Hydroxycarboxylic acid receptor 1: Difference between revisions
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== | {{Infobox protein | ||
| name = Hydroxycarboxylic acid receptor 1 | |||
| image = <!-- Image removed --> | |||
| caption = <!-- Caption removed --> | |||
| symbol = HCAR1 | |||
| HGNCid = 23366 | |||
| chromosome = 12 | |||
| arm = q | |||
| band = 24.31 | |||
}} | |||
'''Hydroxycarboxylic acid receptor 1''' ('''HCAR1'''), also known as '''GPR81''', is a [[G protein-coupled receptor]] (GPCR) that is encoded by the [[HCAR1 gene]] in humans. This receptor is primarily activated by [[lactate]], a key metabolite in [[energy metabolism]]. | |||
== | == Function == | ||
HCAR1 is involved in the regulation of [[lipolysis]] in [[adipose tissue]]. When activated by lactate, HCAR1 inhibits the breakdown of [[fatty acids]], thereby reducing the release of [[free fatty acids]] into the bloodstream. This mechanism is crucial for maintaining [[energy homeostasis]] and is particularly important during [[exercise]] when lactate levels are elevated. | |||
== | == Expression == | ||
HCAR1 is predominantly expressed in [[adipose tissue]], but it is also found in other tissues such as the [[skeletal muscle]] and the [[brain]]. Its expression in the brain suggests a potential role in [[neurotransmission]] and [[neuroprotection]]. | |||
== Clinical Significance == | |||
The modulation of HCAR1 activity has been implicated in various [[metabolic disorders]], including [[obesity]] and [[type 2 diabetes]]. As a result, HCAR1 is considered a potential target for the development of new [[therapeutic agents]] aimed at treating these conditions. | |||
== Research == | |||
Recent studies have explored the role of HCAR1 in [[cancer metabolism]], as cancer cells often exhibit altered lactate production and utilization. Understanding the interaction between HCAR1 and lactate in the [[tumor microenvironment]] could lead to novel approaches in [[cancer therapy]]. | |||
== See Also == | |||
* [[G protein-coupled receptor]] | * [[G protein-coupled receptor]] | ||
* [[ | * [[Lactate]] | ||
* [[Energy metabolism]] | |||
* [[Lipolysis]] | * [[Lipolysis]] | ||
==References== | == References == | ||
<references /> | <references /> | ||
== External Links == | |||
* [https://www.wikimd.com/wiki/Hydroxycarboxylic_acid_receptor_1 Hydroxycarboxylic acid receptor 1 on WikiMD] | |||
{{Receptor-stub}} | |||
{{Protein-stub}} | |||
[[Category:Human proteins]] | |||
[[Category:G protein-coupled receptors]] | [[Category:G protein-coupled receptors]] | ||
[[Category: | [[Category:Metabolism]] | ||
[[Category: | [[Category:Adipose tissue]] | ||
Latest revision as of 04:33, 29 December 2024
Hydroxycarboxylic acid receptor 1 (HCAR1), also known as GPR81, is a G protein-coupled receptor (GPCR) that is encoded by the HCAR1 gene in humans. This receptor is primarily activated by lactate, a key metabolite in energy metabolism.
Function[edit]
HCAR1 is involved in the regulation of lipolysis in adipose tissue. When activated by lactate, HCAR1 inhibits the breakdown of fatty acids, thereby reducing the release of free fatty acids into the bloodstream. This mechanism is crucial for maintaining energy homeostasis and is particularly important during exercise when lactate levels are elevated.
Expression[edit]
HCAR1 is predominantly expressed in adipose tissue, but it is also found in other tissues such as the skeletal muscle and the brain. Its expression in the brain suggests a potential role in neurotransmission and neuroprotection.
Clinical Significance[edit]
The modulation of HCAR1 activity has been implicated in various metabolic disorders, including obesity and type 2 diabetes. As a result, HCAR1 is considered a potential target for the development of new therapeutic agents aimed at treating these conditions.
Research[edit]
Recent studies have explored the role of HCAR1 in cancer metabolism, as cancer cells often exhibit altered lactate production and utilization. Understanding the interaction between HCAR1 and lactate in the tumor microenvironment could lead to novel approaches in cancer therapy.
See Also[edit]
References[edit]
<references />
External Links[edit]
