Difference between revisions 439311741 and 439312088 on enwiki

{{cleanup|date=April 2011}}{{More footnotes|article|date=July 2011}}
'''Zerona''' is a low-level laser device applied for non-invasive body slimming of the waist, hips, and thighs.  It has been shown to disrupt [[adipocyte]], or fat cell, membranes causing the release of stored [[lipids]] and fatty material, in turn, promoting adipocyte collapse.  The device was first introduced to the market in 2008 as an [[off-label use]] device for slimming, but later was granted 510k market(contracted; show full)He-Ne laser on human blood leukocytes |volume=50 |issue=5 |pages=862–6 |journal=Biofizika}}</ref><ref>{{cite journal |pmid=15129632 |year=2004 |last1=Vladimirov |first1=IuA |last2=Klebanov |first2=GI |last3=Borisenko |first3=GG |last4=Osipov |first4=AN |title=Molecular and cellular mechanisms of the low intensity laser radiation effect |volume=49 |issue=2 |pages=339–50 |journal=Biofizika}}</ref><ref name=pmid8570716>{{cite journal |pages=580–7 |doi=10.1111/j.1751-1097.1995.tb02388.x
 |title=PHOTODYNAMICALLY GENERATED 3-β-HYDROXY-5α-CHOLEST-6-ENE-5-HYDROPEROXIDE: TOXIC REACTIVITY IN MEMBRANES and SUSCEPTIBILITY TO ENZYMATIC DETOXIFICATION |year=1995 |last1=Geiger |first1=Peter G. |last2=Korytowski |first2=Witold |last3=Girotti |first3=Albert W. |journal=Photochemistry and Photobiology |volume=62 |issue=3 |pmid=8570716}}</ref> This highly reactive oxygen molecule participates in numerous pathways within a cell. However, as the concentration of ROS elevates a process known as [[lipid peroxidation]] can occur where ROS reacts with lipids found within cell membranes temporarily damaging them.<ref name=pmid16248161/><ref name=pmid8570716/> It has been hypothesized that the Zerona, as a low-level laser device, modulates cell metabolism resulting in a transient rise of ROS which temporarily degrades the membr(contracted; show full)Gijs H. |journal=Physiology & Behavior |volume=94 |issue=2}}</ref><ref name=pmid20107860>{{cite journal |pages=1277–92 |doi=10.1007/s00018-010-0263-4 |title=Adipocyte extracellular matrix composition, dynamics and role in obesity |year=2010 |last1=Mariman |first1=Edwin C. M. |last2=Wang |first2=Ping |journal=Cellular and Molecular Life Sciences |volume=67 |issue=8 |pmid=20107860 |pmc=2839497}}</ref><ref name=pmid19192421>{{cite journal |pages=26–32 |doi=10.1007/s11892-009-0006-9
 |title=Impact of increased adipose tissue mass on inflammation, insulin resistance, and dyslipidemia |year=2009 |last1=Gutierrez |first1=Dario A. |last2=Puglisi |first2=Michael J. |last3=Hasty |first3=Alyssa H. |journal=Current Diabetes Reports |volume=9 |pmid=19192421 |issue=1 |pmc=2735041}}</ref> Excessive body fat results in adipocyte hypertrophy or acquired [[lipodystrophy]].  Significant adipocyte expansion is believed to interrupt the interplay of transcriptional factors and other intracellular components yielding pathological consequences.<ref name=pmid19948207/><ref name=pmid18334583/><ref name=pmid18037457/><ref name=pmid20107860/><ref name=pmid19192421/>

Adipocyte [[hypertrophy]] has been shown to directly disrupt [[angiogenesis]], [[adipogenesis]], extracellular matrix dissolution and reformation, lipogenesis, growth factor production, glucose metabolism, lipid metabolism, enzyme production, immune response, and hormone production.<ref name=pmid17021375>{{cite journal |pages=242S–249S |doi=10.1038/oby.2006.317 |title=Adipose Tissue as an Endocrine Organ |year=2006 |last1=Ahima |first1=Rexford S. |journal=Obesity |volume=14 |pmid=17021375}}</ref> Furthermore, studies have illustrated an alteration in [[gene expression]] recording an upregulation in [[proinflammatory]] factors including classic [[cytokines]] and [[complement factors]].<ref name=pmid17021375/><ref name=pmid18473870>{{cite journal |pmid=18473870 |year=2008 |last1=Heilbronn |first1=LK |last2=Campbell |first2=LV |title=Adipose tissue macrophages, low grade inflammation and insulin resistance in human obesity |volume=14 |issue=12 |pages=1225–30 |journal=Current pharmaceutical design |doi=10.2174/138161208784246153}}</ref><ref name=pmid17505154>{{cite journal |pmid=17505154 |year=2007 |last1=Bahceci |first1=M |last2=Gokalp |first2=D |last3=Bahceci |first3=S |last4=Tuzcu |first4=A |last5=Atmaca |first5=S |last6=Arikan |first6=S |title=The correlation between adiposity and adiponectin, tumor necrosis factor alpha, interleukin-6 and high sensitivity C-reactive protein levels. Is adipocyte size associated with inflammation in adults? |volume=30 |issue=3 |pages=210–4 |journal=Journal of endocrinological invest(contracted; show full)

Directly associated with enlarged fat mass is the chronic disease [[diabetes]]. [[Adiponectin]], a hormone solely produced by adipocytes, has demonstrated insulin sensitive effects promoting anti-diabetic characteristics.<ref name=pmid16642957>{{cite journal |pages=9S–15S |doi=10.1038/oby.2006.276
 |title=Metabolic Actions of Adipocyte Hormones: Focus on Adiponectin |year=2006 |last1=Ahima |first1=Rexford S. |journal=Obesity |volume=14 |issue=2S}}</ref> As a plasma protein, adiponectin has been reported to regulate insulin sensitivity via the activation of AMPK and reduction of mTOR/S6 kinase activity consequentially reducing insulin receptor substrate 1 inhibitory serine phosphorylation in several tissues.<ref name=pmid17021375/><ref name=pmid16642957/> The synthesis of adiponectin is tightly coupled with adipose tissue fat mass, demonstrating a negative relationship with larger masses. Individuals who are classified as obese display a lower plasma adiponectin concentration when compared to non-obese groups. Furthermore, a direct correlation between low adiponectin levels and the onset of type-2 diabetes has been reported. Adiponectin modulation is reflective of the deleterious outcome that manifests when the adipocyte accumulates tremendous volume.{{fact}}

Studies have demonstrated the physiological importance of adipocytes.  [[Lipoatrophy]], a condition in which the total number of adipocytes are reduced, reveals an association with [[insulin resistance]], [[hyperglycemia]], and liver [[steatosis]].<ref>{{cite journal |pages=271–8 |doi=10.1172/JCI7901 |title=Surgical implantation of adipose tissue reverses diabetes in lipoatrophic mice |year=2000 |last1=Gavrilova |first1=Oksana |last2=Marcus-Samuels |first2=Bernice |last3=Graham |first3=David |last4=Kim |first4=Jason K. |last5=Shulman |first5=Gerald I. |last6=Castle |first6=Arthur L. |last7=Vinson |first7=Charles |last8=Eckhaus |first8=Michael |last9=Reitman |first9=Marc L. |journal=Journal of Clinical Investigation |volume=105 |issue=3 |pmid=10675352 |pmc=377444}}</ref> Therefore, preserving cell viability while restoring a lean state is an important strategy as adipocytes exert a protective action by releasing beneficial endocrine hormones. Zerona has been proven to restore a lean state adipocytes without inducing cell apoptosis. It is hypothesized that Zerona could serve as an adjunct to other dietary therapies to promote insulin sensitivity and reduce the risk of diabetes.  The Zerona, based on histological evidence, has proven to reduce adipose tissue fa(contracted; show full)rum Levels Following Low-Level Laser Irradiation: A Noncontrolled, Nonrandomized Pilot Study |journal=The American Journal of Cosmetic Surgery |volume=27 |issue=4 |pages=177–84 |url=http://www.erchonia.com/files/uploads/1/file/Jackson_Reduction%20in%20Cholesterol%20and%20Triglyceride%20Serum%20Levels%20Following%203LT_AJCS_2010.pdf}}</ref> Presently, clinical studies are on-going to elucidate the potential utility of this application.{{fact}}

== References ==
{{reflist}}

[[Category:Laser medicine]]