Insulin Modulates Early-Phase Noradrenaline Response to Glucose Ingestion in Humans

Summary

To clarify the relationship between the early-phase insulin response and the early-phase noradrenaline (NA) response to glucose ingestion in humans, serum NA, adrenaline, immunoreactive insulin (IRI), C-peptide immunoreactivity, potassium, nonesterified fatty acid and plasma glucose levels were measured in 8 non-diabetics and 10 diabetics without autonomic disturbance after oral 75 g glucose load.

Following results were obtained:

1) In non-diabetics, the maximal NA response was observed at 30 min after glucose ingestion, but in diabetics, mean serum NA levels remained unchanged. The effect of glucose ingestion on the NA response was significantly different between non-diabetics and diabetics by the repeated measurements analysis of variance (F ratio = 5.72, P < 0.05).

2) In total group (n=18), at early-phase after glucose ingestion (at 30 min), positive correlation was found between dIRI level and dNA level (r=0.52, P < 0.05), between dIRI level and %dNA level (r=0.56, P < 0.05), between dIRI/dglucose ratio (insulinogenic index) and dNA level (r=0.70, P < 0.01).

3) In four diabetics, NA responses to glucose ingestion were studied again after mild energy restriction for 2 wk. In three of them, both early-phase IRI response and early-phase NA response to glucose ingestion improved after diet therapy, but in the remainder, early-phase NA response to glucose ingestion remained unchanged in accordance with sustained impaired early-phase insulin response to glucose ingestion.

It is suggested that insulin modulates early-phase NA response to glucose ingestion and that the increase in NA levels after glucose ingestion is to control the release of insulin from the pancreatic islets by the central negative feedback mechanism in humans, although its precise mechanism awaits further investigation.

Key-Words

Glucose Ingestion - Insulin - Noradrenaline - Central Negative Feedback Mechanism