Reference : Effect of indomethacin on the metabolic and hormonal response to a standardized break...
Scientific journals : Article
Human health sciences : Pharmacy, pharmacology & toxicology
Human health sciences : Endocrinology, metabolism & nutrition
Effect of indomethacin on the metabolic and hormonal response to a standardized breakfast in normal subjects.
Luyckx, A. S. [> > > >]
Guerten, D. [> > > >]
Scheen, André mailto [Université de Liège - ULiège > Département des sciences cliniques > Diabétologie, nutrition et maladie métaboliques - Médecine interne générale >]
Delporte, Jean-Pierre mailto [Université de Liège - ULiège > Département de pharmacie > Economie du médicament - Phamacie hospitalière >]
Lefebvre, Pierre [Centre Hospitalier Universitaire de Liège - CHU > > Diabétologie,nutrition, maladies métaboliques >]
Jaminet, F. [> > > >]
Acta Diabetologica Latina
Il Ponte
Yes (verified by ORBi)
[en] Adult ; Blood Glucose/analysis ; Fasting ; Fatty Acids, Nonesterified/blood ; Food ; Glucagon/blood ; Humans ; Indomethacin/pharmacology ; Insulin/blood ; Male
[en] We have investigated the influence of a single oral administration of indomethacin on blood glucose, plasma free fatty acids (FFA), alpha-amino-nitrogen, insulin and glucagon concentrations in young healthy subjects. Two groups of 6 subjects were studied, the first received a standardized 500 kcal mixed meal without any previous drug administration (controls) whereas the second group received 50 mg indomethacin 2 h before ingesting an identical meal. Plasma indomethacin concentration reached its maximum (2.36 +/- 0.36 micro g/ml) 15 min after administration and declined to 0.45 +/- 0.04 micro g/ml after 2 h. Indomethacin ingestion was followed by a significant increase in blood glucose and plasma FFA reaching their maximum value at 45 min and returning to basal levels at 120 min. No simultaneous changes in plasma alpha-amino-nitrogen, insulin or glucagon levels were detected during this period. The meal was followed by a rise in blood glucose and plasma insulin as well as by a decrease in plasma FFA concentration. No significant differences were detected between the controls and the subjects receiving indomethacin. In controls, the meal was followed by a rise in plasma alpha-amino-nitrogen and a modest although significant increase in glucagon levels. In indomethacin-treated subjects, the increment of alpha-amino-nitrogen was less marked and the increase in plasma glucagon was not observed. Thus, indomethacin by itself can exert several metabolic effects; however, it does not deteriorate the blood glucose or insulin profile after a regular meal. The present work is the first to demonstrate that an inhibitor of prostaglandin synthesis inhibits the plasma glucagon rise occurring after a physiological stimulus such as a normal meal. On the basis of previous in vitro experiments, we suggest that this effect results from an inhibition of glucagon secretion by the PG synthesis inhibitor.

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