specific Microplate Assay for the Determination of Intra- and Extracellular Ascorbate in Cultured Cells
Published on: April 11, 2014
Ascorbic acid metabolism and polyol pathway in diabetes.
D K Yue1, S McLennan, E Fisher
1Department of Medicine, University of Sydney, New South Wales, Australia.
Diabetes
|February 1, 1989
Summary
Diabetic rats show impaired ascorbic acid (AA) metabolism, with low plasma levels and high urinary excretion. Treatments targeting the polyol pathway, like tolrestat or myo-inositol, normalized these AA levels.
Area of Science:
- Biochemistry
- Endocrinology
- Metabolic Research
Background:
- Plasma ascorbic acid (AA) is reduced in diabetic rats.
- Aldose reductase inhibitors (ARIs) like tolrestat can normalize AA levels.
- The polyol pathway's role in AA metabolism in diabetes requires further investigation.
Purpose of the Study:
- To investigate the relationship between the polyol pathway and ascorbic acid (AA) metabolism in diabetic rats.
- To assess the impact of tolrestat and myo-inositol on AA levels and excretion in diabetic models.
- To explore the potential role of AA metabolic abnormalities in diabetic complications.
Main Methods:
- Induction of diabetes in rats using streptozocin.
- Administration of tolrestat (an aldose reductase inhibitor) and myo-inositol.
- Measurement of plasma and urinary ascorbic acid (AA) concentrations.
- Comparison with galactose-fed rat models.
Main Results:
- Diabetes caused a disturbance in AA metabolism within 1 week, characterized by low plasma AA and increased urinary excretion.
- Both tolrestat and myo-inositol treatments normalized plasma AA levels and reversed increased urinary AA excretion in diabetic rats.
- Ascorbic acid supplementation normalized plasma AA but further increased urinary AA excretion.
- Galactose-fed rats exhibited less severe AA metabolic abnormalities compared to diabetic rats.
Conclusions:
- Experimental diabetes significantly disrupts the regulation of plasma and urinary ascorbic acid (AA) concentration.
- A clear relationship exists between the polyol pathway and AA metabolism, with interventions affecting the polyol pathway impacting AA levels.
- Abnormalities in AA metabolism may contribute to diabetic complications, suggesting aldose reductase inhibitors as a potential therapeutic target.
Related Concept Videos
01:19Overview of Carbohydrate Metabolism
Carbohydrate metabolism is a fundamental biochemical process that ensures a constant supply of energy to living cells. The most important carbohydrate is glucose, which can be broken down via glycolysis to enter into the Krebs cycle and eventually lead to the production of ATP through oxidative phosphorylation.
Glucose transport into cells is facilitated by a family of transport proteins called GLUT (Glucose Transporters). GLUT4 is the primary glucose transporter for insulin-stimulated glucose...
Glucose transport into cells is facilitated by a family of transport proteins called GLUT (Glucose Transporters). GLUT4 is the primary glucose transporter for insulin-stimulated glucose...
01:02Glucose Homeostasis: Regulation of Blood Glucose
Carbohydrates consumed through foods are converted into glucose, a crucial energy source for the body. In the prandial state, high blood glucose levels stimulate the secretion of insulin from the pancreas. Insulin inhibits hepatic glucose production and stimulates glucose uptake and metabolism by muscle and adipose tissue. The excess glucose is converted into glycogen and stored in the liver and muscles.
During fasting, when blood glucose levels are low, the pancreas secretes glucagon. it...
During fasting, when blood glucose levels are low, the pancreas secretes glucagon. it...
01:20Pathophysiology of Diabetes
Diabetes mellitus is a chronic metabolic disorder characterized by hyperglycemia. The four categories of diabetes are type 1 diabetes, type 2 diabetes, other specific types of diabetes, and gestational diabetes.
Type 1 diabetes is characterized by autoimmune-mediated destruction of pancreatic β cells, with environmental factors potentially triggering this process in genetically susceptible individuals. Despite many not having a family history, certain genes increase susceptibility, suggesting a...
Type 1 diabetes is characterized by autoimmune-mediated destruction of pancreatic β cells, with environmental factors potentially triggering this process in genetically susceptible individuals. Despite many not having a family history, certain genes increase susceptibility, suggesting a...
01:26Type I Diabetes II: Pathophysiology
Type 1 diabetes mellitus arises from an immune-mediated destruction of pancreatic β-cells, resulting in an absolute deficiency of insulin. This process develops in genetically susceptible individuals when autoimmunity, environmental exposures, and immunologic dysregulation converge to trigger a targeted attack on the insulin-producing cells of the pancreas. The β-cells are located within the islets of Langerhans and are essential for regulating blood glucose by facilitating cellular uptake of...
01:24Type II Diabetes II: Pathophysiology
PathophysiologyType 2 diabetes mellitus (T2DM ) is a chronic metabolic disorder characterized by insulin resistance and progressive pancreatic β-cell dysfunction, leading to impaired glucose homeostasis. It results from interactions among genetic predisposition, environmental factors, and metabolic stressors, such as overnutrition and a sedentary lifestyle.Insulin Resistance and Glucose DysregulationEarly T2DM involves insulin resistance in skeletal muscle, adipose tissue, and the liver.
01:22Diabetic Ketoacidosis ll: Pathophysiology
Diabetic ketoacidosis (DKA) is a metabolic emergency characterized by hyperglycemia, ketonemia, and metabolic acidosis. It results from severe insulin deficiency and an excess of counterregulatory hormones, leading to uncontrolled lipolysis, ketogenesis, and widespread electrolyte and fluid disturbances.Pathophysiology The central event in DKA is a profound loss of insulin action. Without insulin, glucose uptake in insulin-dependent tissues is impaired, while hepatic glucose production...