Potentiation of glucose-stimulated insulin release by tolazamide and paradoxical absence of glucose facilitation (Staub effect) in non-insulin-dependent diabetes

Alan Reich, Carlos Abraira, Richard Brunken, Ileana Soneru

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

Acceleration of glucose tolerance after repetitive intravenous glucose loads (Staub-Traugott effect) has not previously been tested in non-insulin-dependent diabetes (NIDDM). Six overt, untreated subjects were administered three hourly IV glucose tolerance tests (GTT). The glucose disappearance rate (K) changed very little between loads, indicating a suppressed Staub effect. However, insulin levels increased with each load. The characterstic loss of early phase insulin release after the first intravenous glucose injection was recovered with the third injection. After four months of tolazamide treatment the fasting plasma glucose fell from 180 ± 19 to 134 ± 13 mg/dL. Despite dramatic potentiation of glucose-stimulated insulin release and further improvement of early phase insulin release, K values again failed to progressively rise. This paradox occurred even in three additional subjects tested after two years of tolazamide treatment, suggesting that tolazamide may not ameliorate the postreceptor defects that impede the expression of the Staub effect. The applicability of the glucose facilitatory effect to the treatment of NIDDM might be limited to subjects in whom adjunctive measures have reestablished effective tissue responsiveness to endogenous insulin.

Original languageEnglish
Pages (from-to)367-370
Number of pages4
JournalMetabolism
Volume35
Issue number4
DOIs
StatePublished - Jan 1 1986

Fingerprint

Tolazamide
Insulin
Glucose
Type 2 Diabetes Mellitus
Glucose Tolerance Test
Intravenous Injections
Fasting
Therapeutics

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism

Cite this

Potentiation of glucose-stimulated insulin release by tolazamide and paradoxical absence of glucose facilitation (Staub effect) in non-insulin-dependent diabetes. / Reich, Alan; Abraira, Carlos; Brunken, Richard; Soneru, Ileana.

In: Metabolism, Vol. 35, No. 4, 01.01.1986, p. 367-370.

Research output: Contribution to journalArticle

@article{e09076d62e0e470ba0d78aa0d14716db,
title = "Potentiation of glucose-stimulated insulin release by tolazamide and paradoxical absence of glucose facilitation (Staub effect) in non-insulin-dependent diabetes",
abstract = "Acceleration of glucose tolerance after repetitive intravenous glucose loads (Staub-Traugott effect) has not previously been tested in non-insulin-dependent diabetes (NIDDM). Six overt, untreated subjects were administered three hourly IV glucose tolerance tests (GTT). The glucose disappearance rate (K) changed very little between loads, indicating a suppressed Staub effect. However, insulin levels increased with each load. The characterstic loss of early phase insulin release after the first intravenous glucose injection was recovered with the third injection. After four months of tolazamide treatment the fasting plasma glucose fell from 180 ± 19 to 134 ± 13 mg/dL. Despite dramatic potentiation of glucose-stimulated insulin release and further improvement of early phase insulin release, K values again failed to progressively rise. This paradox occurred even in three additional subjects tested after two years of tolazamide treatment, suggesting that tolazamide may not ameliorate the postreceptor defects that impede the expression of the Staub effect. The applicability of the glucose facilitatory effect to the treatment of NIDDM might be limited to subjects in whom adjunctive measures have reestablished effective tissue responsiveness to endogenous insulin.",
author = "Alan Reich and Carlos Abraira and Richard Brunken and Ileana Soneru",
year = "1986",
month = "1",
day = "1",
doi = "10.1016/0026-0495(86)90157-5",
language = "English",
volume = "35",
pages = "367--370",
journal = "Metabolism: Clinical and Experimental",
issn = "0026-0495",
publisher = "W.B. Saunders Ltd",
number = "4",

}

TY - JOUR

T1 - Potentiation of glucose-stimulated insulin release by tolazamide and paradoxical absence of glucose facilitation (Staub effect) in non-insulin-dependent diabetes

AU - Reich, Alan

AU - Abraira, Carlos

AU - Brunken, Richard

AU - Soneru, Ileana

PY - 1986/1/1

Y1 - 1986/1/1

N2 - Acceleration of glucose tolerance after repetitive intravenous glucose loads (Staub-Traugott effect) has not previously been tested in non-insulin-dependent diabetes (NIDDM). Six overt, untreated subjects were administered three hourly IV glucose tolerance tests (GTT). The glucose disappearance rate (K) changed very little between loads, indicating a suppressed Staub effect. However, insulin levels increased with each load. The characterstic loss of early phase insulin release after the first intravenous glucose injection was recovered with the third injection. After four months of tolazamide treatment the fasting plasma glucose fell from 180 ± 19 to 134 ± 13 mg/dL. Despite dramatic potentiation of glucose-stimulated insulin release and further improvement of early phase insulin release, K values again failed to progressively rise. This paradox occurred even in three additional subjects tested after two years of tolazamide treatment, suggesting that tolazamide may not ameliorate the postreceptor defects that impede the expression of the Staub effect. The applicability of the glucose facilitatory effect to the treatment of NIDDM might be limited to subjects in whom adjunctive measures have reestablished effective tissue responsiveness to endogenous insulin.

AB - Acceleration of glucose tolerance after repetitive intravenous glucose loads (Staub-Traugott effect) has not previously been tested in non-insulin-dependent diabetes (NIDDM). Six overt, untreated subjects were administered three hourly IV glucose tolerance tests (GTT). The glucose disappearance rate (K) changed very little between loads, indicating a suppressed Staub effect. However, insulin levels increased with each load. The characterstic loss of early phase insulin release after the first intravenous glucose injection was recovered with the third injection. After four months of tolazamide treatment the fasting plasma glucose fell from 180 ± 19 to 134 ± 13 mg/dL. Despite dramatic potentiation of glucose-stimulated insulin release and further improvement of early phase insulin release, K values again failed to progressively rise. This paradox occurred even in three additional subjects tested after two years of tolazamide treatment, suggesting that tolazamide may not ameliorate the postreceptor defects that impede the expression of the Staub effect. The applicability of the glucose facilitatory effect to the treatment of NIDDM might be limited to subjects in whom adjunctive measures have reestablished effective tissue responsiveness to endogenous insulin.

UR - http://www.scopus.com/inward/record.url?scp=0022469616&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0022469616&partnerID=8YFLogxK

U2 - 10.1016/0026-0495(86)90157-5

DO - 10.1016/0026-0495(86)90157-5

M3 - Article

VL - 35

SP - 367

EP - 370

JO - Metabolism: Clinical and Experimental

JF - Metabolism: Clinical and Experimental

SN - 0026-0495

IS - 4

ER -