Related Experiment Video
Updated: Jul 28, 2026
11:10
Hyperinsulinemic-euglycemic Clamps in Conscious, Unrestrained Mice
Published on: November 16, 2011
Hyperinsulinism in asphyxiated and small-for-dates infants with hypoglycaemia
Lancet (London, England)
|August 11, 1984
Summary
Hypoglycaemia in newborns is often due to low glycogen. However, this study found hyperinsulinism contributes to low blood sugar in birth-asphyxiated and small-for-dates infants.
Area of Science:
- Neonatal Medicine
- Endocrinology
- Pediatrics
Background:
- Hypoglycaemia is a common neonatal issue.
- Glycogen depletion is the traditionally accepted cause of neonatal hypoglycaemia.
Observation:
- Six infants (3 birth-asphyxiated, 3 small-for-dates) presented with hypoglycaemia.
- These infants exhibited clear signs of hyperinsulinism.
Findings:
- Hyperinsulinism was identified as a significant factor in neonatal hypoglycaemia.
- This challenges the sole reliance on glycogen depletion as the cause.
Implications:
- Suggests a need to investigate hyperinsulinism in affected neonates.
- May lead to revised diagnostic and treatment strategies for neonatal hypoglycaemia.
Related Concept Videos
01:27Glucose Transporters
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:
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:
01:15Hypoglycemia and Glucagon
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...
01:26Hypoglycemia
Hypoglycemia is a blood glucose level below 70 mg/dL. It commonly occurs in individuals using insulin or insulin-secreting drugs, but may also arise in non-diabetic conditions. People with type 1 diabetes are at the highest risk because they depend on exogenous insulin. People with type 2 diabetes are also at risk, especially when treated with insulin or medications such as sulfonylureas, which increase insulin release regardless of blood glucose levels. It develops when insulin levels exceed...
01:29Hyperglycemia
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...
01:21Hyperosmolar Hyperglycemic State
Hyperosmolar Hyperglycemic State, or HHS, is a serious and life-threatening complication of type 2 diabetes mellitus. It is characterized by three main features: severe hyperglycemia, profound dehydration, and elevated serum osmolality, all occurring without significant ketoacidosis.HHS typically develops in older adults or individuals with limited access to fluids. This may result from illness, cognitive impairment, or medications such as diuretics or corticosteroids. These factors reduce...
01:25Diabetic Ketoacidosis l: Introduction
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...