Porth's Essentials of Pathophysiology, 4e

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Gastrointestinal and Hepatobiliary Function

U N I T 8

Amino acids Glycerol

Lactic acid

Liver

Gluconeogenesis

A

Glycogen

Glucose

Triglycerides

Bloodstream

B

C

Dietary fat

Dietary proteins

Phospholipids and complex lipids for cell structures

Storage as triglycerols

Fatty acid

Amino acid

Tissue protein

Plasma proteins

Synthesis

Ketone bodies

Beta oxidation

Transamination/ deamination

Acetyl-CoA

Glucose synthesis (gluconeogenesis)

Synthesis of nonessential amino acids

HMG-CoA

Carbohydrates and amino acids metabolism

Citric acid cycle

Fatty acids

Ketoacids

Cholesterol Bile salts Steroid synthesis

Ammonia

Acetyl-CoA

ATP

Urea cycle

Citric acid cycle

Urea

ATP

FIGURE 30-4. Hepatic pathways for (A) glucose metabolism, (B) lipid metabolism, and (C) protein metabolism and conversion of ammonia to urea. ATP, adenosine triphosphate; HMG-CoA, hydroxymethylglutaryl-CoA.

protein synthesis and degradation. It produces proteins for its own cellular needs, as well as secretory proteins (e.g., plasma proteins, fibrinogen, and coagulation fac- tors) that are released into the circulation. One of the most important of these secretory proteins is albumin. Albumin contributes significantly to the plasma colloi- dal osmotic pressure (see Chapter 8) and to the binding and transport of numerous substances such as hor- mones, fatty acids, and bilirubin. Proteins are made up of amino acids. Protein syn- thesis and degradation involves two major reactions: transamination and deamination 1 (Fig. 30-4C). In trans- amination, an amino group (NH 2 ) is transferred to an acceptor substance. The process is catalyzed by amino- transferases, enzymes that are found in high amounts in the liver. As a result of transamination, amino acids can participate in the intermediary metabolism of car- bohydrates and lipids. During periods of fasting or starvation, amino acids are used for producing glucose

(i.e., gluconeogenesis). Most of the nonessential amino acids are synthesized in the liver by transamination. Oxidative deamination involves the removal of the amino group and a hydrogen atom from an amino acid. This yields ammonia (NH 3 ). Because ammonia is very toxic to body tissues, particularly neurons, the ammonia that is released during the deamination process is rap- idly removed from the blood by the liver and combined with carbon dioxide to form urea. Essentially all urea formed in the body is synthesized by the urea cycle in the liver and then excreted by the kidneys. Although urea is mostly excreted by the kidneys, some diffuses into the intestine, where it is converted to ammonia by enteric bacteria. The intestinal produc- tion of ammonia also results from bacterial deamination of unabsorbed amino acids and proteins derived from the diet, exfoliated cells, or blood in the gastrointestinal tract. Ammonia produced in the intestine is absorbed into the portal circulation and transported to the liver,