These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Origin and utilization of volatile fatty acids in the rat.
    Author: Rémésy C, Demigné C, Chartier F.
    Journal: Reprod Nutr Dev (1980); 1980; 20(4B):1339-49. PubMed ID: 7349486.
    Abstract:
    The arteriovenous differences in the caecum of the rat have been compared for volatile fatty acids (VFA) and for electrolytes. Our results suggest the possibility of an exchange between VFA and chloride at the level of the caecal wall, rather than a net exchange between VFA and bicarbonate; however, the role of bicarbonate or Cl- at the cellular level is still unknown. Acetate uptake by the liver was enhanced when acetate in the afferent plasma was increased in fed as in starved rats, showing that acetyl CoA synthetase was still active during starvation. A release of endogenous acetate was only observed in situations of very active ketogenesis (starvation at the end of pregnancy). In physiological conditions, propionate and butyrate reaching the liver were almost quantitatively removed. However, butyrate was taken up by the liver at a higher rate than propionate after intracecal loads. Propionate was very efficiently utilized as a glucogenic substrate and without noticeable disturbance of lactate metabolism. After administration of acetate loads in starved rats, hepatic ketogenesis increased slightly. There was a marked difference between ketogenesis from butyrate in fed and starved rats. The low ketogenesis from butyrate in the fed rats stressed the important role of metabolic pathways of acetyl-CoA utilization in the control of ketogenesis. In contrast to alanine or lactate, propionate was poorly antiketogenic in the rat.
    [Abstract] [Full Text] [Related] [New Search]