An additional bolus of rapid-acting insulin to normalise postprandial cardiovascular risk factors following a high-carbohydrate high-fat meal in patients with type 1 diabetes: A randomised controlled trial.
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.



A total of 10 males with type 1 diabetes [HbA1c52.5 ± 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.



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.



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.
1 Institute for Sport, Physical Activity & Leisure, Leeds Beckett University, Leeds, UK.|2 Multidisciplinary Cardiovascular Research Centre, University of Leeds, Leeds, UK.
Matthew D
MD
Campbell
3 Human Nutrition Research Centre, Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, UK.
Mark
M
Walker
2 Multidisciplinary Cardiovascular Research Centre, University of Leeds, Leeds, UK.
Ramzi A
RA
Ajjan
2 Multidisciplinary Cardiovascular Research Centre, University of Leeds, Leeds, UK.
Karen M
KM
Birch
4 Department for Health, University of Bath, Bath, UK.
Javier T
JT
Gonzalez
3 Human Nutrition Research Centre, Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, UK.
Daniel J
DJ
West
D000328:Adult; D015415:Biomarkers / Q000097:blood; D001777:Blood Coagulation / Q000187:drug effects; D001786:Blood Glucose / Q000187:drug effects* / Q000378:metabolism; D002318:Cardiovascular Diseases / Q000097:blood / Q000175:diagnosis / Q000209:etiology / Q000517:prevention & control*; D003922:Diabetes Mellitus, Type 1 / Q000097:blood / Q000150:complications / Q000175:diagnosis / Q000188:drug therapy*; D059305:Diet, High-Fat; D004040:Dietary Carbohydrates / Q000008:administration & dosage / Q000378:metabolism*; D004041:Dietary Fats / Q000008:administration & dosage / Q000378:metabolism*; D004739:England; D006801:Humans; D007004:Hypoglycemic Agents / Q000008:administration & dosage*; D018836:Inflammation Mediators / Q000097:blood; D000069057:Insulin Detemir / Q000008:administration & dosage*; D000069036:Insulin Glargine / Q000008:administration & dosage*; D008297:Male; D062407:Meals; D019518:Postprandial Period; D012307:Risk Factors; D013997:Time Factors; D016896:Treatment Outcome; D014280:Triglycerides / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D055815:Young Adult
D015415:Biomarkers; D001786:Blood Glucose; D004040:Dietary Carbohydrates; D004041:Dietary Fats; D007004:Hypoglycemic Agents; D018836:Inflammation Mediators; D014280:Triglycerides; D014409:Tumor Necrosis Factor-alpha; D000069036:Insulin Glargine; D000069057:Insulin Detemir
Type 1 diabetes; cardiovascular risk; high-fat feeding; inflammation; lipaemia