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Diabetes Mellitus: Type 2 and Gestational

Diabetes Mellitus: Type 2 and Gestational

Type 2 diabetes, characterized by insulin resistance, arises when the insulin receptors on cells lose responsiveness to insulin, diminishing the cell's capacity to take up glucose, resulting in elevated blood glucose levels. To receive a diagnosis of Type 2 diabetes, a series of blood glucose tests are necessary to assess whether the blood glucose falls within normal parameters. If the result is out of the normal range, a patient may be diagnosed as prediabetic or diabetic, depending on the...

Type II Diabetes II: Pathophysiology

Type 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.

Hyperglycemia

Hyperglycemia

Hyperglycemia is an abnormally high blood glucose level. It is diagnosed by fasting glucose ≥126 mg/dL, 2-hour oral glucose tolerance test (or OGTT) ≥200 mg/dL, random glucose ≥200 mg/dL with symptoms, or HbA1c ≥6.5%. However, HbA1c results may be unreliable in certain conditions, such as anemia or hemoglobinopathies, and the diagnosis should be confirmed unless classic symptoms are present. Postprandial hyperglycemia is typically considered significant when glucose levels exceed 180 mg/dL two...

Glucose Transporters

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Glucose transporters facilitate the transport of glucose across the cell membrane. In addition to glucose, some glucose transporters can also aid the movement of other hexoses such as fructose, mannose, and galactose.
Facilitated diffusion-glucose transporters (GLUTs) are encoded by the solute-linked carrier (SLC) family 2, subfamily A gene family, or SLC2A. The 14 GLUT protein members are distributed into three classes:

Type II Diabetes I: Introduction

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Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder characterized by insulin resistance, in which target tissues such as the liver, muscle, and adipose tissue respond poorly to insulin. It is also associated with inadequate compensatory insulin secretion, where pancreatic β-cells fail to produce sufficient insulin. Together, these abnormalities lead to persistent hyperglycemia.EtiologyT2DM develops through a complex interaction of genetic predisposition and environmental or...

Type I Diabetes II: Pathophysiology

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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...

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Updated: May 25, 2026

Alternate Immersion in Glucose to Produce Prolonged Hyperglycemia in Zebrafish

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Relationship between erythrocyte GLUT1 function and membrane glycation in type 2 diabetes.

M M Porter-Turner¹, J C Skidmore, M A Khokher

¹School of Health Sciences, University of Wolverhampton, Wolverhampton, UK.

British Journal of Biomedical Science

|January 24, 2012

Summary

Glycation impairs glucose transport in diabetic erythrocytes, reducing uptake and net transport despite unchanged transporter numbers. Binding affinity for glucose transporters increases in diabetes.

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Last Updated: May 25, 2026

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Extracellular Glucose Depletion as an Indirect Measure of Glucose Uptake in Cells and Tissues Ex Vivo

Extracellular Glucose Depletion as an Indirect Measure of Glucose Uptake in Cells and Tissues Ex Vivo

Published on: April 6, 2022

Area of Science:

Physiology
Biochemistry
Endocrinology

Background:

Glycation, a post-translational modification of proteins by sugars, is elevated in diabetes.
Erythrocyte glucose transport is crucial for cellular glucose uptake and metabolic homeostasis.
Understanding glycation's impact on glucose transporters is vital for managing diabetic complications.

Purpose of the Study:

To investigate the effects of glycation on glucose transporter function, number, and phosphorylation in erythrocytes from diabetic patients.
To compare glucose transport parameters between individuals with diabetes and healthy controls.

Main Methods:

Simultaneous measurement of glucose transporter function, numbers, and erythrocyte phosphorylation rates.
Utilized 3-O-methylglucose uptake, D-glucose influx, and 2-deoxyglucose phosphorylation assays.
Quantified glucose transporter numbers and binding affinity using cytochalasin B studies.

Main Results:

Significantly reduced 3-O-methylglucose uptake, D-glucose influx, and net transport in diabetic erythrocytes.
No significant difference in erythrocyte phosphorylation rates or the number of functional glucose transporters.
Increased binding affinity (lower K(d)) of glucose transporters in diabetic individuals.
Negative correlation between HbA1c levels and D-glucose influx.

Conclusions:

Glycation significantly impairs glucose transport function in erythrocytes, independent of transporter number.
Increased glucose transporter binding affinity in diabetes may represent a compensatory mechanism.
These findings highlight altered erythrocyte glucose metabolism in diabetes, potentially impacting glycemic control.