Glucuronidation: Difference between revisions

Latest revision as of 16:24, 16 February 2025

Glucuronidation[edit]

Illustration of glucuronidation of biphenyl amine.

Glucuronidation is a biochemical process that involves the addition of glucuronic acid to substances, facilitating their excretion from the body. This process is a major pathway of phase II metabolism in the liver, where it plays a crucial role in the detoxification and elimination of both endogenous and exogenous compounds.

Mechanism[edit]

Glucuronidation is catalyzed by the family of enzymes known as UDP-glucuronosyltransferases (UGTs). These enzymes transfer glucuronic acid from the cofactor uridine diphosphate glucuronic acid (UDPGA) to a substrate, which can be a drug, hormone, or toxin. The resulting glucuronide conjugates are more water-soluble, allowing for easier excretion via the urinary system or bile.

Substrates[edit]

A wide variety of substrates undergo glucuronidation, including:

Bilirubin
Steroid hormones
Thyroid hormones
Drugs such as acetaminophen, morphine, and ibuprofen
Environmental toxins

Clinical Significance[edit]

Glucuronidation is essential for the metabolism and clearance of many therapeutic drugs. Impairments in this pathway can lead to drug toxicity or ineffective drug therapy. Genetic polymorphisms in UGT enzymes can affect an individual's ability to metabolize certain drugs, influencing drug efficacy and safety.

Related Enzymes[edit]

The UGT enzyme family is divided into several subfamilies, including UGT1A and UGT2B, each with specific substrate affinities. These enzymes are primarily located in the liver, but are also found in other tissues such as the intestine, kidney, and brain.

Related Pages[edit]

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-'''Glucuronidation''' is a [[biochemical]] process that involves the addition of a [[glucuronic acid]] molecule to a [[substrate]]. This process is part of the [[Phase II metabolism]] in the [[liver]], which is responsible for the detoxification of various substances.
+== Glucuronidation ==
-== Process ==
+[[File:GlucuronidationBiphenylAmine.svg|thumb|right|Illustration of glucuronidation of biphenyl amine.]]
-Glucuronidation is catalyzed by the [[enzyme]] [[UDP-glucuronosyltransferase]] (UGT). The UGT enzyme transfers a glucuronic acid molecule from [[uridine diphosphate glucuronic acid]] (UDPGA) to the substrate. This process increases the solubility of the substrate, making it easier for the body to excrete it.
+'''Glucuronidation''' is a biochemical process that involves the addition of [[glucuronic acid]] to substances, facilitating their excretion from the body. This process is a major pathway of [[phase II metabolism]] in the liver, where it plays a crucial role in the detoxification and elimination of both endogenous and exogenous compounds.
-== Role in Drug Metabolism ==
+== Mechanism ==
-Glucuronidation plays a crucial role in the [[metabolism]] of many [[drugs]] and [[xenobiotics]]. By increasing the solubility of these substances, glucuronidation facilitates their excretion from the body. This process is particularly important for drugs that are not easily excreted by the kidneys.
+Glucuronidation is catalyzed by the family of enzymes known as [[UDP-glucuronosyltransferases]] (UGTs). These enzymes transfer glucuronic acid from the cofactor [[uridine diphosphate glucuronic acid]] (UDPGA) to a substrate, which can be a [[drug]], [[hormone]], or [[toxin]]. The resulting glucuronide conjugates are more water-soluble, allowing for easier excretion via the [[urinary system]] or [[bile]].
+== Substrates ==
+A wide variety of substrates undergo glucuronidation, including:
+* [[Bilirubin]]
+* [[Steroid hormones]]
+* [[Thyroid hormones]]
+* [[Drugs]] such as [[acetaminophen]], [[morphine]], and [[ibuprofen]]
+* [[Environmental toxins]]
 == Clinical Significance ==
-Alterations in glucuronidation can have significant clinical implications. For example, individuals with [[Gilbert's syndrome]] have a reduced capacity for glucuronidation, which can lead to an increased risk of drug toxicity. Additionally, certain drugs can inhibit or induce the UGT enzyme, potentially leading to drug-drug interactions.
+Glucuronidation is essential for the metabolism and clearance of many therapeutic drugs. Impairments in this pathway can lead to drug toxicity or ineffective drug therapy. Genetic polymorphisms in UGT enzymes can affect an individual's ability to metabolize certain drugs, influencing drug efficacy and safety.
-== See Also ==
+== Related Enzymes ==
+The UGT enzyme family is divided into several subfamilies, including UGT1A and UGT2B, each with specific substrate affinities. These enzymes are primarily located in the [[liver]], but are also found in other tissues such as the [[intestine]], [[kidney]], and [[brain]].
+== Related Pages ==
 * [[Phase I metabolism]]
-* [[Phase II metabolism]]
+* [[Cytochrome P450]]
+* [[Conjugation reactions]]
 * [[Drug metabolism]]
-* [[Gilbert's syndrome]]
-== References ==
+{{Metabolism}}
-<references />
-{{stub}}
+[[Category:Metabolism]]
 [[Category:Biochemistry]]
-[[Category:Pharmacology]]
-[[Category:Metabolism]]