Fasting ketone levels vary by age: implications for differentiating physiologic from pathologic ketotic hypoglycemia
Komalben Parmar1,2, Maua Mosha3, David A Weinstein2
1Department of Pediatric Endocrinology, Connecticut Children Medical Center, Hartford, CT, USA.
Summary
Fasting serum beta-hydroxybutyrate (BHB) is significantly higher in children aged 3 and under compared to older children. Levels above 1.0 mmol/L are rare and may indicate pathologic ketotic hypoglycemia.
Area of Science:
- Biochemistry
- Pediatric Endocrinology
- Metabolic Disorders
Background:
- Ketone production via beta-oxidation of free fatty acids is a normal physiological process.
- Differentiating physiologic ketosis from pathologic states is crucial for diagnosing carbohydrate metabolism disorders.
- Limited data exists on normal ketone levels in children during fasting periods.
Purpose of the Study:
- To measure fasting serum beta-hydroxybutyrate (BHB) concentrations in healthy children after an overnight fast.
- To establish normative BHB levels in pediatric populations.
- To aid in the differentiation between physiologic and pathologic ketosis in children.
Main Methods:
- Prospective recruitment of 94 healthy children (≤18 years) undergoing elective procedures.
- Exclusion of participants with pre-existing metabolic, endocrine, or inflammatory conditions, or those on specific medications.
- Assessment of serum glucose, cortisol, and BHB levels following an overnight fast.
Main Results:
- Children aged ≤3 years (n=19) exhibited significantly higher mean BHB (0.40 ± 0.06 mmol/L) than those >3 years (n=75) (0.21 ± 0.02 mmol/L).
- Fasting BHB levels >1.0 mmol/L were infrequent (2%), with 74% of participants showing levels <0.3 mmol/L.
- A strong statistical significance (p<0.0001) was observed between the two age groups.
Conclusions:
- Younger children (≤3 years) demonstrate inherently higher fasting BHB concentrations than older children.
- Fasting BHB levels exceeding 1.0 mmol/L in children may warrant further investigation for potential pathologic ketotic hypoglycemia.
- Establishing precise normative ranges for fasting BHB in children is essential for accurate clinical diagnosis.
Keywords:
beta-hydroxybutyratefasting ketosisketotic hypoglycemiapathologic ketotic hypoglycemiapediatrics, idiopathic ketotic hypoglycemiaphysiological ketotic hypoglycemiaMore Related Videos
06:59Characterization of Metabolic Status in Nonhuman Primates with the Intravenous Glucose Tolerance Test
Published on: November 13, 2016
11.0K
08:13Study of In Vivo Glucose Metabolism in High-fat Diet-fed Mice Using Oral Glucose Tolerance Test OGTT and Insulin Tolerance Test ITT
Published on: January 7, 2018
68.8K
Related Concept Videos
01:24Metabolic States of the Body: Fasting and Starvation
1.6K
During the initial hours of fasting, the body uses up its glycogen stores as an energy source. Once these glycogen reserves are depleted, the body begins breaking down stored triglycerides and structural proteins. During this stage, glycerol becomes a key substrate for gluconeogenesis, while free fatty acids undergo beta-oxidation to provide energy for tissues, such as skeletal muscle. In the fasting state, the body spares protein breakdown as much as possible to conserve muscle and structural...
1.6K
01:15Hypoglycemia and Glucagon
306
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...
306
01:18Metabolic States of the Body: The Postabsorptive State
396
The postabsorptive state usually starts about four hours after a meal and lasts until the next meal is eaten. During this time, the digestive system stops absorbing nutrients, and the body uses stored energy reserves to maintain stable blood glucose levels.
Initially, glycogen stored in the liver is broken down to release glucose into the bloodstream, while glycogen in the muscles is broken down to supply glucose for energy directly within the muscle cells. As glycogen stores diminish,...
Initially, glycogen stored in the liver is broken down to release glucose into the bloodstream, while glycogen in the muscles is broken down to supply glucose for energy directly within the muscle cells. As glycogen stores diminish,...
396
01:15Diabetes: Symptoms, Diagnosis, and Complications
612
For most patients, experiencing several weeks of polyuria, polydipsia, fatigue, and significant weight loss may indicate the presence of diabetes. Furthermore, adults displaying the phenotypic appearance of type 2 diabetes (particularly those who are obese and not initially insulin-requiring), may have islet cell autoantibodies, suggesting autoimmune-mediated β cell destruction and a diagnosis of latent autoimmune diabetes of adults (LADA). The categorization of glucose homeostasis is...
612
01:02Glucose Homeostasis: Regulation of Blood Glucose
1.8K
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...
During fasting, when blood glucose levels are low, the pancreas secretes glucagon. it...
1.8K
01:20Inborn Errors of Metabolism
207
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...
207