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Glucose tolerance, insulin sensitivity, and insulin secretion in children born small for gestational age
Margreet A Veening1, Mirjam M Van Weissenbruch, Henriette A Delemarre-Van De Waal
1Department of Pediatrics, Research Institute for Endocrinology, Reproduction and Metabolism, VU University Medical Center, 1007 MB Amsterdam, The Netherlands.
Insights
Children born small for gestational age (SGA) exhibit reduced insulin sensitivity, increasing their risk for noninsulin-dependent diabetes mellitus (NIDDM). Catch-up growth and higher BMI in SGA children may exacerbate this risk.
Area of Science:
- Pediatrics
- Endocrinology
- Metabolic Diseases
Background:
- Intrauterine growth retardation and being born small for gestational age (SGA) are linked to increased risks of adult diseases, including noninsulin-dependent diabetes mellitus (NIDDM).
- NIDDM development can stem from impaired insulin sensitivity, reduced insulin secretion, or a combination of both factors.
Purpose of the Study:
- To investigate glucose tolerance, insulin sensitivity, and insulin secretion in prepubertal children born small for gestational age (SGA) compared to those born appropriate for gestational age (AGA).
Main Methods:
- Oral glucose tolerance tests were conducted to assess glucose tolerance and estimate beta-cell function (using AUC(ins0-120 min)/AUC(gluc0-120 min)).
- Hyperinsulinemic euglycemic clamp studies determined insulin sensitivity (M-value).
- Participants included 29 SGA children and 24 AGA children, all born at term and prepubertal.
Main Results:
- No significant differences in glucose tolerance or beta-cell function were observed between SGA and AGA children.
- Insulin sensitivity (M-value) was significantly lower in SGA children compared to AGA children (12.9 vs. 15.6 mg/kg.min, P=0.009).
- Reduced insulin sensitivity was particularly noted in SGA children with catch-up growth and a body mass index (BMI) greater than 17 kg/m(2).
Conclusions:
- Prepubertal children born SGA demonstrate reduced insulin sensitivity, a potential precursor to NIDDM in adulthood.
- Catch-up growth and elevated BMI in SGA children may heighten the risk of developing NIDDM.
- Interventions focusing on improving fetal growth and managing childhood obesity are crucial for NIDDM prevention in SGA individuals.
Abstract:
Intrauterine growth retardation is associated with an increased risk of developing adult diseases, such as noninsulin-dependent diabetes mellitus (NIDDM). NIDDM could result from a decreased insulin sensitivity or a reduced insulin secretion or a combination of both. Glucose tolerance, insulin sensitivity, and insulin secretion were studied in prepubertal children born small for gestational age (SGA). Twenty-nine SGA children with a mean age of 9.1 +/- 1.1 yr and 24 children born appropriate for gestational age (AGA), with a mean age of 9.0 +/- 1.1 yr, were studied. All children were born at term and were prepubertal. Children were studied on two separate days after 12 h of overnight fasting. Day 1: Glucose tolerance was studied with an oral glucose tolerance test. AUC(ins0-120 min)/AUC(gluc0-120 min) was used to estimate beta-cell function in the two groups. Day 2: A hyperinsulinemic euglycemic clamp study was performed to determine insulin sensitivity (M-value). Glucose tolerance and beta-cell function were not different between the two groups. M-value in SGA children was significantly lower than M-value in AGA children: 12.9 +/- 4.0 mg/kg.min vs. 15.6 +/- 2.3 mg/kg.min [P = 0.009; after adjustment for appropriate gestational age body mass index (BMI), P = 0.001]. The M-value tended to be higher in SGA children without catch-up growth compared with SGA children with catch-up growth (15.8 +/- 4.3 vs. 12.3 +/- 3.8 mg/kg.min; P = 0.079) and was comparable to AGA controls (15.6 +/- 2.3 mg/kg.min). The M-value in SGA children who had shown catch-up growth was comparable to AGA children (13.4 +/- 3.4 vs. 15.6 +/- 2.3 mg/kg.min; P = 0.06), provided they had a BMI of 17 kg/m(2) or less. However, the SGA children with catch-up growth and a BMI greater than 17 kg/m(2) were those having the lowest M-values (9.3 +/- 3.4 mg/kg.min). In conclusion, during oral glucose tolerance tests, no differences were found in glucose tolerance and beta-cell function between the SGA and AGA groups. However, the hyperinsulinemic clamp showed a reduced insulin sensitivity in SGA children, which may contribute to the enhanced risk of developing NIDDM in adult life, especially in SGA children with catch-up growth and a high BMI. The implications of our findings in relation to height are unclear, but might be of potential importance when considering GH treatment. In addition, interventions to improve fetal growth and to control obesity in childhood seem to be important factors in the prevention of NIDDM.