Insulin function in obese children within the low and high ranges of impaired fasting glycemia
Emilia Hagman1, Anna E Ek1, Claude Marcus1
1Department of Clinical Science, Intervention and Technology, Division of Pediatrics, Karolinska Institutet, Stockholm, Sweden.
Insights
Impaired fasting glycemia (IFG) in the 5.6-6.0 mmol/L range did not affect glucose metabolism in obese children. However, higher fasting glucose levels (6.1-6.9 mmol/L) were linked to impaired insulin response and disposition index.
Area of Science:
- Pediatric Endocrinology
- Metabolic Disorders
- Obesity Research
Background:
- Impaired fasting glycemia (IFG) signifies intermediate hyperglycemia, but its impact on insulin-glucose homeostasis in obese children remains unclear.
- Understanding these variations is crucial for early detection and intervention in pediatric metabolic health.
Purpose of the Study:
- To investigate insulin and glucose homeostasis across different fasting glucose levels within the non-diabetic range in Swedish children and adolescents with obesity.
- To determine the specific fasting glucose thresholds associated with impaired metabolic function in this population.
Main Methods:
- Utilized an insulin-modified frequent sample intravenous glucose tolerance test (GTT) in 333 obese children and adolescents.
- Assessed acute insulin response (AIR), insulin sensitivity (SI), and disposition index (DI).
- Categorized participants into three groups based on fasting glucose: normoglycemic (≤5.5 mmol/L), ADA's IFG range (5.6-6.0 mmol/L), and WHO's IFG range (6.1-6.9 mmol/L).
Main Results:
- Fasting glucose levels between 5.6-6.0 mmol/L showed no significant difference in AIR, SI, or DI compared to the normoglycemic group.
- Fasting glucose levels between 6.1-6.9 mmol/L were associated with significantly lower AIR and DI, though SI remained statistically similar.
- IFG within the American Diabetes Association's exclusive range (5.6-6.0 mmol/L) did not correlate with disturbed glucose metabolism.
Conclusions:
- IFG as defined by the ADA (5.6-6.0 mmol/L) in obese children does not appear to be associated with impaired glucose metabolism.
- Higher fasting glucose levels (6.1-6.9 mmol/L) indicate a more significant impact on insulin secretion and overall glucose regulation.
- These findings suggest that IFG may affect metabolic profiles in obese children differently than previously observed in adult populations.
Background/Objective:
Impaired fasting glycemia (IFG) reflects an intermediate hyperglycemia in the fasting state. Which fasting glucose level that actually is associated with impaired insulin-glucose homeostasis in children and adolescents with obesity is unknown. The aim of this study was to investigate how insulin and glucose homeostasis in children and adolescents with obesity in Sweden varies within different fasting glucose levels in the non-diabetic range.
Subjects:
The subjects, n = 333, were divided into three groups based on their fasting glucose level. Normoglycemic range: up to 5.5 mmol/L (n = 268); the exclusive range the American Diabetes Association (ADA) has for IFG diagnosis: 5.6-6.0 mmol/L (n = 44); and IFG according to World Health Organization: 6.1-6.9 mmol/L (n = 21). The three groups were of similar age, degree of obesity, fasting insulin levels, sex, and migrant background distribution.
Methods:
We used an insulin-modified frequent sample intravenous glucose tolerance test to study acute insulin response (AIR), insulin sensitivity (SI), and disposition index (DI) in children and adolescents with obesity. The main outcome measures were AIR, SI, and DI in three groups based on fasting glucose level.
Results:
Fasting glucose levels ranging from 5.6 to 6.0 mmol/L were not associated with a lower AIR, SI, or DI compared with the normoglycemic range. However, glucose levels ranging from 6.1 to 6.9 mmol/L were associated with lower AIR and lower DI, but no statistical differences in SI were present.
Conclusions:
IFG in the exclusive ADA range was not associated with disturbed glucose metabolism. This suggests that IFG contributes to adverse metabolic profile in children differently to what has been described previously in adult obese populations.
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