Sandbox reserved 919: Difference between revisions
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[[Image:HPL_firstimage.png|300 px|left|thumb|Hormone-Sensitive Lipase from [[3dnm]]. Alpha helices and beta sheets are shown in red and yellow, respectively.]] | [[Image:HPL_firstimage.png|300 px|left|thumb|Hormone-Sensitive Lipase from [[3dnm]]. Alpha helices and beta sheets are shown in red and yellow, respectively.]] | ||
Hormone-sensitive [http://proteopedia.org/wiki/index.php/Lipase lipases] (HSL) represent a class of [http://en.wikipedia.org/wiki/Esterase esterases] within the [http://www.proteopedia.org/wiki/index.php/Hydrolase α/β hydrolase] family. HSL catalyzes the cleavage of ester bonds in fatty acid molecules when stimulated by a hormone. <ref name="Holm">PMID:14641008</ref> The activation and mobilization of hormone-sensitive lipase can be triggered by various [http://en.wikipedia.org/wiki/Catecholamine catecholamines] and inhibited by [http://www.proteopedia.org/wiki/index.php/Insulin insulin]. Catecholamines, such as [http://en.wikipedia.org/wiki/Epinephrine epinephrine], are rapidly spread throughout the body during times of energy mobilization, like in the fight of flight response. Conversely, insulin triggers glucose uptake, requiring the storage of energy, opposing HSL's function. HSL is clinically relevant, because the mobilization of or inability to mobilize fats in cells is directly related to fat accumulation seen in [http://en.wikipedia.org/wiki/Atherosclerosis artherosclerosis]and [http://en.wikipedia.org/wiki/Obesity obesity].<ref name= "Yeaman">PMID:14725507</ref> Such diseases are characterized by an accumulation of fats and researchers are investigating whether HSL's activity plays a role or not. <ref name= "Ray">PMID:12765952</ref> Investigation of HSL's structure and function could provide a better clinical understanding of these diseases. <ref name= "Yeaman">PMID:14725507</ref> | Hormone-sensitive [http://proteopedia.org/wiki/index.php/Lipase lipases] (HSL) represent a class of [http://en.wikipedia.org/wiki/Esterase esterases] within the [http://www.proteopedia.org/wiki/index.php/Hydrolase α/β hydrolase] family. HSL catalyzes the cleavage of ester bonds in fatty acid molecules when stimulated by a hormone. <ref name="Holm">PMID:14641008</ref> The activation and mobilization of hormone-sensitive lipase can be triggered by various [http://en.wikipedia.org/wiki/Catecholamine catecholamines] and inhibited by [http://www.proteopedia.org/wiki/index.php/Insulin insulin]. <ref name= "Ray">PMID:12765952</ref> Catecholamines, such as [http://en.wikipedia.org/wiki/Epinephrine epinephrine], are rapidly spread throughout the body during times of energy mobilization, like in the fight of flight response. Conversely, insulin triggers glucose uptake, requiring the storage of energy, opposing HSL's function. HSL is clinically relevant, because the mobilization of or inability to mobilize fats in cells is directly related to fat accumulation seen in [http://en.wikipedia.org/wiki/Atherosclerosis artherosclerosis]and [http://en.wikipedia.org/wiki/Obesity obesity].<ref name= "Yeaman">PMID:14725507</ref> Such diseases are characterized by an accumulation of fats and researchers are investigating whether HSL's activity plays a role or not. <ref name= "Ray">PMID:12765952</ref> Investigation of HSL's structure and function could provide a better clinical understanding of these diseases. <ref name= "Yeaman">PMID:14725507</ref> | ||
Briefly, HSL is stimulated by the binding of catecholamines to β-adrenergic receptors. β-adrenergic receptors coupled with [http://www.proteopedia.org/wiki/index.php/Adenylate_Cyclase adenylate cyclase] (AC) then stimulate G-proteins to increase the levels of cystolic [http://en.wikipedia.org/wiki/Cyclic_adenosine_monophosphate cAMP]. Elevated levels of cAMP leads to an activation [http://www.proteopedia.org/wiki/index.php/Protein_kinase_A protein kinase A] (PKA) leading to phosphorylation of serine residues on HSL activating and translocating HSL to lipid droplets for lipolysis. Conversely, insulin signaling decreases cystolic cAMP levels, resulting in a decreased HSL mobilization. <ref name="Holm">PMID:14641008</ref> | Briefly, HSL is stimulated by the binding of catecholamines to β-adrenergic receptors. β-adrenergic receptors coupled with [http://www.proteopedia.org/wiki/index.php/Adenylate_Cyclase adenylate cyclase] (AC) then stimulate G-proteins to increase the levels of cystolic [http://en.wikipedia.org/wiki/Cyclic_adenosine_monophosphate cAMP]. Elevated levels of cAMP leads to an activation [http://www.proteopedia.org/wiki/index.php/Protein_kinase_A protein kinase A] (PKA) leading to phosphorylation of serine residues on HSL activating and translocating HSL to lipid droplets for lipolysis. Conversely, insulin signaling decreases cystolic cAMP levels, resulting in a decreased HSL mobilization. <ref name="Holm">PMID:14641008</ref> | ||
