Cephalic phase of insulin secretion in response to a meal is unrelated to family history of type 2 diabetes

PLoS One. 2017 Mar 13;12(3):e0173654. doi: 10.1371/journal.pone.0173654. eCollection 2017.

Abstract

The pre-absorptive cephalic phase of insulin secretion is elicited during the first ten min of a meal and before glucose levels rise. Its importance for insulin release during the post-absorptive phase has been well documented in animals but its presence or importance in man has become increasingly controversial. We here examined the presence of an early cephalic phase of insulin release in 31 well matched individuals without (n = 15) or with (n = 16) a known family history of type 2 diabetes (first-degree relatives; FDR). We also examined the potential differences in individuals with or without impaired fasting (IFG) and impaired glucose tolerance (IGT). We here demonstrate that a cephalic phase of insulin secretion was present in all individuals examined and without any differences between control persons and FDR or IFG/IGT. However, the overall importance of the cephalic phase is conjectural since it was unrelated to the subsequent post-absorptive insulin release or glucose tolerance. One of the best predictors of the incremental cephalic phase of insulin release was fasting insulin level and, thus, a relation to degree of insulin sensitivity is likely. In conclusion, an early pre-absorptive and cephalic phase of insulin release is robustly present in man. However, we could not document any relation to family history of Type 2 diabetes nor to the post-absorptive phase and, thus, confirm its importance for subsequent degree of insulin release or glucose tolerance.

MeSH terms

  • Adult
  • C-Peptide / metabolism
  • Case-Control Studies
  • Diabetes Mellitus, Type 2*
  • Eating
  • Fasting / physiology
  • Glucose Intolerance
  • Glucose Tolerance Test
  • Humans
  • Insulin / metabolism*
  • Insulin Secretion
  • Male
  • Meals
  • Middle Aged
  • Pedigree

Substances

  • C-Peptide
  • Insulin

Grants and funding

The present study was funded by grants from the Swedish Medical Research Council, the Swedish Diabetes Foundation and the Novo Nordisk Foundation. It also received support from the Innovative Medicines Initiative Joint Undertaking under EMIF grant agreement 115372. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.