Basal plasma insulin levels exert a qualitative but not quantitative effect on glucose-mediated glucose uptake

S. Del Prato, A. Riccio, S. V. De Kreutzenberg, M. Dorella, A. Tiengo, Ralph A Defronzo

Research output: Contribution to journalArticle

22 Citations (Scopus)

Abstract

We assessed the effect of hyperglycemia on glucose uptake in the presence of normal basal insulin levels or somatostatin-induced hypoinsulinemia in seven normal volunteers during a 200-min hyperglycemic clamp (+9 mmol/l) carried out with [3-3H]glucose and indirect calorimetry. Hyperglycemia increased glucose uptake to 22.4 ± 2.6 and 21.3 ± 1.6 μmol · kg-1 · min-1 with and without insulin replacement, respectively. Normoinsulinemia increased glucose oxidation (Δ = +4.5 ± 0.6 μmol · kg-1 · min-1) and nonoxidative glucose metabolism (Δ = +5.2 ± 1.7 μmol · kg-1 · min- 1), whereas with insulinopenia, glucose oxidation did not change (Δ = -0.3 ± 0.6 μmol · kg -1 · min-1), and nonoxidative glucose metabolism increased (Δ = +8.7 ± 0.8 μmol · kg-1 · min-1). Nonoxidative glucose metabolism was higher during insulinopenic (13.5 ± 1.8 μmol · kg-1 · min-1) than normoinsulinemic hyperglycemia (9.8 ± 2.7 μmol · kg-1 min-1; p < 0.01). Plasma FFA concentration and lipid oxidation were higher with insulinopenia. Blood lactate and alanine concentrations were greater with normoinsulinemia. In conclusion: 1) hyperglycemia promotes glucose uptake by stimulating both nonoxidative and oxidative glucose disposal; 2) the ability of hyperglycemia to enhance total body glucose uptake is similar with and without normoinsulinemia; 3) although acute insulinopenia does not impair the ability of hyperglycemia to stimulate glucose uptake, it plays a critical role in determining the intracellular metabolic fate of glucose taken up in response to hyperglycemia.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Endocrinology and Metabolism
Volume268
Issue number6 31-6
StatePublished - 1995
Externally publishedYes

Fingerprint

insulin
Insulin
uptake mechanisms
Plasmas
Glucose
glucose
hyperglycemia
Hyperglycemia
Metabolism
Oxidation
metabolism
oxidation
Indirect Calorimetry
somatostatin
Clamping devices
calorimetry
Calorimetry
Somatostatin
Alanine
alanine

Keywords

  • glycolysis
  • hyperglycemia
  • insulinopenia
  • intermediary metabolism

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology
  • Physiology
  • Agricultural and Biological Sciences(all)

Cite this

Basal plasma insulin levels exert a qualitative but not quantitative effect on glucose-mediated glucose uptake. / Del Prato, S.; Riccio, A.; De Kreutzenberg, S. V.; Dorella, M.; Tiengo, A.; Defronzo, Ralph A.

In: American Journal of Physiology - Endocrinology and Metabolism, Vol. 268, No. 6 31-6, 1995.

Research output: Contribution to journalArticle

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N2 - We assessed the effect of hyperglycemia on glucose uptake in the presence of normal basal insulin levels or somatostatin-induced hypoinsulinemia in seven normal volunteers during a 200-min hyperglycemic clamp (+9 mmol/l) carried out with [3-3H]glucose and indirect calorimetry. Hyperglycemia increased glucose uptake to 22.4 ± 2.6 and 21.3 ± 1.6 μmol · kg-1 · min-1 with and without insulin replacement, respectively. Normoinsulinemia increased glucose oxidation (Δ = +4.5 ± 0.6 μmol · kg-1 · min-1) and nonoxidative glucose metabolism (Δ = +5.2 ± 1.7 μmol · kg-1 · min- 1), whereas with insulinopenia, glucose oxidation did not change (Δ = -0.3 ± 0.6 μmol · kg -1 · min-1), and nonoxidative glucose metabolism increased (Δ = +8.7 ± 0.8 μmol · kg-1 · min-1). Nonoxidative glucose metabolism was higher during insulinopenic (13.5 ± 1.8 μmol · kg-1 · min-1) than normoinsulinemic hyperglycemia (9.8 ± 2.7 μmol · kg-1 min-1; p < 0.01). Plasma FFA concentration and lipid oxidation were higher with insulinopenia. Blood lactate and alanine concentrations were greater with normoinsulinemia. In conclusion: 1) hyperglycemia promotes glucose uptake by stimulating both nonoxidative and oxidative glucose disposal; 2) the ability of hyperglycemia to enhance total body glucose uptake is similar with and without normoinsulinemia; 3) although acute insulinopenia does not impair the ability of hyperglycemia to stimulate glucose uptake, it plays a critical role in determining the intracellular metabolic fate of glucose taken up in response to hyperglycemia.

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