Assessment of endogenous insulin secretion in insulin treated diabetes predicts postprandial glucose and treatment response to prandial insulin
BMC Endocrine Disorders
© Jones et al.; licensee BioMed Central Ltd. 2012. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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.
This project was supported by the Peninsula NIHR Clinical Research Facility and the Peninsula Collaboration for Leadership in Applied Health Research and Care (PenCLAHRC). ATH, BAK and BMS are supported by the Peninsula NIHR Clinical Research Facility. NIHR have supported AGJ, SVH and PB through academic clinical fellowships and AGJ through a doctoral research fellowship. ATH is an NIHR senior investigator. REJB is supported by a Diabetes UK clinical training fellowship. This article presents independent research commissioned by the National Institute for Health Research (NIHR). The views given in this paper do not necessarily represent those of NIHR, the NHS or the Department of Health. We thank all the study volunteers.
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Vol. 12, article 6
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