Extremity hyperinsulinemia stimulates muscle protein synthesis in severely injured patients

Dennis Gore, Steven Wolf, Arthur P. Sanford, David Herndon, Robert R. Wolfe

Research output: Contribution to journalArticle

54 Citations (Scopus)

Abstract

Insulin has a well-recognized anabolic effect on muscle protein, yet critically ill, severely injured patients are often considered "resistant" to the action of insulin. The purpose of this study was to assess the in vivo effects of hyperinsulinemia on human skeletal muscle in severely injured patients. To accomplish this goal, 14 patients with burns encompassing >40% of their body surface area underwent metabolic evaluation utilizing isotopic dilution of phenylalanine, femoral artery and vein blood sampling, and sequential muscle biopsies of the leg. After baseline metabolic measurements were taken, insulin was infused into the femoral artery at 0.45 mIU·min-1·100 ml leg volume-1 to create a local hyperinsulinemia but with minimal systemic perturbations. Insulin administration increased femoral venous concentration of insulin (P < 0.01) but with only a 4% (insignificant) decrease in the arterial glucose concentration and a 7% (insignificant) decrease in the arterial concentration of phenylalanine. Extremity hyperinsulinemia significantly increased leg blood flow (P < 0.05) and the rate of muscle protein synthesis (P < 0.05). Neither the rate of muscle protein breakdown nor the rate of transmembrane transport of phenylalanine was significantly altered with extremity hyperinsulinemia. In conclusion, this study demonstrates that insulin directly stimulates muscle protein synthesis in severely injured patients.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Endocrinology and Metabolism
Volume286
Issue number4 49-4
DOIs
StatePublished - Apr 2004

Fingerprint

Muscle Proteins
Hyperinsulinism
Extremities
Insulin
Phenylalanine
Leg
Femoral Artery
Muscle
Blood
Anabolic Agents
Femoral Vein
Biopsy
Body Surface Area
Thigh
Burns
Critical Illness
Dilution
Skeletal Muscle
Sampling
Glucose

Keywords

  • Burns
  • Critical illness
  • Hypermetabolic response
  • Insulin resistance
  • Muscle catabolism
  • Phenylalanine

ASJC Scopus subject areas

  • Physiology
  • Endocrinology
  • Biochemistry

Cite this

Extremity hyperinsulinemia stimulates muscle protein synthesis in severely injured patients. / Gore, Dennis; Wolf, Steven; Sanford, Arthur P.; Herndon, David; Wolfe, Robert R.

In: American Journal of Physiology - Endocrinology and Metabolism, Vol. 286, No. 4 49-4, 04.2004.

Research output: Contribution to journalArticle

@article{6657f853367d4187868d87ae3833ee38,
title = "Extremity hyperinsulinemia stimulates muscle protein synthesis in severely injured patients",
abstract = "Insulin has a well-recognized anabolic effect on muscle protein, yet critically ill, severely injured patients are often considered {"}resistant{"} to the action of insulin. The purpose of this study was to assess the in vivo effects of hyperinsulinemia on human skeletal muscle in severely injured patients. To accomplish this goal, 14 patients with burns encompassing >40{\%} of their body surface area underwent metabolic evaluation utilizing isotopic dilution of phenylalanine, femoral artery and vein blood sampling, and sequential muscle biopsies of the leg. After baseline metabolic measurements were taken, insulin was infused into the femoral artery at 0.45 mIU·min-1·100 ml leg volume-1 to create a local hyperinsulinemia but with minimal systemic perturbations. Insulin administration increased femoral venous concentration of insulin (P < 0.01) but with only a 4{\%} (insignificant) decrease in the arterial glucose concentration and a 7{\%} (insignificant) decrease in the arterial concentration of phenylalanine. Extremity hyperinsulinemia significantly increased leg blood flow (P < 0.05) and the rate of muscle protein synthesis (P < 0.05). Neither the rate of muscle protein breakdown nor the rate of transmembrane transport of phenylalanine was significantly altered with extremity hyperinsulinemia. In conclusion, this study demonstrates that insulin directly stimulates muscle protein synthesis in severely injured patients.",
keywords = "Burns, Critical illness, Hypermetabolic response, Insulin resistance, Muscle catabolism, Phenylalanine",
author = "Dennis Gore and Steven Wolf and Sanford, {Arthur P.} and David Herndon and Wolfe, {Robert R.}",
year = "2004",
month = "4",
doi = "10.1152/ajpendo.00258.2003",
language = "English (US)",
volume = "286",
journal = "American Journal of Physiology - Endocrinology and Metabolism",
issn = "0193-1849",
publisher = "American Physiological Society",
number = "4 49-4",

}

TY - JOUR

T1 - Extremity hyperinsulinemia stimulates muscle protein synthesis in severely injured patients

AU - Gore, Dennis

AU - Wolf, Steven

AU - Sanford, Arthur P.

AU - Herndon, David

AU - Wolfe, Robert R.

PY - 2004/4

Y1 - 2004/4

N2 - Insulin has a well-recognized anabolic effect on muscle protein, yet critically ill, severely injured patients are often considered "resistant" to the action of insulin. The purpose of this study was to assess the in vivo effects of hyperinsulinemia on human skeletal muscle in severely injured patients. To accomplish this goal, 14 patients with burns encompassing >40% of their body surface area underwent metabolic evaluation utilizing isotopic dilution of phenylalanine, femoral artery and vein blood sampling, and sequential muscle biopsies of the leg. After baseline metabolic measurements were taken, insulin was infused into the femoral artery at 0.45 mIU·min-1·100 ml leg volume-1 to create a local hyperinsulinemia but with minimal systemic perturbations. Insulin administration increased femoral venous concentration of insulin (P < 0.01) but with only a 4% (insignificant) decrease in the arterial glucose concentration and a 7% (insignificant) decrease in the arterial concentration of phenylalanine. Extremity hyperinsulinemia significantly increased leg blood flow (P < 0.05) and the rate of muscle protein synthesis (P < 0.05). Neither the rate of muscle protein breakdown nor the rate of transmembrane transport of phenylalanine was significantly altered with extremity hyperinsulinemia. In conclusion, this study demonstrates that insulin directly stimulates muscle protein synthesis in severely injured patients.

AB - Insulin has a well-recognized anabolic effect on muscle protein, yet critically ill, severely injured patients are often considered "resistant" to the action of insulin. The purpose of this study was to assess the in vivo effects of hyperinsulinemia on human skeletal muscle in severely injured patients. To accomplish this goal, 14 patients with burns encompassing >40% of their body surface area underwent metabolic evaluation utilizing isotopic dilution of phenylalanine, femoral artery and vein blood sampling, and sequential muscle biopsies of the leg. After baseline metabolic measurements were taken, insulin was infused into the femoral artery at 0.45 mIU·min-1·100 ml leg volume-1 to create a local hyperinsulinemia but with minimal systemic perturbations. Insulin administration increased femoral venous concentration of insulin (P < 0.01) but with only a 4% (insignificant) decrease in the arterial glucose concentration and a 7% (insignificant) decrease in the arterial concentration of phenylalanine. Extremity hyperinsulinemia significantly increased leg blood flow (P < 0.05) and the rate of muscle protein synthesis (P < 0.05). Neither the rate of muscle protein breakdown nor the rate of transmembrane transport of phenylalanine was significantly altered with extremity hyperinsulinemia. In conclusion, this study demonstrates that insulin directly stimulates muscle protein synthesis in severely injured patients.

KW - Burns

KW - Critical illness

KW - Hypermetabolic response

KW - Insulin resistance

KW - Muscle catabolism

KW - Phenylalanine

UR - http://www.scopus.com/inward/record.url?scp=1642330098&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=1642330098&partnerID=8YFLogxK

U2 - 10.1152/ajpendo.00258.2003

DO - 10.1152/ajpendo.00258.2003

M3 - Article

VL - 286

JO - American Journal of Physiology - Endocrinology and Metabolism

JF - American Journal of Physiology - Endocrinology and Metabolism

SN - 0193-1849

IS - 4 49-4

ER -