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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...

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Without prolonged fasting, healthy individuals maintain blood glucose levels above 3.5 mM due to a well-adapted neuroendocrine counterregulatory system that effectively prevents acute hypoglycemia, a potentially life-threatening condition. The primary clinical scenarios for hypoglycemia encompass diabetes treatment, inappropriate production of endogenous insulin or insulin-like substances by tumors, and the use of glucose-lowering agents in non-diabetic individuals. Notably, hypoglycemia in the...

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DefinitionDiabetic ketoacidosis (DKA) is an acute, life-threatening complication of diabetes mellitus, characterized by a triad of hyperglycemia (blood glucose >250 mg/dL), ketonemia or ketonuria, and metabolic acidosis (arterial pH <7.30 and serum bicarbonate <18 mEq/L). It results from insulin deficiency combined with elevated levels of counterregulatory hormones—glucagon, catecholamines, cortisol, and growth hormone—leading to increased lipolysis, hepatic ketone production, and...

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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...

Type II Diabetes Mellitus III: Clinical Manifestations and Diagnosis

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Type 2 diabetes mellitus develops gradually and is often asymptomatic in early stages.Clinical ManifestationsWhen symptoms appear, they include fatigue, blurred vision, pruritus, delayed wound healing, and recurrent infections, particularly candidal infections. Peripheral neuropathy may present as numbness or tingling in the extremities. Classic hyperglycemia symptoms—polyuria, polydipsia, and polyphagia—are less common. Most patients are overweight and frequently have associated hypertension...

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Related Experiment Video

Updated: Jun 27, 2026

Hyperinsulinemic-euglycemic Clamps in Conscious, Unrestrained Mice

Hyperinsulinemic-euglycemic Clamps in Conscious, Unrestrained Mice

Published on: November 16, 2011

Diagnostic difficulties in glucokinase hyperinsulinism.

T Meissner¹, J Marquard, N Cobo-Vuilleumier

¹Department of General Pediatrics, University Children's Hospital, Düsseldorf, Germany. thomas.meissner@med.uni-duesseldorf.de

Hormone and Metabolic Research = Hormon- Und Stoffwechselforschung = Hormones Et Metabolisme

|December 5, 2008

Summary

Glucokinase hyperinsulinism, a rare condition, presents diagnostic challenges due to variable insulin levels. Genetic testing of the GCK-gene is crucial for diagnosing this form of congenital hyperinsulinism.

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Last Updated: Jun 27, 2026

Hyperinsulinemic-euglycemic Clamps in Conscious, Unrestrained Mice

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Published on: November 16, 2011

Characterization of Metabolic Status in Nonhuman Primates with the Intravenous Glucose Tolerance Test

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Published on: November 13, 2016

Homogeneous Time-resolved Förster Resonance Energy Transfer-based Assay for Detection of Insulin Secretion

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Published on: May 10, 2018

Area of Science:

Endocrinology
Genetics
Metabolic Disorders

Background:

Congenital hyperinsulinism (CHI) encompasses genetic disorders of insulin dysregulation.
Glucokinase hyperinsulinism (GCK-HI) is a rare CHI subtype caused by activating glucokinase gene mutations.
Overactive glucokinase in pancreatic beta-cells leads to excessive insulin secretion.

Observation:

A case of persistent hyperinsulinism with diagnostic difficulties is presented.
The patient experienced neonatal hypoglycemia and later developmental delay.
Fasting tests showed low glucose and suppressed insulin levels, complicating diagnosis.

Findings:

A novel heterozygous missense mutation (c.1354G>C, p.Val452Leu) in the GCK-gene was identified and functionally validated.
Diagnostic criteria for GCK-HI are inconsistent, with low insulin levels sometimes observed during hypoglycemia.
An extra-pancreatic glucose-lowering effect may mask hyperinsulinism, leading to underdiagnosis.

Implications:

Genetic analysis of the GCK-gene is recommended for unexplained hypoglycemia, even without documented hyperinsulinism.
Early diagnosis is vital to prevent developmental delays and mental handicaps associated with GCK-HI.
This study highlights the need for comprehensive diagnostic approaches for rare endocrine disorders.