Neonatal Gastrointestinal Growth and Function: Are They Regulated by Composition of Feeds?

Weaver, Lawrence T.; Landymore-Lim, Lisa; Lucas, Alan

doi:10.1159/000243369

Cited by 16 publications

(11 citation statements)

References 26 publications

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“…Moreover, the lack of CEL in the digestive tract not only led to nutritional deficit in neonates, but evidence suggests that the undigested lipid is injurious to the intestinal epithelium of these mice, especially in the ileum (75)(76)(77)(78)(79). Taken together, these results suggest the importance of CEL in caring for premature and low birthweight infants, who typically have poor gastrointestinal function and are prone to inflammatory diseases of the bowel (80)(81)(82)(83). The physiological significance for the lack of CEL in rat and cow milk has not been determined.…”

Section: Triglyceride Absorptionmentioning

confidence: 96%

Carboxyl ester lipase

Hui

Howles

2002

Journal of Lipid Research

196

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Carboxyl ester lipase (CEL), previously named cholesterol esterase or bile salt-stimulated (or dependent) lipase, is a lipolytic enzyme capable of hydrolyzing cholesteryl esters, tri-, di-, and mono-acylglycerols, phospholipids, lysophospholipids, and ceramide. The active site catalytic triad of serine-histidine-aspartate is centrally located within the enzyme structure and is partially covered by a surface loop. The carboxyl terminus of the protein regulates enzymatic activity by forming hydrogen bonds with the surface loop to partially shield the active site. Bile salt binding to the loop domain frees the active site for accessibility by water-insoluble substrates. CEL is synthesized primarily in the pancreas and lactating mammary gland, but the enzyme is also expressed in liver, macrophages, and in the vessel wall. In the gastrointestinal tract, CEL serves as a compensatory protein to other lipolytic enzymes for complete digestion and absorption of lipid nutrients. Importantly, CEL also participates in chylomicron assembly and secretion, in a mechanism mediated through its ceramide hydrolytic activity. Cell culture studies suggest a role for CEL in lipoprotein metabolism and oxidized LDL-induced atherosclerosis. Thus, this enzyme, which has a wide substrate reactivity and diffuse anatomic distribution, may have multiple functions in lipid and lipoprotein metabolism, and atherosclerosis. Carboxyl ester lipase (CEL), previously named pancreatic cholesterol esterase and also known as bile salt-stimulated (or -dependent) lipase, is a nonspecific lipolytic enzyme capable of hydrolyzing cholesteryl esters, tri-, di-, and mono-acylglycerols, phospholipids, lysophospholipids, and ceramide (1-3). The hydrolysis of water-insoluble carboxyl esters with long chain fatty acyl groups by CEL requires its activation by bile salt. However, CEL hydrolysis of water-soluble substrates such as carboxyl esters with short chain fatty acids or lysophospholipids does not have an absolute dependence on bile salt activation. The CEL protein is synthesized primarily in the pancreatic acinar cells and lactating mammary glands of higher mammals. Small amounts of CEL are found in other tissues, particularly the liver, macrophages, endothelial cells, and eosinophils (4-10). Extensive research has been performed in recent years on the structure-function relationship of this protein as well as its physiological role in lipid metabolism. A significant body of work has also been devoted to studying CEL processing and transport in pancreatic acinar cells. The latter topic was reviewed recently (11) and will be discussed only briefly in this article when appropriate. This article will present an updated review on the structure-function studies of CEL as well as an in-depth discussion on the current understanding of its role in lipid metabolism. PROTEIN STRUCTURE-FUNCTION RELATIONSHIP Active siteThe nucleotide sequence of CEL from various species shows that it is a highly conserved protein belonging to the ␣ / ␤ hydrolase family. The carb...

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Section: Triglyceride Absorptionmentioning

confidence: 96%

Carboxyl ester lipase

Hui

Howles

2002

Journal of Lipid Research

196

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“…Similar to humans, mitotic activity was increased in formula-fed compared with suckled animals (26,30) . However, in precocial species, such as the guinea-pig, born more mature than rat pups and therefore more similar to humans, no such gut hypertrophy in response to formula-feeding has been observed (31) . In piglets, also believed to be more similar to human neonates, results are contradictory, since formula-feeding for the first 7 d of life resulted in an early increase in apoptotic index and a decrease in mitotic index but no significant variation in villous length or crypt depth (32,33) .…”

Section: Mucosa Morphologymentioning

confidence: 99%

Breast-v.formula-feeding: impacts on the digestive tract and immediate and long-term health effects

2010

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The health benefits of breast-feeding have been recognised for a long time. In particular, breast-feeding is associated with lower incidence of necrotising enterocolitis and diarrhoea during the early period of life and with lower incidence of inflammatory bowel diseases, type 2 diabetes and obesity later in life. The higher nutritional and protective degree of human milk is related to its nutritional composition that changes over the lactation period and to the biological activities of specific components while lower growth rate of breast-fed infants may be attributed to their self-regulation of milk intake at a lower level than formula-fed infants. Many results now suggest that the developmental changes in intestinal and pancreatic function that occur postnatally are modulated by the diet. Indeed, formula-feeding induces intestinal hypertrophy and accelerates maturation of hydrolysis capacities; it increases intestinal permeability and bacterial translocation, but does not induce evident differences in microbiota composition. Whether these changes would be beneficial for enhancing absorptive capacities and for educating the gut-associated immune system remains to be further studied. Moreover, it is evident that formula-feeding increases basal blood glucose and decreases plasma ketone body concentrations, while discrepancies on postprandial glycaemia, insulin and incretin responses in both human studies and experimental studies are inconclusive. Manipulating the composition of formula, by reducing protein content, adding prebiotics, growth factors or secretory IgA can modulate intestinal and pancreatic function development, and thereby may reduce the differential responses between breast-fed and formula-fed neonates. However, the developmental responses of the digestive tract to different feeding strategies must be elucidated in terms of sensitivity to developing diseases, taking into account the major role of the intestinal microbiota.

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“…Specifically, measures of villous height, epithelial barrier integrity, intestinal permeability, brush border disaccharidase and aminopeptidase activity and glucose transport are a few of the functional parameters shown to be improved in different animal species when fed specific growth factors present in mother's milk [40][41][42]. It should be noted that some studies have not found a growth difference between neonates fed formula or mother's milk, suggesting that macronutrients contained in the diet may be just as important as growth factors for gut growth [43,44]. However, these studies were performed in term neonates, supporting the view that the trophic response of mother's milk relative to formula may be most pronounced in preterm infants.…”

Section: Milk Diets and Gut Development In Preterm Neonatesmentioning

confidence: 99%