Insulin does not stimulate protein synthesis acutely in prepubertal children with insulin-dependent diabetes mellitus

Maria G. Vogiatzi, K Sreekumaran Nair, Philip R. Beckett, Kenneth C. Copeland

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Abstract

Insulin treatment in adult type I diabetic patients decreases protein loss primarily by inhibiting protein breakdown without stimulating protein synthesis. In young growing rodents, insulin treatment has been reported to stimulate protein synthesis. We examined whether insulin stimulates protein synthesis in normally growing prepubertal children with insulin-dependent diabetes mellitus. Five prepubertal children with insulin-dependent diabetes mellitus (aged 8.6-11.25 yr) were studied in the postabsorptive state on two occasions: once during insulin deprivation (I-; blood glucose, 325 ± 67.8 mg/dL; mean ± SD) and once during insulin administration for 4 h (I+; blood glucose, 96 ± 23.6 mg/dL). Leucine kinetics were measured using a 4-h primed continuous infusion of L-[1-19C]leucine. Serum insulin concentrations were lower (I- vs. I+. 0.6 ± 0.3 vs. 7.5 ± 4.3 μU/mL; mean ± SD; P = 0.02), whereas serum β-hydroxybutyrate (I- vs. I+, 3.4 ± 0.5 vs. 0.9 ± 0.5 mg/dL; P < 0.001) and free fatty acid concentrations (I- vs. I +, 2.9 ± 0.4 vs. 0.9 ± 0.4 mEq/L; P < 0.001) were higher in the insulin-deprived state than during insulin administration Leucine Ra, an index of protein breakdown (I - vs. I +, 200.5 ± 23.4 vs. 167 ± 17 μmol/kg·h; P = 0.008), and leucine oxidation (I- vs. I+, 56.5 ± 20.7 vs. 29.6 ± 9.3 μmol/kg·h;P = 0.03) were reduced by insulin treatment. Nonoxidative leucine disposal, an index of protein synthesis, was not affected by insulin treatment (I- vs. I+ 144 ± 20.8 vs. 137.5 ± 13.5 μmol/kg·h; P = 0.4). We conclude that the acute decline in net protein loss during insulin treatment in growing prepubertal children, like that in adults, is due primarily to an inhibition of protein breakdown without stimulation of protein synthesis.

Original languageEnglish (US)
Pages (from-to)4083-4087
Number of pages5
JournalJournal of Clinical Endocrinology and Metabolism
Volume82
Issue number12
StatePublished - 1997

Fingerprint

Medical problems
Type 1 Diabetes Mellitus
Insulin
Leucine
Proteins
Blood Glucose
Hydroxybutyrates
Therapeutics
Serum
Nonesterified Fatty Acids
Rodentia

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology, Diabetes and Metabolism

Cite this

Insulin does not stimulate protein synthesis acutely in prepubertal children with insulin-dependent diabetes mellitus. / Vogiatzi, Maria G.; Nair, K Sreekumaran; Beckett, Philip R.; Copeland, Kenneth C.

In: Journal of Clinical Endocrinology and Metabolism, Vol. 82, No. 12, 1997, p. 4083-4087.

Research output: Contribution to journalArticle

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abstract = "Insulin treatment in adult type I diabetic patients decreases protein loss primarily by inhibiting protein breakdown without stimulating protein synthesis. In young growing rodents, insulin treatment has been reported to stimulate protein synthesis. We examined whether insulin stimulates protein synthesis in normally growing prepubertal children with insulin-dependent diabetes mellitus. Five prepubertal children with insulin-dependent diabetes mellitus (aged 8.6-11.25 yr) were studied in the postabsorptive state on two occasions: once during insulin deprivation (I-; blood glucose, 325 ± 67.8 mg/dL; mean ± SD) and once during insulin administration for 4 h (I+; blood glucose, 96 ± 23.6 mg/dL). Leucine kinetics were measured using a 4-h primed continuous infusion of L-[1-19C]leucine. Serum insulin concentrations were lower (I- vs. I+. 0.6 ± 0.3 vs. 7.5 ± 4.3 μU/mL; mean ± SD; P = 0.02), whereas serum β-hydroxybutyrate (I- vs. I+, 3.4 ± 0.5 vs. 0.9 ± 0.5 mg/dL; P < 0.001) and free fatty acid concentrations (I- vs. I +, 2.9 ± 0.4 vs. 0.9 ± 0.4 mEq/L; P < 0.001) were higher in the insulin-deprived state than during insulin administration Leucine Ra, an index of protein breakdown (I - vs. I +, 200.5 ± 23.4 vs. 167 ± 17 μmol/kg·h; P = 0.008), and leucine oxidation (I- vs. I+, 56.5 ± 20.7 vs. 29.6 ± 9.3 μmol/kg·h;P = 0.03) were reduced by insulin treatment. Nonoxidative leucine disposal, an index of protein synthesis, was not affected by insulin treatment (I- vs. I+ 144 ± 20.8 vs. 137.5 ± 13.5 μmol/kg·h; P = 0.4). We conclude that the acute decline in net protein loss during insulin treatment in growing prepubertal children, like that in adults, is due primarily to an inhibition of protein breakdown without stimulation of protein synthesis.",
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