Experimentally induced acute hyperinsulinemia stimulates endogenous nitric oxide production in humans

Detection using urinary NO2-/NO3- excretion

Hirokazu Tsukahara, Kiyoshi Kikuchi, Kumi Tsumura, Kouki Kimura, Ikue Hata, Masahiro Hiraoka, Masakatsu Sudo

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

Insulin-mediated glucose metabolism in skeletal muscle is associated with a proportional increase in muscle perfusion. The vasodilatory effect of insulin is thought to be mediated in part by endothelium-derived nitric oxide (NO). The present study was performed to determine whether acute hyperinsulinemia has any stimulatory effect on endogenous NO production in humans. Bolus intravenous injection of insulin (0.1 IU/kg body weight) caused a significant increase in urinary excretion of NO2-/NO3-together with s significant decrease in blood pressure, whereas saline infusion alone had no effect on these parameters. The increased NO response to insulin was almost comparable to that obtained with infusion of 30 g L-arginine. The acute effect of hyperinsulinemia on endogenous NO formation supports the concept that NO may mediate the vasodilatory action of insulin in humans.

Original languageEnglish
Pages (from-to)406-409
Number of pages4
JournalMetabolism: Clinical and Experimental
Volume46
Issue number4
DOIs
Publication statusPublished - 1997
Externally publishedYes

Fingerprint

Hyperinsulinism
Nitric Oxide
Insulin
Concept Formation
Intravenous Injections
Arginine
Skeletal Muscle
Perfusion
Body Weight
Blood Pressure
Glucose
Muscles

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism

Cite this

Experimentally induced acute hyperinsulinemia stimulates endogenous nitric oxide production in humans : Detection using urinary NO2-/NO3- excretion. / Tsukahara, Hirokazu; Kikuchi, Kiyoshi; Tsumura, Kumi; Kimura, Kouki; Hata, Ikue; Hiraoka, Masahiro; Sudo, Masakatsu.

In: Metabolism: Clinical and Experimental, Vol. 46, No. 4, 1997, p. 406-409.

Research output: Contribution to journalArticle

Tsukahara, Hirokazu ; Kikuchi, Kiyoshi ; Tsumura, Kumi ; Kimura, Kouki ; Hata, Ikue ; Hiraoka, Masahiro ; Sudo, Masakatsu. / Experimentally induced acute hyperinsulinemia stimulates endogenous nitric oxide production in humans : Detection using urinary NO2-/NO3- excretion. In: Metabolism: Clinical and Experimental. 1997 ; Vol. 46, No. 4. pp. 406-409.
@article{370ded3cc10f45f5a5536c5ea6ab1a75,
title = "Experimentally induced acute hyperinsulinemia stimulates endogenous nitric oxide production in humans: Detection using urinary NO2-/NO3- excretion",
abstract = "Insulin-mediated glucose metabolism in skeletal muscle is associated with a proportional increase in muscle perfusion. The vasodilatory effect of insulin is thought to be mediated in part by endothelium-derived nitric oxide (NO). The present study was performed to determine whether acute hyperinsulinemia has any stimulatory effect on endogenous NO production in humans. Bolus intravenous injection of insulin (0.1 IU/kg body weight) caused a significant increase in urinary excretion of NO2-/NO3-together with s significant decrease in blood pressure, whereas saline infusion alone had no effect on these parameters. The increased NO response to insulin was almost comparable to that obtained with infusion of 30 g L-arginine. The acute effect of hyperinsulinemia on endogenous NO formation supports the concept that NO may mediate the vasodilatory action of insulin in humans.",
author = "Hirokazu Tsukahara and Kiyoshi Kikuchi and Kumi Tsumura and Kouki Kimura and Ikue Hata and Masahiro Hiraoka and Masakatsu Sudo",
year = "1997",
doi = "10.1016/S0026-0495(97)90056-1",
language = "English",
volume = "46",
pages = "406--409",
journal = "Metabolism: Clinical and Experimental",
issn = "0026-0495",
publisher = "W.B. Saunders Ltd",
number = "4",

}

TY - JOUR

T1 - Experimentally induced acute hyperinsulinemia stimulates endogenous nitric oxide production in humans

T2 - Detection using urinary NO2-/NO3- excretion

AU - Tsukahara, Hirokazu

AU - Kikuchi, Kiyoshi

AU - Tsumura, Kumi

AU - Kimura, Kouki

AU - Hata, Ikue

AU - Hiraoka, Masahiro

AU - Sudo, Masakatsu

PY - 1997

Y1 - 1997

N2 - Insulin-mediated glucose metabolism in skeletal muscle is associated with a proportional increase in muscle perfusion. The vasodilatory effect of insulin is thought to be mediated in part by endothelium-derived nitric oxide (NO). The present study was performed to determine whether acute hyperinsulinemia has any stimulatory effect on endogenous NO production in humans. Bolus intravenous injection of insulin (0.1 IU/kg body weight) caused a significant increase in urinary excretion of NO2-/NO3-together with s significant decrease in blood pressure, whereas saline infusion alone had no effect on these parameters. The increased NO response to insulin was almost comparable to that obtained with infusion of 30 g L-arginine. The acute effect of hyperinsulinemia on endogenous NO formation supports the concept that NO may mediate the vasodilatory action of insulin in humans.

AB - Insulin-mediated glucose metabolism in skeletal muscle is associated with a proportional increase in muscle perfusion. The vasodilatory effect of insulin is thought to be mediated in part by endothelium-derived nitric oxide (NO). The present study was performed to determine whether acute hyperinsulinemia has any stimulatory effect on endogenous NO production in humans. Bolus intravenous injection of insulin (0.1 IU/kg body weight) caused a significant increase in urinary excretion of NO2-/NO3-together with s significant decrease in blood pressure, whereas saline infusion alone had no effect on these parameters. The increased NO response to insulin was almost comparable to that obtained with infusion of 30 g L-arginine. The acute effect of hyperinsulinemia on endogenous NO formation supports the concept that NO may mediate the vasodilatory action of insulin in humans.

UR - http://www.scopus.com/inward/record.url?scp=0030901426&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0030901426&partnerID=8YFLogxK

U2 - 10.1016/S0026-0495(97)90056-1

DO - 10.1016/S0026-0495(97)90056-1

M3 - Article

VL - 46

SP - 406

EP - 409

JO - Metabolism: Clinical and Experimental

JF - Metabolism: Clinical and Experimental

SN - 0026-0495

IS - 4

ER -