TY - JOUR
T1 - Insulin does not stimulate protein synthesis acutely in prepubertal children with insulin-dependent diabetes mellitus
AU - Vogiatzi, Maria G.
AU - Nair, K. Sreekumaran
AU - Beckett, Philip R.
AU - Copeland, Kenneth C.
N1 - Copyright:
Copyright 2017 Elsevier B.V., All rights reserved.
PY - 1997
Y1 - 1997
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=0030816897&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0030816897&partnerID=8YFLogxK
U2 - 10.1210/jc.82.12.4083
DO - 10.1210/jc.82.12.4083
M3 - Article
C2 - 9398718
AN - SCOPUS:0030816897
SN - 0021-972X
VL - 82
SP - 4083
EP - 4087
JO - Journal of Clinical Endocrinology and Metabolism
JF - Journal of Clinical Endocrinology and Metabolism
IS - 12
ER -