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Introduction: Glycaemic control is an important predictor of mortality in sepsis. Various international organizations including the Surviving Sepsis campaign recommend glycaemic control in critical illness with a glucose target between 6.1-10 mmol/L. The NICE-SUGARTrial in 2009 was a landmark in the debate over tight versus liberal glycaemic control in the critically ill and subsequent guidelines have been adjusted to reflect a move towards moderate glycaemic control. Methods: We conducted a nationwide study comparing glucose targets used in intensive care units in the United Kingdom in 2007 with those used in 2014 to 2015 to see the impact of the NICE-SUGAR study and subsequent guideline changes. Results: We received a combined response from 81% of intensive care units in the UK. There was an increase in the average median glucose target in 2014/2015 compared with 2007 (7.8 versus 7.2; p < 0.01). However, there is still much variability in glucose targets used in critical care in the UK. Conclusions: There is an overall trend towards using a more moderate glucose target in critical care in the UK reflecting changes in international guidelines. However, it is likely that controversies, which still exist in the literature, are reflected in the variability of glycaemic control targets. It is possible that the advent of closed-loop or continuous glucose monitoring may have a further impact on this.

Islet amyloid polypeptide is a normal constituent of islet Beta cells and is derived from a larger precursor by removal of flanking peptides at the carboxy (C) and amino (N) terminals. The role of these flanking peptides in the formation of amyloid in Type 2 (non-insulin-dependent) diabetes mellitus and in insulinomas is unknown. The C-terminal flanking peptide of islet amyloid polypeptide was localised by immunocytochemistry in human and monkey pancreatic islets from Type 2 diabetic and non-diabetic individuals by use of specific polyclonal antisera. Immunoreactivity for the C-terminal peptide was found in insulin-containing cells in both diabetic and non-diabetic tissue: no antibody binding was detected in islet amyloid of Type 2 diabetic man or of monkeys although a positive reaction occurred with antisera for islet amyloid polypeptide. The C-terminal peptide was localised by immunogold electron microscopy in the insulin granules in both diabetic and non-diabetic individuals but, unlike islet amyloid polypeptide, was not detected in lysosomes. The absence of immunoreactivity for the C-terminal peptide in amyloid suggests that incomplete cleavage of this flanking peptide from islet amyloid polypeptide is not a factor in the formation of islet amyloid.

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