Digestion of human milk fat in healthy infants

Abstract

Lipid digestion is critical for infant development, and yet, the interconnection between lipid digestion and the microbiota is largely understudied. This review focuses on digestion of the human milk fat globule and summarizes the current understanding of the mechanisms underlying this process in infants. We first discuss the partial hydrolysis of milk fat in the stomach, which leads to rearrangement of lipid droplets, creating a lipid-water interface necessary for duodenal lipolysis. In the first few months of life, secretion of pancreatic triglyceride lipase, phospholipase A 2 , and bile salts is immature. The dominant lipases aiding fat digestion in the newborn small intestine are therefore pancreatic lipase-related protein 2 and bile salt-stimulated lipase from both the exocrine pancreas and milk. We summarize the interaction between ionic fatty acids and cations to form insoluble fatty acid soaps and how it is influenced by various factors, including cation availability, pH, and bile salt concentration, as well as saturation and chain length of fatty acids. We further argue that the formation of the soap complex does not contribute to lipid bioavailability. Next, the possible roles that the gut microbiota plays in lipid digestion and absorption are discussed. Finally, we provide a perspective on how the manufacturing process of infant formula and dairy products may alter the physical properties and structure of lipid droplets, thereby altering the rate of lipolysis.

Comparative Proteomics of Human Milk From Eight Cities in China During Six Months of Lactation in the Chinese Human Milk Project Study

“…The crucial protein that handled fat metabolism in HM was CEL, which was found to be the seventh abundant protein ( Table 2 ) and also significantly expressed protein across the cities ( Supplementary Table 2 ). CEL from HM played a major role in infant lipid utilization by replacing pancreatic triglycerides lipase (PTL), which is secreted by the pancreas, while the pancreas condition is immature ( 38 , 43 ). The present research found five significantly expressed proteins in different cities, namely CEL, APOH, APOA2, LPL, and APOE which were enriched in the triglycerides metabolic process.…”

Lipid Composition, Digestion, and Absorption Differences among Neonatal Feeding Strategies: Potential Implications for Intestinal Inflammation in Preterm Infants

“…In infants, gastric lipase is highly effective as it does not require bile salt interaction nor low pH [84], and the enzyme is critical for lipid digestion, as lipases released downstream cannot similarly penetrate the MFGM [85]. While in the stomach, partial digestion of proteins and gastric lipase activity, together, cause coalescence of smaller MFGs into larger, and fewer, droplets [86]. Maternal enzymes present in HM are also active in the infant's stomach and are likely responsible for some of the protein digestion occurring in the early stages [81].…”

“…The pancreas secretes a variety of digestive enzymes into the duodenum, including trypsin, elastase, carboxypeptidases, pancreatic triglyceride lipase (PTL), phospholipase A2 (PLA2), BSSL (also known as carboxyl ester lipase [CEL] or bile salt-dependent lipase [BSDL]), and pancreatic lipase-related protein 2 (PLRP2) [83]. Concurrent with the excretion of pancreatic juice, the gallbladder releases bile salts into the intestinal lumen, but the concentration of bile salts released is extremely low as compared with an adult, often dropping below that required to properly emulsify lipids to micelles [86], especially in preterm infants [88]. While bile acid (BA) synthesis rates in premature infants are significant [89], there is thought to be a lag in development of BA secretory processes [90].…”

“…PLRP2 is capable of hydrolyzing a wide spectrum of lipids, including TGs and phospholipids, and its activity correlates negatively with luminal bile salt concentrations [95], seemingly in perfect concert with neonatal intestinal physiology. BSSL, released in low concentrations by the infant pancreas, requires primary bile salt activation to enable hydrolysis of a broad array of lipid classes [86], including LCPUFAs not hydrolyzed effectively by PLRP2 [95]. Importantly, BSSL is also secreted by the mammary gland throughout the duration of lactation, providing a critical secondary, and majority, source of the enzyme for both term and preterm infants [96].…”

“…The majority of non-esterified fatty acids (NEFA) and 2-monoacylglycerols produced through BSSL activity are emulsified into micelles for enterocyte uptake, largely in the jejunum.These lipid breakdown products are subsequently re-esterified to TGs within the intestinal epithelium, packaged into chylomicrons, and exported systemically via lymph [99]. However, very high dietary fat intake or a relative inability to digest TGs, in preterm infants especially [100], can result in the channeling of lipids to the ileum, where they are much less effectively absorbed [86]. Neither term nor preterm infants fully absorb lipids, with the former excreting up to 10%, and the latter up to 30%, of the dietary lipid load [76].…”