Related Experiment Video
Updated: Jun 8, 2026
06:27
Accelerated Type 1 Diabetes Induction in Mice by Adoptive Transfer of Diabetogenic CD4+ T Cells
Published on: May 6, 2013
CD36 deficiency predisposing young children to fasting hypoglycemia
Hironori Nagasaka1, Tohru Yorifuji, Tomozumi Takatani
1Division of Metabolism, Chiba Children's Hospital, Chiba 266-0007, Japan. nagasa-hirono@k2.dion.ne.jp
Metabolism: Clinical and Experimental
|October 16, 2010
Summary
Type I CD36 deficiency, a defect in fatty acid transport, significantly predisposes preschool children to hypoglycemia. This contrasts with type II CD36 deficiency, which does not show this predisposition.
Area of Science:
- Biochemistry
- Pediatrics
- Metabolic Disorders
Background:
- Fatty acid (FA) β-oxidation defects are known causes of hypoglycemia.
- CD36 is a crucial membrane transporter for long-chain fatty acids.
Purpose of the Study:
- To investigate whether CD36 deficiency predisposes children to hypoglycemia.
- To differentiate the hypoglycemic risk associated with different types of CD36 deficiency.
Main Methods:
- Compared carbohydrate and FA metabolism in 51 hypoglycemic children and 49 controls during prolonged fasting (12-16 hours).
- Assessed CD36 expression on platelets and monocytes to identify phenotypes.
- Analyzed blood glucose, insulin, free fatty acid (FFA), and ketone body concentrations.
Main Results:
- Six children had type I CD36 deficiency; none of the controls did. Hypoglycemia was recurrent in this group.
- Type I CD36 deficiency group exhibited significantly lower blood glucose and insulin levels compared to controls and other hypoglycemic groups.
- Free FA levels were elevated 1.5-2.0 fold in type I CD36 deficiency, while ketone bodies were lower.
Conclusions:
- Type I CD36 deficiency is a significant risk factor for hypoglycemia in preschool children.
- Type II CD36 deficiency does not appear to predispose children to hypoglycemia.
- CD36's role in fatty acid transport is critical for maintaining glucose homeostasis during fasting.
Related Concept Videos
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...
01:27Glucose 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:
01:26Hypoglycemia
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...
01:12Type I Diabetes I: Introduction
Type 1 diabetes mellitus is a chronic metabolic disorder characterized by an absolute deficiency of insulin resulting from the autoimmune destruction of pancreatic β-cells. Although it can occur at any age, it is most commonly diagnosed in childhood, adolescence, or early adulthood. The loss of insulin production impairs cellular glucose uptake, resulting in persistent hyperglycemia and necessitating lifelong insulin therapy.Autoimmune Destruction of β-CellsThe hallmark of type 1 diabetes is an...
01:20Inborn Errors of Metabolism
Phenylketonuria (PKU) is a protein metabolism disorder characterized by high blood levels of the amino acid phenylalanine. This results from a mutation in the gene responsible for phenylalanine hydroxylase, an enzyme that converts phenylalanine into tyrosine. When this enzyme is deficient, phenylalanine builds up in the blood, leading to symptoms such as vomiting, rashes, seizures, growth deficiency, and severe mental retardation. An early diagnosis and a diet restricting phenylalanine intake...
01:19Type I Diabetes III: Clinical Manifestations
Type 1 diabetes mellitus typically presents with rapid-onset symptoms due to the body’s inability to utilize glucose in the absence of insulin. Since insulin is required for glucose uptake into cells, its deficiency leads to hyperglycemia and cellular energy deprivation, resulting in characteristic clinical features.Polyuria and PolydipsiaOne of the earliest, most prominent symptoms is polyuria (excessive urination). When blood glucose concentrations rise above the renal threshold, the kidneys...