Failure of glucagon suppression contributes to postprandial hyperglycaemia in IDDM.

Dinneen S, Alzaid A, Turk D, Rizza R

Diabetologia1 Mar 1995Cited by 131 (Europe PMC)

PMID7758881DOI10.1007/bf00400639PepBankPUB-07758881

Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: Publisher copyright. Results still quote short attributed sentences.

Results from this study6

6 results from studies that gave the peptide. 6 results from people.

01HumanNon-randomized trialPharmacokinetics
In IDDM subjects, constant glucagon produced higher concentrations than delayed glucagon during the first 2 h: 108 versus 63 pg/ml.
In plain wordsIn IDDM subjects, constant glucagon produced higher blood glucagon concentrations than delayed glucagon.
Peptide
Glucagon
Outcome
IncreaseGlucagon concentration
Study
n = 9
Comparator
Glucagon started 2 h after glucose ingestion
Outcome group
Pharmacokinetics · Pharmacology
Studied dose
Dose not stated
Measurements
Glucagon concentration
108 pg/ml
constant; +/- 2
Glucagon concentration
63 pg/ml
suppressed; +/- 1
Source sentences
Summary
This resulted in lower (p < 0.001) glucagon concentrations during the first 2 h of the suppressed than during the constant glucagon study days (63 +/- 1 vs 108 +/- 2 pg/ml).
3 context sentences(design, population, supporting numbers)
Summary · context
To determine if, and the mechanism by which, lack of postprandial suppression of glucagon contributes to hyperglycaemia, nine subjects with insulin-dependent diabetes mellitus (IDDM) ingested 50 g of glucose containing both [2-3H] glucose and [6-3H] glucose on two occasions.
Summary · context
[6-14C] glucose, insulin and low-dose somatostatin were infused intravenously at the same rates on both occasions.
Summary · context
A basal glucagon infusion was started either at the same time ("constant glucagon") or 2 h following ("suppressed glucagon") glucose ingestion.
Report a problemFND-0775888101
02HumanNon-randomized trialEfficacy outcome
In IDDM subjects, constant glucagon increased postprandial glucose compared with delayed glucagon: 10.3 versus 8.1 mmol/l.
In plain wordsIn IDDM subjects, constant glucagon produced higher glucose after a meal than delayed glucagon.
Peptide
Glucagon
Outcome
IncreasePostprandial glucose concentration
Study
n = 9
Comparator
Glucagon started 2 h after glucose ingestion
Outcome group
Glycemic control · Metabolic and weight
Studied dose
Dose not stated
Measurements
Postprandial glucose
10.3 mmol/l
constant; +/- 0.9
Postprandial glucose
8.1 mmol/l
suppressed; +/- 0.7
Source sentences
Summary
Lack of suppression of glucagon led to higher (p < 0.01) postprandial glucose concentrations (10.3 +/- 0.9 vs 8.1 +/- 0.7 mmol/l) and a greater (p < 0.02) integrated glycaemic response.
3 context sentences(design, population, supporting numbers)
Summary · context
To determine if, and the mechanism by which, lack of postprandial suppression of glucagon contributes to hyperglycaemia, nine subjects with insulin-dependent diabetes mellitus (IDDM) ingested 50 g of glucose containing both [2-3H] glucose and [6-3H] glucose on two occasions.
Summary · context
[6-14C] glucose, insulin and low-dose somatostatin were infused intravenously at the same rates on both occasions.
Summary · context
A basal glucagon infusion was started either at the same time ("constant glucagon") or 2 h following ("suppressed glucagon") glucose ingestion.
Report a problemFND-0775888102
03HumanNon-randomized trialEfficacy outcome
In IDDM subjects, constant glucagon increased the integrated glycaemic response compared with delayed glucagon.
In plain wordsIn IDDM subjects, constant glucagon increased the overall glucose response compared with delayed glucagon.
Peptide
Glucagon
Outcome
IncreaseIntegrated glycaemic response
Study
n = 9
Comparator
Glucagon started 2 h after glucose ingestion
Outcome group
Glycemic control · Metabolic and weight
Studied dose
Dose not stated
Source sentences
Summary
Lack of suppression of glucagon led to higher (p < 0.01) postprandial glucose concentrations (10.3 +/- 0.9 vs 8.1 +/- 0.7 mmol/l) and a greater (p < 0.02) integrated glycaemic response.
3 context sentences(design, population, supporting numbers)
Summary · context
To determine if, and the mechanism by which, lack of postprandial suppression of glucagon contributes to hyperglycaemia, nine subjects with insulin-dependent diabetes mellitus (IDDM) ingested 50 g of glucose containing both [2-3H] glucose and [6-3H] glucose on two occasions.
Summary · context
[6-14C] glucose, insulin and low-dose somatostatin were infused intravenously at the same rates on both occasions.
Summary · context
A basal glucagon infusion was started either at the same time ("constant glucagon") or 2 h following ("suppressed glucagon") glucose ingestion.
Report a problemFND-0775888103
04HumanNon-randomized trialMechanism
In IDDM subjects, constant glucagon increased hepatic glucose release versus delayed glucagon using the [6-3H] tracer: 2.6 versus 2.0 mmol.kg-1 per 6 h.
In plain wordsIn IDDM subjects, constant glucagon increased liver glucose release compared with delayed glucagon, as measured with the first tracer.
Peptide
Glucagon
Outcome
IncreasePostprandial hepatic glucose release using [6-3H] glucose
Study
n = 9
Comparator
Glucagon started 2 h after glucose ingestion
Outcome group
Glycemic control · Metabolic and weight
Studied dose
Dose not stated
Measurements
Hepatic glucose release
2.6 mmol.kg-1 per 6 h
constant; +/- 0.2
Hepatic glucose release
2 mmol.kg-1 per 6 h
suppressed; +/- 0.2
Source sentences
Summary
The excessive rise in glucose was due to higher (p < 0.02) rates of postprandial hepatic glucose release during the constant than during the suppressed glucagon study days, whether measured using either [6-3H] glucose (2.6 +/- 0.2 vs 2.0 +/- 0.2 mmol.kg-1 per 6 h) or [2-3H] glucose (3.0 +/- 0.3 vs 2…
3 context sentences(design, population, supporting numbers)
Summary · context
To determine if, and the mechanism by which, lack of postprandial suppression of glucagon contributes to hyperglycaemia, nine subjects with insulin-dependent diabetes mellitus (IDDM) ingested 50 g of glucose containing both [2-3H] glucose and [6-3H] glucose on two occasions.
Summary · context
[6-14C] glucose, insulin and low-dose somatostatin were infused intravenously at the same rates on both occasions.
Summary · context
A basal glucagon infusion was started either at the same time ("constant glucagon") or 2 h following ("suppressed glucagon") glucose ingestion.
Report a problemFND-0775888104
05HumanNon-randomized trialMechanism
In IDDM subjects, constant glucagon increased hepatic glucose release versus delayed glucagon using the [2-3H] tracer: 3.0 versus 2.4 mmol.kg-1 per 6 h.
In plain wordsIn IDDM subjects, constant glucagon increased liver glucose release compared with delayed glucagon, as measured with the second tracer.
Peptide
Glucagon
Outcome
IncreasePostprandial hepatic glucose release using [2-3H] glucose
Study
n = 9
Comparator
Glucagon started 2 h after glucose ingestion
Outcome group
Glycemic control · Metabolic and weight
Studied dose
Dose not stated
Measurements
Hepatic glucose release
3 mmol.kg-1 per 6 h
constant; +/- 0.3
Hepatic glucose release
2.4 mmol.kg-1 per 6 h
suppressed; +/- 0.2
Source sentences
Summary
The excessive rise in glucose was due to higher (p < 0.02) rates of postprandial hepatic glucose release during the constant than during the suppressed glucagon study days, whether measured using either [6-3H] glucose (2.6 +/- 0.2 vs 2.0 +/- 0.2 mmol.kg-1 per 6 h) or [2-3H] glucose (3.0 +/- 0.3 vs 2…
3 context sentences(design, population, supporting numbers)
Summary · context
To determine if, and the mechanism by which, lack of postprandial suppression of glucagon contributes to hyperglycaemia, nine subjects with insulin-dependent diabetes mellitus (IDDM) ingested 50 g of glucose containing both [2-3H] glucose and [6-3H] glucose on two occasions.
Summary · context
[6-14C] glucose, insulin and low-dose somatostatin were infused intravenously at the same rates on both occasions.
Summary · context
A basal glucagon infusion was started either at the same time ("constant glucagon") or 2 h following ("suppressed glucagon") glucose ingestion.
Report a problemFND-0775888105
06HumanNon-randomized trialMechanism
In IDDM subjects, glucose disappearance, initial splanchnic glucose clearance and hepatic glucose cycling did not differ between constant and delayed glucagon.
In plain wordsIn IDDM subjects, glucose disappearance, initial abdominal glucose clearance and liver glucose cycling did not differ between constant and delayed glucagon.
Peptide
Glucagon
Outcome
No significant changeGlucose disappearance, initial splanchnic glucose clearance and hepatic glucose cycling
Study
n = 9
Comparator
Glucagon started 2 h after glucose ingestion
Outcome group
Glycemic control · Metabolic and weight
Studied dose
Dose not stated
Source sentences
Summary
Glucose disappearance, initial splanchnic glucose clearance and hepatic glucose cycling did not differ on the two occasions.
3 context sentences(design, population, supporting numbers)
Summary · context
To determine if, and the mechanism by which, lack of postprandial suppression of glucagon contributes to hyperglycaemia, nine subjects with insulin-dependent diabetes mellitus (IDDM) ingested 50 g of glucose containing both [2-3H] glucose and [6-3H] glucose on two occasions.
Summary · context
[6-14C] glucose, insulin and low-dose somatostatin were infused intravenously at the same rates on both occasions.
Summary · context
A basal glucagon infusion was started either at the same time ("constant glucagon") or 2 h following ("suppressed glucagon") glucose ingestion.
Report a problemFND-0775888106

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

Version 2Current
28 Oct 2026, 02:03 UTC
Study results updated
Version 1
27 Oct 2026, 16:35 UTC
First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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