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Bovine colostrum (BC) contains bioactive components that have been shown to enhance gastrointestinal development and increase nutrient absorptive capacity in neonatal animals.
Absorptive enterocytes perform their nutrient absorptive and digestive functions via nutrient transport proteins and hydrolytic enzymes [ 3- 5].
However, it is worth noting that this transport route evolved early in the amniote lineage, and that neither the chorionic ectoderm as the entry point for nutrient absorption, nor the allantoic vasculature as the nutrient transport venue, nor the association of these two as the main nutrient absorptive organ, is unique to the eutherian mammals.
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Enterocytes would appear to be the obvious cellular mediators of these effects; changes in oxygen supply may modulate the metabolic state of these absorptive cells, and long-term adaptations to nutrient scarcity may result from differential nutrient absorption and/or utilization.
In most taxa, the midgut serves as the primary site of digestion as well as nutrient absorption and is therefore often characterized by the presence of glands and caeca that serve secretory or absorptive functions.
SLC9A3 is present in the brush-border of intestinal Na + -absorptive cells and renal proximal tubules, playing an important role in gastrointestinal and renal Na + absorption [ 73], and suggesting it may be involved in food digestion and nutrient absorption, and in turn, abdominal fat deposition.
Moderate amounts of fat increase nutrient absorption.
These processes involve rapid exocytosis of the major non-nutrient Na+ absorptive pathway, NHE3 via activation of the type I receptor and activation of complex transduction pathways.
There is a whole cascade of events from food assembly, preparation, to digestive breakup starting in the mouth, to the complex stomach and intestinal events, involving biochemical processes to finally present the functional molecules and nutrients to the absorptive sites at the intestinal wall.
Acetycholine (ACh) is released by intra-pancreatic vagal nerve endings and activates muscarinic acetylcholine receptors (mAChRs) on pancreatic β-cells during both the pre-absorptive (cephalic phase) and absorptive phases of nutrient intake [ 1– 3].
Independent of reduced nutrient intake, HS alters post-absorptive carbohydrate (basal and stimulated) metabolism, characterized primarily by increased basal insulin concentrations and insulin response to a GTT.
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