Delayed gastric emptying rate as a potential mechanism for lowered glycemia after eating sourdough bread: studies in humans and rats using test products with added organic acids or an organic salt.
The possible effects of organic acids or an organic salt on the rate of gastric emptying was studied to identify the cause for reduced postmeal responses of blood glucose and insulin to foods containing such components, eg, sourdough bread. Paracetamol was included in bread products with added lactic acid or sodium propionate and used as a marker for the rate of gastric emptying in healthy subjects. In parallel, postprandial glycemia, insulinemia, and satiety were evaluated. The influence of lactic acid, propionic acid, and sodium propionate was also studied in rats after they were tube-fed with glucose solutions. The bread products with lactic acid or sodium propionate both lowered blood glucose and insulin responses. The bread with sodium propionate also prolonged satiety. The reason for the lowered metabolic responses with sodium propionate was probably a lowered gastric emptying rate, as judged from reduced blood paracetamol concentrations; there was no such effect observed with bread with added lactic acid. A similar amount of lactic acid in solution tube-fed to rats did not affect the disappearance of glucose from the stomach. In contrast with the finding in humans, sodium propionate had no effect on the rate of gastric emptying in rats whereas an equimolar solution of propionic acid reduced gastric emptying rate in rats. Possibly, less of this acid was produced in the gastric contents after a bolus load of a sodium propionate solution (in rats) than in an eating situation. Also, the pH and/or the osmolarity may be important, and when provided in excessive amounts, lactic acid reduced the gastric emptying rate in rats. A hydrochloric acid solution of similar pH was much less effective in this respect.
Liljeberg
H G
HG
Department of Applied Nutrition and Food Chemistry, Chemical Center, University of Lund, Sweden. Helena.Liljeberg@inl.lth.se
Björck
I M
IM
D000082:Acetaminophen / Q000097:blood / Q000493:pharmacokinetics; D019342:Acetic Acid / Q000494:pharmacology*; D000328:Adult; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism*; D001939:Bread; D005260:Female; D005746:Gastric Emptying / Q000502:physiology*; D005753:Gastric Mucosa / Q000378:metabolism; D006003:Glycogen / Q000378:metabolism*; D006801:Humans; D006851:Hydrochloric Acid / Q000494:pharmacology*; D007328:Insulin / Q000097:blood; D007408:Intestinal Absorption / Q000187:drug effects / Q000502:physiology; D008297:Male; D008875:Middle Aged; D011422:Propionates / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012527:Satiation / Q000502:physiology; D013270:Stomach / Q000502:physiology
D001786:Blood Glucose; D007328:Insulin; D011422:Propionates; D000082:Acetaminophen; D006003:Glycogen; C514135:sodium propionate; C029658:propionic acid; D019342:Acetic Acid; D006851:Hydrochloric Acid