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Physiology, Digestion

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Last Update: September 12, 2022.


Digestion is the process of mechanically and enzymatically breaking down food into substances for absorption into the bloodstream. The food contains three macronutrients that require digestion before they can be absorbed: fats, carbohydrates, and proteins. Through the process of digestion, these macronutrients are broken down into molecules that can traverse the intestinal epithelium and enter the bloodstream for use in the body. Digestion is a form of catabolism or breaking down of substances that involves two separate processes: mechanical digestion and chemical digestion. Mechanical digestion involves physically breaking down food substances into smaller particles to more efficiently undergo chemical digestion. The role of chemical digestion is to further degrade the molecular structure of the ingested compounds by digestive enzymes into a form that is absorbable into the bloodstream. Effective digestion involves both of these processes, and defects in either mechanical digestion or chemical digestion can lead to nutritional deficiencies and gastrointestinal pathologies.

Through the gastrointestinal system, the nutritional substances, minerals, vitamins, and fluids, enter the body. Lipids, proteins, and complex carbohydrates are broken down into small and absorbable units (digested), principally in the small intestine. The products of digestion, including vitamins, minerals, and water, which cross the mucosa and enter the lymph or the blood (Absorption). 

Digestion of the major food macronutrients is an orderly process involving the action of a large number of digestive enzymes. Enzymes from the salivary and the lingual glands digest carbohydrates and fats, enzymes from the stomach digest proteins, and enzymes from the exocrine glands of the pancreas digest carbohydrates, proteins, lipids, RNA, and DNA. Other enzymes that help in the digestive process are found in the luminal membranes and the cytoplasm of the cells that lines the small intestine. The action of the enzymes is promoted by the hydrochloric acid (HCl), which is secreted by the stomach, and bile from the liver.

The mucosal cells in the small intestines are called enterocytes. In the small intestines, they have a brush border made up of numerous microvilli lining their apical surface. This border is rich in enzymes. It is lined on its luminal side by a layer that is rich in neutral and amino sugars, the glycocalyx. The membranes of the mucosal cells contain the glycoprotein enzymes that hydrolyze carbohydrates and peptides, and glycocalyx is made up in part of the carbohydrate portion of these glycoproteins that extend into the lumen of the intestine. Following the brush border and the glycocalyx is an unstirred layer similar to the layer adjacent to the biologic membrane. Solutes must diffuse across this layer to reach the mucosal cells. The mucous coat overlying the cells also continues a significant barrier to diffusion. Most substances pass from the lumen if the intestines into the enterocytes and then out of the enterocytes to the interstitial fluids.

Cellular Level

Digestion begins immediately in the oral cavity with both mechanical and chemical digestion. Mechanical digestion in the oral cavity consists of grinding of food into smaller pieces by the teeth, a process called mastication. Chemical digestion in the mouth is minor but consists of salivary amylase (ptyalin, or alpha-amylase) and lingual lipase, both contained in the saliva. Salivary amylase is chemically identical to pancreatic amylase and digests starch into maltose and maltotriose, working at a pH optimum of 6.7 to 7.0. Lingual lipase, also contained in the saliva, hydrolyzes the ester bonds in triglycerides to form diacylglycerols and monoacylglycerols.[1] After sufficient digestion in the oral cavity, the partially digested foodstuff, or bolus, is swallowed into the esophagus. No digestion occurs in the esophagus.

After passage through the esophagus, the bolus will enter the stomach and undergo mechanical and chemical digestion. Mechanical digestion in the stomach occurs via peristaltic contractions of the smooth muscle from the fundus towards the contracted pylorus, termed propulsion. Once the bolus is near the pylorus, the antrum functions to grind the material by forceful peristaltic contractions that force the bolus against a tightly constricted pylorus. The churning by the antrum serves to reduce the size of the food particles and is called grinding. Only particles smaller than 2mm in diameter can pass through the contracted pylorus into the duodenum. The rest of the bolus is pushed back towards the body of the stomach for further mechanical and chemical digestion. This backward movement of the bolus from the pylorus to the body is termed retropulsion and also serves to aid in mechanical digestion. This sequence of propulsion, grinding, and retropulsion repeats until the food particles are small enough to pass through the pylorus into the duodenum. All chyme not pushed through the pylorus during the active digestion process is eventually swept into the duodenum through a relaxed pylorus by a series of strong peristaltic contractions in the stomach. This activity occurs during the inter-digestive phase called migrating motor complexes (MMCs) that function to move the bolus in an aboral fashion to prevent stagnation and bacterial accumulation.

There is significant chemical digestion in the stomach. Two types of glands exist in the gastric mucosa that aid in chemical digestion: oxyntic glands and pyloric glands. Oxyntic glands are located in the body of the stomach and contain parietal cells and chief cells. Parietal cells secrete hydrochloric acid, concentrated to approximately 160 mmol/L and a pH of 0.8. Hydrochloric acid secreted by the parietal cells serves three main functions: 1) to create a hostile environment for pathogenic microorganisms taken in through the mouth, 2) to denature proteins and make them more accessible for enzymatic degradation by pepsin, and 3) to activate the zymogen pepsinogen to its active form, pepsin. Parietal cells also secrete a substance called intrinsic factor, necessary for the absorption of Vitamin B12 in the terminal ileum. Oxyntic glands also contain chief cells that secrete the zymogen pepsinogen. Pepsinogen is the precursor to the proteolytic enzyme pepsin and must be activated to pepsin by the acidic pH of the stomach (below 3.5) or from autoactivation by pepsin itself. Pepsin will then act on the internal peptide bonds of proteins at the optimal pH of 2 to 3. The pyloric glands are found in the antrum of the stomach and contain mucous cells and G-cells. Mucous cells secrete a bicarbonate-rich mucous onto the surface of the gastric mucosa to protect it from the acidic contents of the stomach. The G-cells secrete gastrin, a hormone that acts in an endocrine fashion to stimulate the secretion of hydrochloric acid by parietal cells.[2] No digestion of carbohydrates occurs in the stomach.

The majority of chemical digestion occurs in the small intestine. Digested chyme from the stomach passes through the pylorus and into the duodenum. Here, chyme will mix with secretions from both the pancreas and the duodenum. Mechanical digestion will still occur to a minor extent as well. The pancreas produces many digestive enzymes, including pancreatic amylase, pancreatic lipase, trypsinogen, chymotrypsinogen, procarboxypeptidase, and proelastase.[3] These enzymes are separated from the acidic environment of the stomach and function optimally in the more basic environment of the small intestine where the pH ranges from 6 to 7 due to bicarbonate secreted by the pancreas. Pancreatic amylase, like salivary amylase, functions to digest starch into maltose and maltotriose. Pancreatic lipase, secreted by the pancreas with an important coenzyme called colipase, functions to hydrolyze the ester bonds in triglycerides to form diacylglycerols and monoacylglycerols. Trypsinogen, chymotrypsinogen, procarboxypeptidase, and proelastase are all precursors to active peptidases. The pancreas does not secrete the active form of the peptidases; otherwise, autodigestion could occur, as is the case in pancreatitis. Instead, trypsinogen, chymotrypsinogen, procarboxypeptidase, and proelastase convert to trypsin, chymotrypsin, carboxypeptidase, and elastase, respectively.[3] This conversion occurs as enterokinase, a duodenal enzyme, converts trypsinogen to trypsin. Trypsin can then convert chymotrypsinogen, procarboxypeptidase, and proelastase to their active forms. Trypsin, chymotrypsin, and elastase are all endopeptidases that hydrolyze internal peptide bonds of proteins, while the carboxypeptidases are exopeptidases that hydrolyze terminal peptide bonds on proteins. These pancreatic zymogens leave the pancreas through the main pancreatic duct (of Wirsung) and join the common bile duct forming the ampulla of Vater and empty into the descending portion of the duodenum via the major duodenal papilla. The common bile duct carries bile that was made in the liver and stored in the gallbladder. Bile contains a mixture of bile salts, cholesterol, fatty acids, bilirubin, and electrolytes that help emulsify hydrophobic lipids in the small intestine, which is necessary for access and action by pancreatic lipase, which is hydrophilic.

Once in the duodenum, there will be an activation cascade beginning with enterokinase produced by the duodenum to activate trypsinogen to trypsin, and trypsin will activate the other pancreatic peptidases. Importantly, the duodenum also contributes several digestive enzymes such as disaccharidases and dipeptidase. The disaccharidases include maltase, lactase, and sucrase. Maltase cleaves the glycosidic bond in maltose, producing two glucose monomers, lactase cleaves the glycosidic bond in lactose, producing glucose and galactose, and sucrase cleaves the glycosidic bond in sucrose, producing glucose and fructose. Dipeptidase cleaves the peptide bond in dipeptides. At this point, the mouth, stomach, and small intestine have broken down fat in the form of triglycerides to fatty acids and monoacylglycerol, carbohydrate in the form of starch and disaccharides to monosaccharides, and large proteins into amino acids and oligopeptides. Thus, the digestive process has converted macronutrients into forms that are absorbable into the bloodstream for bodily use.[4]

Organ Systems Involved

Gastrointestinal System:

  • Oral cavity
  • Stomach
  • Small intestine
  • Liver
  • Gall bladder
  • Pancreas


Digestion is a process that converts nutrients in ingested food into forms that can be absorbed by the gastrointestinal tract. Proper digestion requires both mechanical and chemical digestion and occurs in the oral cavity, stomach, and small intestine. Additionally, digestion requires the secretions from accessory digestive organs such as the pancreas, liver, and gallbladder. The oral cavity, stomach, and small intestine function as three separate digestive compartments with differing chemical environments. The oral cavity provides significant mechanical digestive functions and minor chemical digestion at a pH between 6.7 and 7.0. The oral cavity requires separation from the acidic environment of the stomach with a pH of 0.8 to 3.5. As such, enzymes such as alpha-amylase secreted by salivary glands in the oral cavity and also by the pancreas cannot function in the stomach, and thus digestion of carbohydrates does not occur in the stomach. However, in the stomach, significant digestion of proteins into polypeptides and oligopeptides occurs by the action of pepsin, which functions optimally at a pH of 2.0 to 3.0.

Minor digestion of lipids into fatty acids and monoacylglycerols also occurs by the action of gastric lipase secreted by chief cells in oxyntic glands of the body of the stomach. Importantly, this acidic environment of the stomach is also separated from the more basic environment of the small intestine by the tonically constricted pylorus. This functions to create an environment where the digestive enzymes produced by the pancreas and duodenum can function optimally at a pH of 6 to 7, a more basic environment than the stomach created by bicarbonate secreted by the pancreas. These separate yet coordinated digestive functions are essential to the body’s ability to absorb and utilize necessary nutrients. A defect in any aspect of this process can result in malabsorption and malnutrition amongst other gastrointestinal pathologies.

Related Testing

Clinical tests for defects in digestion or deficiencies in digestive enzymes are often indicated after a patient presents with gastrointestinal symptoms. An example is testing for lactose intolerance due to a lactase defect or deficiency. Lactase is a disaccharidase produced by the pancreas that hydrolyzes the glycosidic bond in lactose to form the carbohydrate monomers glucose and galactose; this is necessary, as glucose and galactose are absorbable by the SGLT1 cotransporters on the luminal surface of enterocytes in the small intestine, but lactose cannot.[5] As such, in lactose intolerance, lactose remains undigested in the lumen of the small intestine and serves as an osmotic force that draws fluid into the lumen of the small intestine, causing osmotic diarrhea. A common test for lactose intolerance involves the oral administration of a bolus of lactose to the patient. Blood glucose levels are then measured at periodic intervals. In a patient with normal lactase function, blood glucose levels will rise after oral administration of a lactose bolus because lactase will digest lactose into glucose and galactose, with the glucose absorbed into the bloodstream, and thus blood glucose levels will rise.

In a patient with defective or deficient lactase, a rise in blood glucose levels after oral administration of a lactose bolus will not occur because lactose will remain undigested in the lumen of the small intestine and no glucose will enter the bloodstream. A second test for lactose intolerance involves a similar administration of oral lactose and then a measurement of hydrogen gas levels in the breath. In a patient with lactose intolerance, lactose will remain undigested and pass into the colon. Colonic bacteria can use lactose as an energy source, producing hydrogen gas as a byproduct.[6] This production of hydrogen gas by colonic bacteria not only causes bloating and flatulence but is also measurable during exhalation. Thus, a patient with lactose intolerance will show increased hydrogen gas levels in the breath after administration of oral lactose, whereas a patient with normal lactase function will not.[7]

Clinical Significance

Defects in any aspect of digestion can result in uncomfortable gastrointestinal symptoms and the inability to absorb certain nutrients. Several defects of digestion are discussed below.

As mentioned previously, lactose intolerance results from defective or deficient lactase and can result in bloating, flatulence, diarrhea, and the inability to acquire glucose and galactose from lactose. Management can involve avoiding dairy products, which contain significant amounts of lactose. In this case, supplemental calcium may be necessary. Additionally, beta-galactosidase (lactase) tablets are available as supplements for people who are lactose intolerant.

Paralytic ileus is a condition where the normal peristaltic movements of the gastrointestinal tract are inhibited due to abdominal surgery or the use of anticholinergics. Inhibitory neurons in the myenteric plexus between the inner circular and outer longitudinal muscle layers of the gastrointestinal tract release excessive vasoactive intestinal peptide (VIP) or nitric oxide (NO), inhibitory neurotransmitters that prevent peristalsis. Anticholinergics can interfere with the action of acetylcholine, a stimulatory neurotransmitter from the parasympathetic nervous system that stimulates peristalsis. In both cases, peristalsis is inhibited, hindering the movement and mechanical digestion of food through the gastrointestinal tract.

Sjogren syndrome is an autoimmune condition that destroys the salivary and lacrimal glands. Without the production of saliva, the patient develops xerostomia or dry mouth. The lack of saliva results in difficulty speaking and swallowing, dental caries, and halitosis.[8]

Zollinger-Ellison syndrome is a condition where a gastrinoma produces excessive gastrin, leading to overstimulation of gastric parietal cells and excessive hydrochloric acid production. This can result in ulceration of the lining of the gastrointestinal tract, extreme discomfort, and hematemesis. Treatment includes proton pump inhibitors such as omeprazole, H2 receptor antagonists such as ranitidine, and removal of the offending tumor.[9]

Cystic fibrosis, aside from respiratory effects, also has consequences for the digestive tract. In cystic fibrosis, the CFTR chloride channel is defective. This channel is important in the pancreas for transporting chloride into the lumen of the pancreatic ducts, in order to draw Na and water into the lumen. This serves to make the pancreatic secretions less viscous and allow their passage through the duct of Wirsung and into the duodenum. If this CFTR chloride channel is defective, such as is the case in cystic fibrosis, the pancreatic secretions become extremely viscous and clog the pancreatic ducts.[10] This not only prevents the digestion of proteins, fats, and carbohydrates in the lumen of the small intestine but also causes premature activation of pancreatic digestive enzymes within the pancreas, causing autodigestion and pancreatitis. The inability to digest fats can lead to steatorrhea and fat-soluble vitamin deficiencies. Patients with pancreatic insufficiency secondary to cystic fibrosis or other causes can take oral pancreatic enzyme supplements to aid in digestion.

Cholelithiasis, or gallstones, are solidified particles of bile that can obstruct the common bile duct. This results in the inability of bile to enter the lumen of the duodenum, and, as such, fats are not emulsified. Pancreatic lipase cannot access the triglycerides, and fats remain undigested. This also results in steatorrhea and can lead to deficiencies in fat-soluble vitamins. Treatment often involves the removal of the gallbladder or cholecystectomy.[11]

Review Questions


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Schubert ML. Physiologic, pathophysiologic, and pharmacologic regulation of gastric acid secretion. Curr Opin Gastroenterol. 2017 Nov;33(6):430-438. [PubMed: 28787289]
Pandiri AR. Overview of exocrine pancreatic pathobiology. Toxicol Pathol. 2014 Jan;42(1):207-16. [PMC free article: PMC4360889] [PubMed: 24190915]
Kiela PR, Ghishan FK. Physiology of Intestinal Absorption and Secretion. Best Pract Res Clin Gastroenterol. 2016 Apr;30(2):145-59. [PMC free article: PMC4956471] [PubMed: 27086882]
Forsgård RA. Lactose digestion in humans: intestinal lactase appears to be constitutive whereas the colonic microbiome is adaptable. Am J Clin Nutr. 2019 Aug 01;110(2):273-279. [PMC free article: PMC6669050] [PubMed: 31175813]
Sakai D, Hirooka Y, Kawashima H, Ohno E, Ishikawa T, Suhara H, Takeyama T, Koya T, Tanaka H, Iida T, Nishio R, Suzuki H, Uetsuki K, Matsushita M, Yamamura T, Furukawa K, Funasaka K, Nakamura M, Miyahara R, Watanabe O, Ishigami M, Tsuruta A, Shin W, Goto H. Increase in breath hydrogen concentration was correlated with the main pancreatic duct stenosis. J Breath Res. 2018 Mar 12;12(3):036004. [PubMed: 29445052]
Mattar R, de Campos Mazo DF, Carrilho FJ. Lactose intolerance: diagnosis, genetic, and clinical factors. Clin Exp Gastroenterol. 2012;5:113-21. [PMC free article: PMC3401057] [PubMed: 22826639]
Stefanski AL, Tomiak C, Pleyer U, Dietrich T, Burmester GR, Dörner T. The Diagnosis and Treatment of Sjögren's Syndrome. Dtsch Arztebl Int. 2017 May 26;114(20):354-361. [PMC free article: PMC5471601] [PubMed: 28610655]
Bardram L, Thomsen P, Stadil F. Gastric endocrine cells in omeprazole-treated and untreated patients with the Zollinger-Ellison syndrome. Digestion. 1986;35 Suppl 1:116-22. [PubMed: 3792668]
Borowitz D. CFTR, bicarbonate, and the pathophysiology of cystic fibrosis. Pediatr Pulmonol. 2015 Oct;50 Suppl 40:S24-S30. [PubMed: 26335950]
Dosch AR, Imagawa DK, Jutric Z. Bile Metabolism and Lithogenesis: An Update. Surg Clin North Am. 2019 Apr;99(2):215-229. [PubMed: 30846031]

Disclosure: Justin Patricia declares no relevant financial relationships with ineligible companies.

Disclosure: Amit Dhamoon declares no relevant financial relationships with ineligible companies.

Copyright © 2023, StatPearls Publishing LLC.

This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ), which permits others to distribute the work, provided that the article is not altered or used commercially. You are not required to obtain permission to distribute this article, provided that you credit the author and journal.

Bookshelf ID: NBK544242PMID: 31334962


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