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Effect of 24 hour fast in obese children
Insights
Fasting in obese children reveals reduced fat mobilization and increased branched-chain amino acids, suggesting peripheral insulin resistance. These findings highlight key metabolic differences in childhood obesity.
Area of Science:
- Pediatrics
- Metabolic Research
- Endocrinology
Background:
- Childhood obesity is a growing health concern with complex metabolic underpinnings.
- Understanding metabolic responses to fasting in obese children is crucial for developing effective interventions.
Purpose of the Study:
- To investigate the metabolic effects of a 24-hour fast in obese children compared to healthy controls.
- To identify potential biomarkers and physiological differences associated with obesity in pediatric populations.
Main Methods:
- A 24-hour fasting study was conducted on 21 obese children (aged 7-14) and 8 healthy controls.
- Measurements included blood glucose, plasma cortisol, free fatty acids (FFA), ketonuria, serum alanine, and branched-chain amino acids.
- Glucagon stimulation tests were performed before and after the fast.
Main Results:
- Obese children showed a less pronounced drop in blood glucose and higher post-fast ketonuria compared to controls.
- While FFA increased in both groups, levels were lower in obese children, indicating reduced fat mobilization.
- Obese children exhibited a significant rise in branched-chain amino acids and demonstrated peripheral insulin resistance, evidenced by hyperinsulinism during glucagon tests.
Conclusions:
- Childhood obesity is characterized by impaired fat mobilization and altered amino acid metabolism during fasting.
- Peripheral insulin resistance is a key feature in obese children, even with normal protein gluconeogenesis.
- These metabolic differences may represent a significant biological characteristic of pediatric obesity.
Abstract:
Effects of a 24 hour fast were studied in 21 obese children aged 7 to 14 and in 8 controls. Mean blood glucose (BG) during fast dropped more in controls (0.88 to 0.54 g/l) than in obese (0.90 to 0.63 g/l) Plasma cortisol changes were similar in the 2 groups, FFA increased (p less than 0.01) in the 2 groups, but the 24 hour mean level was higher in controls (4.0 mEq/l) than in obese (2.06 mEq/l). At the end of the fast, a ketonuria was present in all obese children except 2. Serum alanine dropped similarly in obese (28 to 24 muM p. cent ml) and in controls (30 to 22 muM p. cent ml). All obese exhibited at the end of the fast a significant rise (p less than 0.01) of branched chain aminoacids, not observed in controls. Responses to glucagon (0.03 mg/kg I.M.) were studied before and after fast. At time 0, BG response was higher and more prolonged in obese in spite of hyperinsulinism. At time 24 hours, BG raised from 0.50 to 0.74 g/1 and insulin from 8 to 35 muU/ml in controls, while in obese BG raised from 0.63 to 1.06 g/l and insulin from 25 to 88 muU/ml. Concomitant hyperinsulinsim and biological criteria of hypoinsulinism demonstrated in obese children the peripheral resistance to insulin. The contrast between a normal degree of protein gluconeogenesis and a reduced rate of fat mobilization during fast may be a major biological feature of obesity in childhood.
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