Postprandial Aminogenic Insulin and Glucagon Secretion Can Stimulate Glucose Flux in Humans.
Level 3 - non-randomized controlled study
Controlled crossover physiological trial in healthy humans (randomization not specified in abstract)
PubMed 30833465 · doi:10.2337/db18-1138
What was done
Eight healthy participants completed a water control trial and a multidose whey protein ingestion trial designed to augment the protein-induced endocrine response. Glucose kinetics, including endogenous glucose production (EGP) and rate of glucose disposal (Rd), were quantified using stable isotope tracer methodology alongside measurements of amino acids, insulin, glucagon, and free fatty acids.
What was found
Protein ingestion induced hyperaminoacidemia, an approximately sixfold basal rise in insulin, and an approximately eightfold basal rise in glucagon, while suppressing free fatty acids. Both glucose disposal (Rd) and endogenous glucose production (EGP) increased by ~25%, maintaining euglycemia. Physiological hyperglucagonemia overrode the hepatic actions of insulin, preventing insulin-mediated EGP suppression despite postprandial inhibition of adipose lipolysis.
Why it matters
These findings show that postprandial glucagon acts in synergy with insulin after protein intake to stimulate hepatic glucose production, matching peripheral glucose uptake and preventing hypoglycemia. This reframes glucagon as an active postprandial regulatory hormone with direct implications for glucagon receptor agonist and antagonist therapies.
Limits
The sample size is very small (n = 8), and the abstract does not state whether treatment order was randomized. The study included only healthy participants, precluding conclusions about individuals with impaired glucose tolerance or diabetes. Dosing specifics and long-term effects beyond the acute postprandial window were not reported.
Cited by
- partial High protein intake can trigger gluconeogenesis and cause an insulin reaction or glucose spike.