Aim:To evaluate an additional rapid-acting insulin bolus on postprandial lipaemia, inflammation and pro-coagulation following high-carbohydrate high-fat feeding in people with type 1 diabetes. Methods: A total of 10 males with type 1 diabetes [HbA 1c 52.5 ± 5.9 mmol/mol (7.0% ± 0.5%)] underwent three conditions: (1) a low-fat (LF) meal with normal bolus insulin, (2), a high-fat (HF) meal with normal bolus insulin and (3) a high-fat meal with normal bolus insulin with an additional 30% insulin bolus administered 3-h post-meal (HFA). Meals had identical carbohydrate and protein content and bolus insulin dose determined by carbohydrate-counting. Blood was sampled periodically for 6-h post-meal and analysed for triglyceride, non-esterified-fatty acids, apolipoprotein B48, glucagon, tumour necrosis factor alpha, fibrinogen, human tissue factor activity and plasminogen activator inhibitor-1. Continuous glucose monitoring captured interstitial glucose responses. Results: Triglyceride concentrations following LF remained similar to baseline, whereas triglyceride levels following HF were significantly greater throughout the 6-h observation period. The additional insulin bolus (HFA) normalised triglyceride similarly to low fat 3-6 h following the meal. HF was associated with late postprandial elevations in tumour necrosis factor alpha, whereas LF and HFA was not. Fibrinogen, plasminogen activator inhibitor-1 and tissue factor pathway levels were similar between conditions. Conclusion: Additional bolus insulin 3 h following a high-carbohydrate high-fat meal prevents late rises in postprandial triglycerides and tumour necrosis factor alpha, thus improving cardiovascular risk profile.

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The purpose of the present study was to examine whether the expression of capillary-derived appetite peptides accurately reflects concentrations of their venous equivalents. Fingertip capillary (2×0.3 mL) and venous blood samples (2×4 mL) were collected simultaneously from 19 healthy adult volunteers [mean age 24.1 (SD 5.7) years, body mass 73.7 (SD 10.9) kg;], for determination of acylated ghrelin, GLP-17–36, glucagon, insulin and leptin. Samples were obtained at baseline (t=0 min) and at 30, 60, 90 and 120 min following consumption of a standardised breakfast. Bland-Altman plots were constructed with their 95% limits of agreement and confidence intervals. All analysis was computed using time-averaged area under the curve data (AUC). Where data were heteroscedastic, data were log transformed and reported as ratio limits of agreement (LOA). With the exception of acylated ghrelin (r2=0.51), venous and capillary blood samples displayed strong correlations between all hormonal peptides (r2≥0.84). GLP-17–36 and glucagon illustrated no systematic difference between capillary and venous blood samples (0.44±0.63 and −0.19±7.63 pg·mL−1, respectively). Capillary leptin, acylated ghrelin and insulin, on average, underestimated their venous equivalents. Mean log transformed ratio LOA for leptin, insulin and acylated ghrelin were 0.89 (1.19), 0.82 (1.79) and 0.44 (3.12), respectively. Fingertip capillary blood sampling appears appropriate in appetite-related research. Further research is warranted to clarify the acceptability of capillary sampling in lieu of venous blood sampling for the determination appetite peptides.