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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 Homeostasis: Pancreatic Islets and Insulin Secretion

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The pancreatic islets comprising only 1%-2% of the volume are highly vascularized and innervated mini-organs. They contain five endocrine cell types, including β cells that secrete insulin, which is synthesized as a single polypeptide chain, preproinsulin, processed to proinsulin, and finally to insulin and C-peptide. This process is complex and regulated, involving the Golgi complex, the endoplasmic reticulum, and the secretory granules of the β cell.
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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.

cAMP-dependent Protein Kinase Pathways

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Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...

Hormones Regulating Blood Glucose

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Insulin is released by beta cells of the pancreas when blood glucose levels are high. It facilitates glucose absorption and utilization in insulin-dependent cells with insulin receptors on their plasma membranes. Insulin promotes glucose uptake by increasing the number of glucose transport proteins in the cell membrane, allowing glucose to enter the cell. As a result, glucose utilization and ATP production are enhanced.
In addition to accelerating glucose uptake and utilization, insulin has...

Glucose Homeostasis: Regulation of Blood Glucose

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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...

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Updated: Jun 28, 2026

Alternate Immersion in Glucose to Produce Prolonged Hyperglycemia in Zebrafish

Alternate Immersion in Glucose to Produce Prolonged Hyperglycemia in Zebrafish

Published on: May 5, 2021

High glucose-induced IKK-Hsp-90 interaction contributes to endothelial dysfunction.

Sumathy Mohan¹, Ryszard Konopinski, Bo Yan

¹Department of Pathology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Dr., San Antonio, TX 78229, USA. mohan@uthscsa.edu

American Journal of Physiology. Cell Physiology

|October 24, 2008

Summary

High glucose in diabetes increases inhibitor kappaB kinase-beta (IKKbeta) interaction with heat shock protein-90 (Hsp-90) in endothelial cells. This interaction impairs nitric oxide (NO) production, contributing to vascular dysfunction.

Related Experiment Videos

Last Updated: Jun 28, 2026

Alternate Immersion in Glucose to Produce Prolonged Hyperglycemia in Zebrafish

Alternate Immersion in Glucose to Produce Prolonged Hyperglycemia in Zebrafish

Published on: May 5, 2021

Area of Science:

Molecular Biology
Endothelial Cell Biology
Diabetes Research

Background:

Diabetes mellitus is characterized by endothelial dysfunction, linked to reduced nitric oxide (NO) bioavailability.
Heat shock protein-90 (Hsp-90) is known to regulate endothelial nitric oxide synthase (eNOS) activity.
Hsp-90 interacts with kinases like inhibitor kappaB kinases (IKK) in nonvascular cells.

Purpose of the Study:

To investigate the interaction between Hsp-90 and IKKbeta in endothelial cells under high glucose (HG) conditions.
To determine if this interaction contributes to the diminished Hsp-90-eNOS interaction and reduced NO bioavailability in diabetes.

Main Methods:

Investigated Hsp-90 and IKKbeta interaction in vascular endothelial cells exposed to high glucose.
Utilized co-immunoprecipitation to detect protein interactions.
Assessed IKKbeta expression and activity using Western blotting and kinase assays.
Employed Hsp-90 inhibitors (geldanamycin, Radicicol) and an IKKbeta inhibitor (wedelolactone) or siRNA to block specific pathways.

Main Results:

High glucose significantly augmented the interaction between IKKbeta and Hsp-90 in endothelial cells.
HG also increased IKKbeta's transcriptional and translational expression, as well as its catalytic activity.
Inhibition of Hsp-90 or IKKbeta restored Hsp-90-eNOS interaction and improved NO production under HG conditions.

Conclusions:

High glucose promotes an interaction between IKKbeta and Hsp-90 in endothelial cells.
This HG-induced IKKbeta-Hsp-90 interaction is a novel mechanism contributing to reduced eNOS activity and NO bioavailability in diabetes.
Targeting the IKKbeta-Hsp-90 pathway may offer therapeutic potential for diabetic vascular complications.