Insulin-like growth factor-I in man enhances lipid mobilization and oxidation induced by a growth hormone pulse

T. L. Bianda, Mehboob Hussain, A. Keller, Y. Glatz, O. Schmitz, J. S. Christiansen, K. G M M Alberti, E. R. Froesch

Research output: Contribution to journalArticle

Abstract

Growth hormone (GH) secretion is suppressed during insulin-like growth factor-I (IGF-I) administration. The aim of the study was to examine whether IGF-I alters the metabolic response to a GH pulse. Seven healthy male subjects (age 27 ± 4 years, BMI 21.8 ± 1.7 kg/m2) were treated with NaCl 0.9% (saline) or IGF-I (8 μg · kg-1 · h-1) for 5 days by continuous subcutaneous infusion in a randomized, crossover fashion while receiving an isocaloric diet (30 kcal · kg-1 · day-1). On the third treatment day an intravenous bolus of 0.5 U GH was administered. Forearm muscle metabolism was examined by measuring arterialized and deep venous blood samples, forearm blood flow by occlusion plethysmography and substrate oxidation by indirect calorimetry. IGF-I treatment significantly reduced insulin concentrations by 80% (p <0.02) and C-peptide levels by 78% (p <0.02), as assessed by area under the curve. Non-esterified fatty acid (NEFA), glycerol and 3-OH-butyrate levels were elevated and alanine concentration decreased. Forearm blood flow rose from 2.10 ± 0.43 (saline) to 2.79 ± 0.37 ml · 100 ml-1 · min-1 (IGF-I) (p <0.02). GH-pulse: 10 h after i.v. GH injection serum GH peaked at 40.9 ± 7.4 ng/ml. GH did not influence circulating levels of total IGF-I, C-peptide, insulin or glucose, but caused a further increase in NEFA, glycerol and 3-OH-butyrate levels, indicating enhanced lipolysis and ketogenesis. This effect of GH was much more pronounced during IGF-I: NEFA rose from 702 ± 267 (saline) and 885 ± 236 (IGF-I) to 963 ± 215 (saline) (p <0.05) and 1815 ± 586 μmol/l (IGF-I) (p <0.02), respectively; after 5 h, 3-OH-butyrate rose from 242 ± 234 (saline) and 340 ± 280 (IGF-I) to 678 ± 638 (saline) (p <0.02) and 1115 ± 578 μmol/l (IGF-I) (p <0.02) respectively. After injection of GH, forearm uptake of 3-OH-butyrate was markedly elevated only in the subjects treated with IGF-I: from 44 ± 195 to 300 ± 370 aftr 20 min (p <0.03) and to 287 ± 91 nmol · 100 ml-1 · min-1 after 120 min (p <0.02). In conclusion, the lipolytic and ketogenic response to GH was grossly enhanced during IGF-I treatment, and utilization of ketone bodies by skeletal muscle was increased.

Original languageEnglish (US)
Pages (from-to)961-969
Number of pages9
JournalDiabetologia
Volume39
Issue number8
DOIs
StatePublished - 1996
Externally publishedYes

Fingerprint

Lipid Mobilization
Insulin-Like Growth Factor I
Growth Hormone
Butyrates
Forearm
Fatty Acids
C-Peptide
Glycerol
Insulin
Subcutaneous Infusions
Ketone Bodies
Indirect Calorimetry
Injections
Plethysmography
Lipolysis

Keywords

  • 'dawn' phenomenon
  • Energy expenditure
  • Ketogenesis
  • Lipolysis
  • Substrate oxidation

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism

Cite this

Bianda, T. L., Hussain, M., Keller, A., Glatz, Y., Schmitz, O., Christiansen, J. S., ... Froesch, E. R. (1996). Insulin-like growth factor-I in man enhances lipid mobilization and oxidation induced by a growth hormone pulse. Diabetologia, 39(8), 961-969. https://doi.org/10.1007/s001250050538

Insulin-like growth factor-I in man enhances lipid mobilization and oxidation induced by a growth hormone pulse. / Bianda, T. L.; Hussain, Mehboob; Keller, A.; Glatz, Y.; Schmitz, O.; Christiansen, J. S.; Alberti, K. G M M; Froesch, E. R.

In: Diabetologia, Vol. 39, No. 8, 1996, p. 961-969.

Research output: Contribution to journalArticle

Bianda, TL, Hussain, M, Keller, A, Glatz, Y, Schmitz, O, Christiansen, JS, Alberti, KGMM & Froesch, ER 1996, 'Insulin-like growth factor-I in man enhances lipid mobilization and oxidation induced by a growth hormone pulse', Diabetologia, vol. 39, no. 8, pp. 961-969. https://doi.org/10.1007/s001250050538
Bianda, T. L. ; Hussain, Mehboob ; Keller, A. ; Glatz, Y. ; Schmitz, O. ; Christiansen, J. S. ; Alberti, K. G M M ; Froesch, E. R. / Insulin-like growth factor-I in man enhances lipid mobilization and oxidation induced by a growth hormone pulse. In: Diabetologia. 1996 ; Vol. 39, No. 8. pp. 961-969.
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T1 - Insulin-like growth factor-I in man enhances lipid mobilization and oxidation induced by a growth hormone pulse

AU - Bianda, T. L.

AU - Hussain, Mehboob

AU - Keller, A.

AU - Glatz, Y.

AU - Schmitz, O.

AU - Christiansen, J. S.

AU - Alberti, K. G M M

AU - Froesch, E. R.

PY - 1996

Y1 - 1996

N2 - Growth hormone (GH) secretion is suppressed during insulin-like growth factor-I (IGF-I) administration. The aim of the study was to examine whether IGF-I alters the metabolic response to a GH pulse. Seven healthy male subjects (age 27 ± 4 years, BMI 21.8 ± 1.7 kg/m2) were treated with NaCl 0.9% (saline) or IGF-I (8 μg · kg-1 · h-1) for 5 days by continuous subcutaneous infusion in a randomized, crossover fashion while receiving an isocaloric diet (30 kcal · kg-1 · day-1). On the third treatment day an intravenous bolus of 0.5 U GH was administered. Forearm muscle metabolism was examined by measuring arterialized and deep venous blood samples, forearm blood flow by occlusion plethysmography and substrate oxidation by indirect calorimetry. IGF-I treatment significantly reduced insulin concentrations by 80% (p <0.02) and C-peptide levels by 78% (p <0.02), as assessed by area under the curve. Non-esterified fatty acid (NEFA), glycerol and 3-OH-butyrate levels were elevated and alanine concentration decreased. Forearm blood flow rose from 2.10 ± 0.43 (saline) to 2.79 ± 0.37 ml · 100 ml-1 · min-1 (IGF-I) (p <0.02). GH-pulse: 10 h after i.v. GH injection serum GH peaked at 40.9 ± 7.4 ng/ml. GH did not influence circulating levels of total IGF-I, C-peptide, insulin or glucose, but caused a further increase in NEFA, glycerol and 3-OH-butyrate levels, indicating enhanced lipolysis and ketogenesis. This effect of GH was much more pronounced during IGF-I: NEFA rose from 702 ± 267 (saline) and 885 ± 236 (IGF-I) to 963 ± 215 (saline) (p <0.05) and 1815 ± 586 μmol/l (IGF-I) (p <0.02), respectively; after 5 h, 3-OH-butyrate rose from 242 ± 234 (saline) and 340 ± 280 (IGF-I) to 678 ± 638 (saline) (p <0.02) and 1115 ± 578 μmol/l (IGF-I) (p <0.02) respectively. After injection of GH, forearm uptake of 3-OH-butyrate was markedly elevated only in the subjects treated with IGF-I: from 44 ± 195 to 300 ± 370 aftr 20 min (p <0.03) and to 287 ± 91 nmol · 100 ml-1 · min-1 after 120 min (p <0.02). In conclusion, the lipolytic and ketogenic response to GH was grossly enhanced during IGF-I treatment, and utilization of ketone bodies by skeletal muscle was increased.

AB - Growth hormone (GH) secretion is suppressed during insulin-like growth factor-I (IGF-I) administration. The aim of the study was to examine whether IGF-I alters the metabolic response to a GH pulse. Seven healthy male subjects (age 27 ± 4 years, BMI 21.8 ± 1.7 kg/m2) were treated with NaCl 0.9% (saline) or IGF-I (8 μg · kg-1 · h-1) for 5 days by continuous subcutaneous infusion in a randomized, crossover fashion while receiving an isocaloric diet (30 kcal · kg-1 · day-1). On the third treatment day an intravenous bolus of 0.5 U GH was administered. Forearm muscle metabolism was examined by measuring arterialized and deep venous blood samples, forearm blood flow by occlusion plethysmography and substrate oxidation by indirect calorimetry. IGF-I treatment significantly reduced insulin concentrations by 80% (p <0.02) and C-peptide levels by 78% (p <0.02), as assessed by area under the curve. Non-esterified fatty acid (NEFA), glycerol and 3-OH-butyrate levels were elevated and alanine concentration decreased. Forearm blood flow rose from 2.10 ± 0.43 (saline) to 2.79 ± 0.37 ml · 100 ml-1 · min-1 (IGF-I) (p <0.02). GH-pulse: 10 h after i.v. GH injection serum GH peaked at 40.9 ± 7.4 ng/ml. GH did not influence circulating levels of total IGF-I, C-peptide, insulin or glucose, but caused a further increase in NEFA, glycerol and 3-OH-butyrate levels, indicating enhanced lipolysis and ketogenesis. This effect of GH was much more pronounced during IGF-I: NEFA rose from 702 ± 267 (saline) and 885 ± 236 (IGF-I) to 963 ± 215 (saline) (p <0.05) and 1815 ± 586 μmol/l (IGF-I) (p <0.02), respectively; after 5 h, 3-OH-butyrate rose from 242 ± 234 (saline) and 340 ± 280 (IGF-I) to 678 ± 638 (saline) (p <0.02) and 1115 ± 578 μmol/l (IGF-I) (p <0.02) respectively. After injection of GH, forearm uptake of 3-OH-butyrate was markedly elevated only in the subjects treated with IGF-I: from 44 ± 195 to 300 ± 370 aftr 20 min (p <0.03) and to 287 ± 91 nmol · 100 ml-1 · min-1 after 120 min (p <0.02). In conclusion, the lipolytic and ketogenic response to GH was grossly enhanced during IGF-I treatment, and utilization of ketone bodies by skeletal muscle was increased.

KW - 'dawn' phenomenon

KW - Energy expenditure

KW - Ketogenesis

KW - Lipolysis

KW - Substrate oxidation

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