The physiological response to digestion in snakes: A feast for the integrative physiologist.
Alkalosis
Animals
Boidae
/ physiology
Digestion
/ physiology
Feeding Behavior
/ physiology
Gastric Acid
/ metabolism
Gastrointestinal Tract
/ metabolism
Heart Rate
Hydrogen-Ion Concentration
Hypoventilation
Metabolism
Models, Biological
Oxygen Consumption
Postprandial Period
/ physiology
Respiration
Stroke Volume
Acid-base balance
Alkaline tide
Cardiovascular
Gastric acid secretion
Metabolism
Respiratory
Specific dynamic action
Journal
Comparative biochemistry and physiology. Part A, Molecular & integrative physiology
ISSN: 1531-4332
Titre abrégé: Comp Biochem Physiol A Mol Integr Physiol
Pays: United States
ID NLM: 9806096
Informations de publication
Date de publication:
04 2021
04 2021
Historique:
received:
16
12
2020
revised:
28
12
2020
accepted:
28
12
2020
pubmed:
6
1
2021
medline:
26
10
2021
entrez:
5
1
2021
Statut:
ppublish
Résumé
Many snakes can subdue and swallow very large prey after many months of fasting. The functional capacity and the mass of the gastrointestinal organs regress during fasting, but are quickly restored upon feeding. This phenotypic flexibility appears to be energetically inexpensive, and represents a key adaptation that enables snakes to match digestive performance without compromising bodily energy stores prior to nutrient absorption. The reorganization of the intestines resembles the unfolding of an accordion where the individual enterocytes expand, primarily in response to luminal presence of nutrients. The very large rise in postprandial metabolism (specific dynamic action), where the rate of oxygen consumption can increase four- to six-fold, is likely due to a global rise in protein synthesis in all tissues. The rise in oxygen consumption is sustained by a pronounced tachycardia that, in part, is caused by un-identified humoral factor(s) with positive chronotropic effects, and a rise in stroke volume, where venous return may be augmented by a rise in venous tone. The immediate stimulation of gastric acid secretion causes a metabolic alkalosis (the alkaline tide), but pH remains unchanged due to a rise in arterial PCO
Identifiants
pubmed: 33400953
pii: S1095-6433(20)30244-0
doi: 10.1016/j.cbpa.2020.110891
pii:
doi:
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
110891Informations de copyright
Copyright © 2020 Elsevier Inc. All rights reserved.