Insulin action in uremia

Ralph A Defronzo, D. Smith, A. Alvestrand

Research output: Contribution to journalArticle

70 Citations (Scopus)

Abstract

The evidence appears overwhelming that insulin resistance is the major cause of the carbohydrate intolerance observed in chronically uremic subjects and that the primary site of this insulin resistance resides in peripheral tissues, muscle. Diminished lipoprotein lipase activity, perhaps related to decreased insulin sensitivity, is in large part responsible for the hypertriglyceridemia. However, there is some evidence that increased VLDL-synthesis also contributes to the disturbance in lipid metabolism. This latter abnormality may be related to the high circulating insulin levels that result from the insulin resistance. In contrast to glucose and lipid metabolism, the plasma amino acid and potassium lowering effects of insulin are normal in uremic individuals. Whether there is an impaired ability of insulin to stimulate protein synthesis and inhibit protein degradation remains to be delineated.

Original languageEnglish (US)
JournalKidney International
Volume24
Issue numberSUPPL. 16
StatePublished - 1983
Externally publishedYes

Fingerprint

Uremia
Insulin Resistance
Insulin
Lipid Metabolism
Lipoprotein Lipase
Hypertriglyceridemia
Proteolysis
Potassium
Amino Acids
Glucose
Muscles
Proteins

ASJC Scopus subject areas

  • Nephrology

Cite this

Defronzo, R. A., Smith, D., & Alvestrand, A. (1983). Insulin action in uremia. Kidney International, 24(SUPPL. 16).

Insulin action in uremia. / Defronzo, Ralph A; Smith, D.; Alvestrand, A.

In: Kidney International, Vol. 24, No. SUPPL. 16, 1983.

Research output: Contribution to journalArticle

Defronzo, RA, Smith, D & Alvestrand, A 1983, 'Insulin action in uremia', Kidney International, vol. 24, no. SUPPL. 16.
Defronzo RA, Smith D, Alvestrand A. Insulin action in uremia. Kidney International. 1983;24(SUPPL. 16).
Defronzo, Ralph A ; Smith, D. ; Alvestrand, A. / Insulin action in uremia. In: Kidney International. 1983 ; Vol. 24, No. SUPPL. 16.
@article{645fe4e5a9324d069b3ad543fc1dff80,
title = "Insulin action in uremia",
abstract = "The evidence appears overwhelming that insulin resistance is the major cause of the carbohydrate intolerance observed in chronically uremic subjects and that the primary site of this insulin resistance resides in peripheral tissues, muscle. Diminished lipoprotein lipase activity, perhaps related to decreased insulin sensitivity, is in large part responsible for the hypertriglyceridemia. However, there is some evidence that increased VLDL-synthesis also contributes to the disturbance in lipid metabolism. This latter abnormality may be related to the high circulating insulin levels that result from the insulin resistance. In contrast to glucose and lipid metabolism, the plasma amino acid and potassium lowering effects of insulin are normal in uremic individuals. Whether there is an impaired ability of insulin to stimulate protein synthesis and inhibit protein degradation remains to be delineated.",
author = "Defronzo, {Ralph A} and D. Smith and A. Alvestrand",
year = "1983",
language = "English (US)",
volume = "24",
journal = "Kidney International",
issn = "0085-2538",
publisher = "Nature Publishing Group",
number = "SUPPL. 16",

}

TY - JOUR

T1 - Insulin action in uremia

AU - Defronzo, Ralph A

AU - Smith, D.

AU - Alvestrand, A.

PY - 1983

Y1 - 1983

N2 - The evidence appears overwhelming that insulin resistance is the major cause of the carbohydrate intolerance observed in chronically uremic subjects and that the primary site of this insulin resistance resides in peripheral tissues, muscle. Diminished lipoprotein lipase activity, perhaps related to decreased insulin sensitivity, is in large part responsible for the hypertriglyceridemia. However, there is some evidence that increased VLDL-synthesis also contributes to the disturbance in lipid metabolism. This latter abnormality may be related to the high circulating insulin levels that result from the insulin resistance. In contrast to glucose and lipid metabolism, the plasma amino acid and potassium lowering effects of insulin are normal in uremic individuals. Whether there is an impaired ability of insulin to stimulate protein synthesis and inhibit protein degradation remains to be delineated.

AB - The evidence appears overwhelming that insulin resistance is the major cause of the carbohydrate intolerance observed in chronically uremic subjects and that the primary site of this insulin resistance resides in peripheral tissues, muscle. Diminished lipoprotein lipase activity, perhaps related to decreased insulin sensitivity, is in large part responsible for the hypertriglyceridemia. However, there is some evidence that increased VLDL-synthesis also contributes to the disturbance in lipid metabolism. This latter abnormality may be related to the high circulating insulin levels that result from the insulin resistance. In contrast to glucose and lipid metabolism, the plasma amino acid and potassium lowering effects of insulin are normal in uremic individuals. Whether there is an impaired ability of insulin to stimulate protein synthesis and inhibit protein degradation remains to be delineated.

UR - http://www.scopus.com/inward/record.url?scp=0020913209&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0020913209&partnerID=8YFLogxK

M3 - Article

VL - 24

JO - Kidney International

JF - Kidney International

SN - 0085-2538

IS - SUPPL. 16

ER -