Effect of the First Feeding on Enterocytes of Newborn Rats
Maria A Nikonova1, Irina S Sesorova1, Ivan D Dimov2
1Department of Anatomy, Ivanovo State Medical Academy, 153012 Ivanovo, Russia.
Insights
Newly born rats exhibit unique enterocyte lipid transport mechanisms, including apical endocytosis. First feeding triggers changes similar to lipid overload, with macrophages capturing chylomicrons to prevent blood entry.
Area of Science:
- Cell Biology
- Gastroenterology
- Lipid Metabolism
Background:
- Enterocyte lipid absorption is crucial for nutrient transport.
- Chylomicron formation and transport are key processes in the lymphatic system.
- Developmental changes in enterocyte function are not fully understood.
Purpose of the Study:
- To investigate the enterocyte-to-lymphatic lipid transport barrier in newborn rats.
- To compare lipid transport in newborn rats before and after their first feeding.
- To understand how initial feeding impacts chylomicron processing and lymphatic uptake.
Main Methods:
- Microscopic examination of enterocytes, blood capillaries, and lymphatic capillaries in newborn rats.
- Analysis of enterocyte structures, including endoplasmic reticulum (ER), Golgi complex (GC), and endosomal networks.
- Observation of chylomicron (ChM) transport and macrophage interactions post-first feeding.
Main Results:
- Newborn rat enterocytes display apical endocytosis and a distinct endosomal network, unlike adults.
- Enterocytes uptake membranes from amniotic fluid, processed via the Golgi complex.
- First feeding induces alterations resembling lipid overload, with enlarged chylomicrons being captured by macrophages in the lymphatic system, preventing blood entry.
Conclusions:
- Neonatal enterocytes possess unique pathways for membrane and potentially lipid uptake before feeding.
- Post-feeding, enterocyte lipid processing shifts, leading to enlarged chylomicrons.
- Macrophages play a critical role in sequestering chylomicrons in the lymph, limiting immediate systemic circulation.
Abstract:
The transcytosis of lipids through enterocytes occurs through the delivery of lipid micelles to the microvilli of enterocytes, consumption of lipid derivates by the apical plasma membrane (PM) and then their delivery to the membrane of the smooth ER attached to the basolateral PM. The SER forms immature chylomicrons (iChMs) in the ER lumen. iChMs are delivered at the Golgi complex (GC) where they are subjected to additional glycosylation resulting in maturation of iChMs. ChMs are secreted into the intercellular space and delivered into the lumen of lymphatic capillaries (LCs). The overloading of enterocytes with lipids induces the formation of lipid droplets inside the lipid bilayer of the ER membranes and transcytosis becomes slower. Here, we examined components of the enterocyte-to-lymphatic barriers in newly born rats before the first feeding and after it. In contrast to adult animals, enterocytes of newborns rats exhibited apical endocytosis and a well-developed subapical endosomal tubular network. These enterocytes uptake membranes from amniotic fluid. Then these membranes are transported across the polarized GC and secreted into the intercellular space. The enterocytes did not contain COPII-coated buds on the granular ER. The endothelium of blood capillaries situated near the enterocytes contained only a few fenestrae. The LCs were similar to those in adult animals. The first feeding induced specific alterations of enterocytes, which were similar to those observed after the lipid overloading of enterocytes in adult rats. Enlarged chylomicrons were stopped at the level of the LAMP2 and Neu1 positive post-Golgi structures, secreted, fused, delivered to the interstitial space, captured by the LCs and transported to the lymph node, inducing the movement of macrophages from lymphatic follicles into its sinuses. The macrophages captured the ChMs, preventing their delivery into the blood.
