The transporter of interest may normally be expressed during the Small Intestinal Phase of the Integrated Response to a Meal, such as in the case of cystinuria. Amino acid transporters generally have broad specificity and transport a subset of amino acids, with some overlap in their affinity for specific amino acids. Some amino acid transporters are symporters that transport their substrate amino acids together with the obligatory uptake of Na+.

In addition to amino acids, the small intestine is capable of taking up short peptides through a transporter called peptide transporter 1 (PepT1). PepT1 is a symporter that transports peptides in conjunction with protons. Amino acids released from these peptides, which are not needed by the enterocyte, are exported across the basolateral membrane and enter the bloodstream through blood capillaries. They are then transported to the liver via the portal vein. PepT1 is also important in the clinical context as it can facilitate the uptake of peptidomimetic drugs, including antibiotics and cancer chemotherapeutic agents. The mechanisms by which amino acids and peptidomimetic drugs leave the enterocyte are not fully understood but are believed to involve additional transport proteins.

The redundancy in uptake mechanisms for the products of protein digestion highlights the significance of this process and also suggests that deficiencies in specific amino acid assimilation across the intestine are relatively uncommon. However, mutations in proteins responsible for specific amino acid transport can lead to pathology in other organs. Cysteinuria is an example of a disease that involves mutations in various amino acid transporters capable of transporting cysteine. Although cysteine can also be assimilated across the gut in the form of peptides, nutritional deficiencies do not occur despite the lack of intestinal uptake mechanisms for this particular amino acid. On the other hand, cysteine can only be poorly reabsorbed from the urine of patients with cystinuria, leading to the formation of kidney stones due to the relative insolubility of this amino acid. Pathophysiology can also arise as a result of mutations in SLC6A19, a Na+-independent transporter of neutral amino acids, resulting in a condition known as Hartnup disease. Hartnup disease is a relatively rare inborn error of metabolism that causes the loss of neutral amino acids in urine, leading to psychiatric issues, intellectual disability, short stature, headaches, and an unsteady gait, although nutritional deficiencies are not typically observed.

Lipids, which are substances more soluble in organic solvents than in water, constitute the third major class of macronutrients in the human diet. Lipids provide a greater number of calories per gram compared to proteins or carbohydrates, making them nutritionally significant. However, excessive consumption of lipids can contribute to obesity. Lipids also dissolve volatile compounds that contribute to the taste and aroma of food.
The Small Intestinal Phase of the Integrated Response to a Meal which the transporter of interest may normally be expressed (e.g., cystinuria). In general, amino acid transporters have reasonably broad specificity and usually transport a subset of amino acids (e.g., neutral, anionic, or cationic) but with some overlap in their affinity for particular amino acids. Furthermore, some (but not all) of the amino acid transporters are symporters that carry their substrate amino acids in conjunction with obligatory uptake of Na+ .
The small intestine is also notable for its ability to take up short peptides (see
Fig. 30.14 ). The primary transporter responsible for such uptake is called peptide transporter 1 (PepT1) and is a symporter that transports peptides in conjunction with protons. Amino acids liberated from these peptides that are not required by the enterocyte are in turn exported across the basolateral membrane and enter blood capillaries to be transported to the liver via the portal vein. PepT1 is also of clinical interest because it can mediate the uptake of so-called peptidomimetic drugs, which include a variety of antibiotics as well as cancer chemotherapeutic agents. The mechanisms by which amino acids and peptidomimetic drugs exit the enterocyte are not fully understood but are presumed to involve additional transport proteins.
Theredundancyinuptakemechanismsfortheproductsofproteindigestionunderscorestheimportanceofthisprocessandalsomeansthatdeficienciesinspecificaminoacidassimilationacrosstheintestinearerelativelyrare.However,undercertaincircumstances,mutationsinproteinsresponsibleforspecificaminoacidtransportcanleadtopathologyinotherorgans.Oneexampleisthediseaseofcysteinuria,whichisamolecularlyheterogeneousdiseaseinvolvingmutationsinavarietyofaminoacidtransporterscapableoftransportingcysteine.Becausecysteinecanalsobeassimilatedacrossthegutintheformofpeptides,nutritionaldeficienciesdonotoccurdespitealackofintestinaluptakemechanismsforthisparticularaminoacid.Incontrast,cysteinecanonlybepoorlyreabsorbedfromtheurineofpatientssufferingfromcystinuria,andkidneystonescanformbecausethisaminoacidisrelativelyinsoluble.PathophysiologycanalsoarisesecondarytomutationsinSLC6A19, aNa+-independenttransporterofneutralaminoacids,andresultinaconditionknownasHartnup disease, arelativelyrareinbornerrorofmetabolismthatcauseslossofneutralaminoacidsinurine,resultinginpsychiatricissues,intellectualdisability,shortstature,headaches,andunsteadygait,althoughnotnutritionaldeficienciesperse.
Lipids, defined as substances that are more soluble in organic solvents than in water, are the third major class of macronutrients making up the human diet. Lipids supply more significant calories on a per-gram basis than proteins or carbohydrates do and are thus of major nutritional significance; they also have a propensity to contribute to obesity if consumed in excessive amounts. Lipids also dissolve volatile compounds that contribute to food’s taste and aroma.