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Open Access Research article

Assessment of endogenous insulin secretion in insulin treated diabetes predicts postprandial glucose and treatment response to prandial insulin

Angus G Jones1*, Rachel EJ Besser1, Beverley M Shields1, Timothy J McDonald12, Suzy V Hope1, Bridget A Knight1 and Andrew T Hattersley1

Author Affiliations

1 Peninsula NIHR Clinical Research Facility, Peninsula Medical School, University of Exeter, Exeter, UK

2 Royal Devon and Exeter Hospital, Barrack Road, Exeter, EX2 5DW, UK

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BMC Endocrine Disorders 2012, 12:6  doi:10.1186/1472-6823-12-6

Published: 8 June 2012

Abstract

Background

In patients with both Type 1 and Type 2 diabetes endogenous insulin secretion falls with time which changes treatment requirements, however direct measurement of endogenous insulin secretion is rarely performed. We aimed to assess the impact of endogenous insulin secretion on postprandial glucose increase and the effectiveness of prandial exogenous insulin.

Methods

We assessed endogenous insulin secretion in 102 participants with insulin treated diabetes (58 Type 1) following a standardised mixed meal without exogenous insulin. We tested the relationship between endogenous insulin secretion and post meal hyperglycaemia. In 80 participants treated with fast acting breakfast insulin we repeated the mixed meal with participants’ usual insulin given and assessed the impact of endogenous insulin secretion on response to exogenous prandial insulin.

Results

Post meal glucose increment (90 minute - fasting) was inversely correlated with endogenous insulin secretion (90 minute C-peptide) (Spearman’s r = −0.70, p < 0.001). Similar doses of exogenous prandial insulin lowered glucose increment more when patients had less endogenous insulin; by 6.4(4.2-11.1) verses 1.2(0.03-2.88) mmol/L (p < 0.001) for patients in the lowest verses highest tertiles of endogenous insulin.

Conclusions

In insulin treated patients the measurement of endogenous insulin secretion may help predict the degree of postprandial hyperglycaemia and the likely response to prandial insulin.

Keywords:
Diabetes; C-peptide; Postprandial; Glucose; Insulin