SUMMARYIn passing from islets to the exocrine part of the gland, pancreatic capillaries change their character. Islet capillaries are significantly wider than exocrine (5 27 ,tm, diameter compared with 4 35 jsm), thinner walled and have many more fenestrations tm-' of endothelium (1 3 compared with 0 13). The point of transition at the edge of the islet is very abrupt, for capillaries that are in contact with both endocrine and exocrine tissue ('edge capillaries') have significantly more fenestrae on the side facing the endocrine cells than the side facing exocrine (1-46 fenestrae um-1 compared with 0 3 ,um-1). The structure of these edge capillaries suggests that the factors operating to induce the formation of fenestrae do so over extremely short distances. The relationship between fenestrations, the high blood flow and high water flux seen in endocrine glands is discussed.

Objective: Glucagon and glucagon-like peptide-1 (GLP-1) originate from the common precursor, proglucagon, and their plasma concentrations have been reported to be increased during inflammatory conditions. Increased blood glucose levels are frequently observed in septic patients, and therefore we hypothesized that glucagon, but not GLP-1, is increased in individuals with inflammation. Design: Prospective longitudinal cohort study. Materials and Methods: We measured glucagon and GLP-1 in plasma sampled consecutively in three cohorts consisting of patients with infective endocarditis (n=16), urosepsis (n=28) and post-operative inflammation following percutaneous aortic valve implantation or thoracic endovascular aortic repair (n=5). Correlations between C-Reactive Protein (CRP), a marker of systemic inflammation, and glucagon and GLP-1 concentrations were investigated. Additionally, glucagon and GLP-1 concentrations were measured after a bolus infusion of lipopolysaccharide (LPS, 1ng/kg) in nine healthy young males. Results: Glucagon and CRP were positively and significantly correlated (r=0.27; P=0.0003), whereas no significant association between GLP-1 and CRP was found (r=0.08, P=0.30). LPS infusion resulted in acute systemic inflammation reflected by increased temperature, pulse, tumor necrosis factor-α (TNFα), interleukin-6 (IL-6) and concomitantly increased concentrations of glucagon (P<0.05) but not GLP-1. Conclusions :Systemic inflammation caused by bacterial infections or developed as a non-infected condition is associated with increased plasma concentration of glucagon, but not GLP-1. Hyperglucagonemia may contribute to the impaired glucose control in patients with systemic inflammatory diseases.

Glucagon, the hyperglycaemic glycogenolytic factor of the pancreas, was discovered by Kimball and Murlin in 1923 (1). It was crystallized by Staub, Sinn and Behrens in 1953 (2, 3). Glucagon is believed to cause a rise in blood sugar by acting at the site of liver Phosphorylase—converting inactive Phosphorylase to active Phosphorylase (4).