Verdauungsrückstände (Fett, Stickstoff, Zucker, Wasser): the pathway in the body

Verdauungsrückstände (Fett, Stickstoff, Zucker, Wasser) is part of the pathway “Digestion and absorption”. This page shows the whole pathway; the station of Verdauungsrückstände (Fett, Stickstoff, Zucker, Wasser) is highlighted.

Where this laboratory value sits: Digestive residues — leftovers in the stool. Whatever the small intestine did not absorb reaches the colon. In the stool, fat, nitrogen as a measure of protein, sugar and water content are determined. Source 4, 10

In brief

Digestion is the breakdown of food into building blocks the gut can absorb: protein into amino acids, fat into fatty acids, sugars into simple sugars. What the small intestine does not absorb is fermented or decomposed by bacteria in the colon, which sets the stool pH.

The pathway step by step

Each station states what the compound does there. Three signs: ↑ supplies — builds up or makes available · ↓ depletes — inhibits, consumes or withholds · ↕ both, depending on amount. Behind it stands what the statement rests on: established physiology, observed in studies, or contested. The signs do not grade; they name the direction.

1. Chief cells → Pepsinogen 1 Pepsinogen 1 (also pepsinogen A) is the inactive precursor of pepsin. A small part passes from the glands into the blood and is measured in serum. Source 1, 3↑ supplies As a precursor, pepsinogen is safely packaged: it splits nothing while it is inside the cell. Only stomach acid turns it into the active enzyme. established physiology Source 1
   ⚖ When the balance tips

   too much — If the stomach lining is irritated or acid production is inhibited, for example with proton pump inhibitors, pepsinogen 1 in the blood rises.

   too little — If there are fewer chief cells, pepsinogen 1 in the blood falls; less pepsin is then formed and protein is less pre-digested in the stomach.

   observed in studies · Source 14, 3

2. Pepsinogen 1 → Pepsin · Stomach acid (HCl) In acidic gastric juice, pepsinogen cuts off a piece of itself and becomes pepsin. Pepsin already formed speeds up this conversion. Source 1↑ supplies Pepsin breaks food protein into shorter pieces, making it accessible to the pancreatic enzymes. It works only in acid; in the small intestine it becomes inactive. established physiology Source 1, 4
   ⚖ When the balance tips

   too much — If a lot of pepsin is active, more protein is already partly digested in the stomach, and the pancreatic enzymes receive shorter pieces.

   too little — If there is little acid, hardly any pepsinogen is activated; protein then reaches the small intestine largely intact and is split there by the pancreatic enzymes alone.

   established physiology · Source 1, 2

3. Food protein → Peptides Pepsin In the stomach, pepsin cuts the long chains into shorter pieces, the peptides. In the small intestine, trypsin, chymotrypsin and elastase from the pancreas continue the work. Source 1, 5↑ supplies Peptides are more accessible than whole proteins: enzymes of the pancreas and the gut cells break them down further until amino acids and di- or tripeptides remain. established physiology Source 5, 4
   ⚖ When the balance tips

   too much — If more peptides arise than the pancreatic enzymes can break down further, they pass into lower sections of the gut.

   too little — If the stomach produces few peptides, the pancreatic enzymes carry out most of the protein splitting.

   established physiology · Source 5

4. Peptides → Amino acids Trypsin, elastase Single amino acids and di- or tripeptides are absorbed into the gut cells via transporters and pass from there into the blood. Source 4↑ supplies The absorbed amino acids are available to the body as building blocks for its own proteins and as fuel. established physiology Source 4
   ⚖ When the balance tips

   too much — If many amino acids are absorbed, the liver uses the excess; it converts the nitrogen into urea.

   too little — If little is absorbed, more protein stays in the gut, and the nitrogen content of the stool rises.

   established physiology · Source 4

5. Dietary fat → Fatty acids Pancreatic lipase · Bile acids, Colipase Pancreatic lipase, anchored by colipase, splits two fatty acids off the glycerol. Together with bile acids, the products form small micelles. Source 5, 6↑ supplies In the micelles, fatty acids, monoglycerides and fat-soluble vitamins cross the watery layer to the surface of the gut cells, where they are absorbed. established physiology Source 6
   ⚖ When the balance tips

   too much — If more fatty acids are released than the gut cells can absorb, they move into lower sections of the gut and partly appear in the stool.

   too little — Without lipase or bile acids, fat remains as triglyceride; the stool becomes fattier, and fat-soluble vitamins are lost with it.

   established physiology · Source 6, 5

6. Fatty acids → I-FABP I-FABP (intestinal fatty acid-binding protein, FABP2) occurs almost only in cells of the small-intestinal lining, especially at the villus tips. It binds absorbed fatty acids inside the cell. Source 8, 9↑ supplies I-FABP keeps long-chain fatty acids in solution inside the cell and hands them on to the pathways that rebuild fat for transport. In animal models it is not indispensable for this. observed in studies Source 8
   ⚖ When the balance tips

   too much — If many fatty acids reach the gut cell, more I-FABP is loaded with them and passes them on for rebuilding into fat.

   too little — Without I-FABP, gut cells in animal models still absorb fat; what changes is rather weight gain and energy balance.

   observed in studies · Source 8

7. I-FABP → I-FABP in blood When cells of the small-intestinal lining die, I-FABP passes into the blood. It stays there only briefly and is quickly excreted by the kidneys. Source 9↓ depletes In the blood, I-FABP has no known task; it shows how many gut cells have recently lost their contents, and thus a current state of the lining. observed in studies Source 9
   ⚖ When the balance tips

   too much — If many gut cells die, for example when blood flow to the gut is reduced, I-FABP in the blood rises quickly; with reduced kidney function it stays longer.

   too little — If the cells of the lining stay intact, hardly any I-FABP passes into the blood.

   observed in studies · Source 9

   Field of research — I-FABP in the blood is being studied as a marker of damage to the gut lining. Source 16

8. Disaccharides → Simple sugars Lactase, sucrase Enzymes on the surface of the gut cells, such as lactase and sucrase, split disaccharides into simple sugars. Glucose and galactose are absorbed together with sodium. Source 7, 4↑ supplies The absorbed simple sugars travel with the blood to the liver and are available as fuel. Water follows the sodium into the gut cells. established physiology Source 4
   ⚖ When the balance tips

   too much — If many simple sugars are released at once, uptake can reach its limit, and some move on into the colon.

   too little — If splitting at the cell surface is weak, for example when little lactase is made, the disaccharide remains unsplit in the gut.

   established physiology · Source 7

9. Disaccharides → Digestive residues Whatever the small intestine did not absorb reaches the colon. In the stool, fat, nitrogen as a measure of protein, sugar and water content are determined. Source 4, 10↕ both, depending on amount The residues feed colonic bacteria: sugars and fibre are fermented, protein is decomposed. Unsplit substances hold water in the gut and make the stool softer. established physiology Source 10, 12
   ⚖ When the balance tips

   too much — If many residues reach the colon, for example with low enzyme output, few bile acids or rapid transit, the stool becomes richer in fat, protein or water.

   too little — If few residues reach the colon, the food has been largely absorbed; a low water content often goes with slow transit.

   established physiology · Source 4, 10

10. Digestive residues → Fermentation Colonic bacteria ferment sugars, starch residues and fibre. This produces short-chain fatty acids such as acetate, propionate and butyrate, as well as lactic acid and gases. Source 10↕ both, depending on amount The acids fuel the gut cells and acidify the gut contents. If a great deal is fermented, more gas forms as well, and the contents become distinctly acidic. established physiology Source 10, 11
    ⚖ When the balance tips

    too much — If a lot is fermented, the pH in the colon falls; acid-sensitive bacteria are pushed back, and lactic-acid producers increase.

    too little — If little is fermented, for example on a low-fibre diet, the gut contents stay less acidic, and protein-decomposing bacteria gain ground.

    observed in studies · Source 11, 12

11. Digestive residues → Protein putrefaction When protein reaches the colon, bacteria decompose it mainly in the distal part. This produces ammonia, branched-chain fatty acids, phenols, indoles and hydrogen sulphide. Source 12↓ depletes Ammonia raises the pH; in cell experiments some putrefaction products strain the gut cells. They also shape the smell of stool and wind. observed in studies Source 12
    ⚖ When the balance tips

    too much — If protein putrefaction predominates, the gut contents become more alkaline, and more putrefaction products such as ammonia and phenols form.

    too little — If little protein reaches the colon or fermentation predominates, only few putrefaction products form.

    observed in studies · Source 12

12. Fermentation → Stool pH Stool pH reflects the environment in the colon. The proximal colon is usually more acidic than the distal part because more fermentation occurs there; the value varies with diet. Source 13, 10↕ both, depending on amount A mildly acidic environment favours bifidobacteria and lactobacilli and holds back acid-sensitive microbes. At acidic pH, ammonia is mostly present as ammonium, which passes less readily into the blood. observed in studies Source 11, 12
    ⚖ When the balance tips

    too much — If the pH is high because little acid forms or protein putrefaction predominates, acid-sensitive microbes can multiply more easily.

    too little — If the pH is low because a lot of sugar is fermented or the acids are no longer absorbed during rapid transit, the stool becomes soft and acidic.

    observed in studies · Source 11, 10, 13

13. Protein putrefaction → Stool pH Stool pH reflects the environment in the colon. The proximal colon is usually more acidic than the distal part because more fermentation occurs there; the value varies with diet. Source 13, 10↕ both, depending on amount A mildly acidic environment favours bifidobacteria and lactobacilli and holds back acid-sensitive microbes. At acidic pH, ammonia is mostly present as ammonium, which passes less readily into the blood. observed in studies Source 11, 12
    ⚖ When the balance tips

    too much — If the pH is high because little acid forms or protein putrefaction predominates, acid-sensitive microbes can multiply more easily.

    too little — If the pH is low because a lot of sugar is fermented or the acids are no longer absorbed during rapid transit, the stool becomes soft and acidic.

    observed in studies · Source 11, 10, 13

Further stations

• Chief cells — in the body of the stomach Chief cells lie in the glands of the body of the stomach. They make pepsinogen and release it into the gastric juice; a small part reaches the blood. Source 1↑ supplies Chief cells supply the precursor of the main protein-splitting enzyme of the stomach. How much pepsinogen is made depends on how many gland cells the lining of the stomach body carries. established physiology Source 1, 3
  ⚖ When the balance tips

  too much — If chief cells are strongly stimulated, for example by nerve signals and messengers during a meal, they release more pepsinogen into the stomach and the blood.

  too little — If the lining of the stomach body regresses, there are fewer chief cells; less pepsinogen and usually less stomach acid are then produced.

  established physiology · Source 3, 2

  Field of research — Pepsinogen in the blood is being studied as an indicator of the state of the stomach lining. Source 15

• Food protein — long amino acid chains Food protein consists of long chains of amino acids. It can only be absorbed once it has been broken into single amino acids or very short pieces. Source 4↑ supplies Food protein supplies the amino acids from which the body builds its own proteins. Whatever is not broken down passes into the colon. established physiology Source 4
  ⚖ When the balance tips

  too much — If more protein arrives than the stomach and small intestine can break down, some passes into the colon and is broken down there by bacteria.

  too little — If little protein arrives, it is almost completely broken down and absorbed, and hardly any reaches the colon.

  established physiology · Source 4, 12

• Dietary fat — mainly triglycerides Dietary fat consists mainly of triglycerides: three fatty acids on one glycerol. Bile acids break it into fine droplets in the small intestine. Source 6↑ supplies Fat supplies a lot of energy and carries the fat-soluble vitamins A, D, E and K. Only as fine droplets does it offer the enzymes enough surface. established physiology Source 6, 4
  ⚖ When the balance tips

  too much — If more fat arrives than lipase and bile acids can handle, some passes undigested into the colon and appears in the stool.

  too little — If little fat arrives, it is almost completely broken down; but with little fat, fewer fat-soluble vitamins arrive too.

  established physiology · Source 6

• Disaccharides — lactose, sucrose Disaccharides such as milk sugar (lactose) and table sugar (sucrose), along with starch fragments, arrive in the small intestine. The gut can only absorb simple sugars. Source 7, 4↑ supplies Disaccharides are a rapidly available energy source once split. Unsplit, they remain in the gut contents and draw water there. established physiology Source 4, 7
  ⚖ When the balance tips

  too much — If more disaccharide arrives than the enzymes can split, the rest moves into the colon; there it is fermented and holds water in the gut.

  too little — If little disaccharide arrives, it is almost completely split and absorbed, and hardly any sugar is found in the stool.

  established physiology · Source 7, 10

Cofactors in this pathway

• Stomach acid (HCl) — Activates pepsinogen to pepsin and keeps gastric juice acidic enough for pepsin to work Source 1, 2
• Bile acids — Break fat into droplets and form micelles with the breakdown products for absorption Source 6In the ORY catalogue as a laboratory value: Gallensäuren (Stuhl)
• Colipase — Anchors pancreatic lipase on the fat droplets coated with bile acids Source 5
• Pancreatic elastase — One of the protein-splitting enzymes of the pancreas that breaks peptides down further in the small intestine Source 5In the ORY catalogue as a laboratory value: Pankreatische Elastase-1 (PE-1)
• Zinc — Component of the pancreatic carboxypeptidases that cleave amino acids from the end of peptides Source 5In the ORY catalogue as a laboratory value: Zink
• Sodium — Carried into the gut cell together with glucose and galactose via the transporter SGLT1 Source 4In the ORY catalogue as a laboratory value: Natrium (intrazellulär)

Sources

1. Kageyama T. Pepsinogens, progastricsins, and prochymosins: structure, function, evolution, and development. Cell Mol Life Sci 2002 · PubMed 11915945
2. Schubert ML. Physiologic, pathophysiologic, and pharmacologic regulation of gastric acid secretion. Curr Opin Gastroenterol 2017 · PubMed 28787289
3. Samloff IM, Varis K, Ihamaki T et al. Relationships among serum pepsinogen I, serum pepsinogen II, and gastric mucosal histology. Gastroenterology 1982 · PubMed 7084603
4. Goodman BE. Insights into digestion and absorption of major nutrients in humans. Adv Physiol Educ 2010 · PubMed 20522896
5. Whitcomb DC, Lowe ME. Human pancreatic digestive enzymes. Dig Dis Sci 2007 · PubMed 17205399
6. Ko CW, Qu J, Black DD et al. Regulation of intestinal lipid metabolism: current concepts and relevance to disease. Nat Rev Gastroenterol Hepatol 2020 · PubMed 32015520
7. Hooton D, Lentle R, Monro J et al. The Secretion and Action of Brush Border Enzymes in the Mammalian Small Intestine. Rev Physiol Biochem Pharmacol 2015 · PubMed 26345415
8. Gajda AM, Storch J. Enterocyte fatty acid-binding proteins (FABPs): different functions of liver and intestinal FABPs in the intestine. Prostaglandins Leukot Essent Fatty Acids 2015 · PubMed 25458898
9. Pelsers MM, Namiot Z, Kisielewski W et al. Intestinal-type and liver-type fatty acid-binding protein in the intestine. Tissue distribution and clinical utility. Clin Biochem 2003 · PubMed 14563446
10. Cummings JH, Macfarlane GT. The control and consequences of bacterial fermentation in the human colon. J Appl Bacteriol 1991 · PubMed 1938669
11. Duncan SH, Louis P, Thomson JM et al. The role of pH in determining the species composition of the human colonic microbiota. Environ Microbiol 2009 · PubMed 19397676
12. Windey K, De Preter V, Verbeke K. Relevance of protein fermentation to gut health. Mol Nutr Food Res 2012 · PubMed 22121108
13. Fallingborg J. Intraluminal pH of the human gastrointestinal tract. Dan Med Bull 1999 · PubMed 10421978
14. Di Mario F, Ingegnoli A, Altavilla N et al. Influence of antisecretory treatment with proton pump inhibitors on serum pepsinogen I levels. Fundam Clin Pharmacol 2005 · PubMed 16011738
15. Agréus L, Kuipers EJ, Kupcinskas L et al. Rationale in diagnosis and screening of atrophic gastritis with stomach-specific plasma biomarkers. Scand J Gastroenterol 2012 · PubMed 22242613
16. Ho SSC, Keenan JI, Day AS. The Role of Gastrointestinal-Related Fatty Acid-Binding Proteins as Biomarkers in Gastrointestinal Diseases. Dig Dis Sci 2020 · PubMed 31529416

Whole pathway: Digestion and absorption

Related pathways

• Gut fermentation and breath gases — simple sugars
• Ketone bodies — fatty acids
• Pancreatic elastase — amino acids
• Triglycerides — dietary fat
• Clostridioides difficile — Gallensäuren (Stuhl), Zink

As of 2026-10-05. Draft, written by Claude to schema v2; sources checked in PubMed; expert approval pending
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