Difference between revisions 741392899 and 741407606 on enwiki

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{{Article for deletion/dated|page=Zerona|timestamp=20160927062427|year=2016|month=September|day=27|substed=yes|help=off}}
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(contracted; show full)baseline, weeks one and two, and a two-week post-procedure follow-up measurement. After two weeks the active treatment group averaged a cumulative reduction of 3.54&nbsp;inches compared to the control group which averaged a cumulative reduction of just 0.68&nbsp;inches. At the two-week post-procedure follow-up, active group participants did not exhibit a significant gain in their measurements. No adverse events or side-effects were reported during the clinical trial.<ref name=pmid20014253/>


== Ongoing research ==
{{Off-topic|date=July 2014}}
The adipocyte or fat cell is described as an endocrine organ cell responsible for the synthesis of bioactive peptides which participate in autocrine, paracrine, and endocrine pathways.  The physical adaptability of the adipocyte is extraordinary, enabling it to expand nearly 1,000 fold in volume and 10 fold in diameter in order to store excessive fuel as triglycerides.<ref>{{cite journal |pmid=9843879 |year=1998 |last1=Marques |first1=BG |last2=Hausman |first2=DB |last3=Martin |first3=RJ |title=Association of fat cell size and paracrine growth factors in development of hyperplastic obesity |volume=275 |issue=6 Pt 2 |pages=R1898–908 |journal=The American journal of physiology}}</ref> During periods of limited food intake fat tissue rapidly transitions to an abundant provider of non-esterfied free fatty acids which upon their release into the circulatory system can undergo beta-oxidation to supply energy.  The storage capacity of adipocytes remains a key component of its function but has been shown to modulate the synthesis of bioactive peptides, specifically adipose-derived hormones.<ref name="pmid19948207"/><ref name="pmid18334583"/>

Studies have revealed a correlation between deregulated adipose tissue function and excessive fat mass having deleterious effects on the endocrine and immune systems.<ref name=pmid19948207>{{cite journal |pages=69–78 |doi=10.1016/j.mce.2009.11.011 |title=The autocrine and paracrine roles of adipokines |year=2010 |last1=Karastergiou |first1=Kalypso |last2=Mohamed-Ali |first2=Vidya |journal=Molecular and Cellular Endocrinology |volume=318 |pmid=19948207 |issue=1–2}}</ref><ref name=pmid18334583>{{cite journal |pages=2255–62 |doi=10.1210/jc.2007-2188 |title=Adipokine Protein Expression Pattern in Growth Hormone Deficiency Predisposes to the Increased Fat Cell Size and the Whole Body Metabolic Derangements |year=2008 |last1=Ukropec |first1=J. |last2=Penesova |first2=A. |last3=Skopkova |first3=M. |last4=Pura |first4=M. |last5=Vlcek |first5=M. |last6=Radikova |first6=Z. |last7=Imrich |first7=R. |last8=Ukropcova |first8=B. |last9=Tajtakova |first9=M. |last10=Koška |first10=Juraj |last11=Zórad |first11=Štefan |last12=Belan |first12=Vítazoslav |last13=Vaňuga |first13=Peter |last14=Payer |first14=Juraj |last15=Eckel |first15=Juergen |last16=Klimeš |first16=Iwar |last17=Gašperíková |first17=Daniela |journal=Journal of Clinical Endocrinology & Metabolism |volume=93 |issue=6|display-authors=8 }}</ref><ref name=pmid18037457>{{cite journal |pages=206–18 |doi=10.1016/j.physbeh.2007.10.010 |title=The role of adipose tissue dysfunction in the pathogenesis of obesity-related insulin resistance |year=2008 |last1=Goossens |first1=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–9S |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 investigation |doi=10.1007/bf03347427}}</ref> A rise in pro-inflammatory [[adipokines]] coupled with cytokine production may promote the onset of metabolic disorders like [[atherosclerosis]].<ref name=pmid19723556>{{cite journal |pmid=19723556 |year=2010 |last1=Galic |first1=S|last2=Oakhill |first2=JS |title=Adipose tissue as an endocrine organ |volume=316 |issue=2 |pages=129–39 |journal=Molecule Cell Endocrinology |doi=10.1016/j.mce.2009.08.018}}
</ref>

Positively correlated with increased adipose tissue size are pro-inflammatory factors: [[tumor necrosis factor-α]] (TNF-α), [[interleukin-6]] (IL-6), and [[C-reactive protein]]. Participating in [[paracrine]] and [[autocrine]] signaling, adipocyte impairment may account for metabolic dysfunction as adipose tissue communicates with multiple body systems including nervous, immune, skeletal, cardiovascular, and gastrointestinal.<ref name=pmid17021375/> Positive caloric intake can result in adipocyte [[hypertrophy]] modulating adipose tissue function and increasing a patient’s risk of developing serious metabolic disorders.

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=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.<ref name=pmid17021375/>

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.  Zerona, based on histological evidence, has proven to reduce adipose tissue fat mass of the waist, hips, and thighs while preventing fat cell death. The formation of the transitory pore within the adipocyte membrane results in adipocyte cell collapse and its return to a lean state.  Reduced fat mass is associated with the synthesis of beneficial hormones like adiponectin which promotes insulin sensitivity within numerous tissues.

A 2010 article in the ''American Journal of Cosmetic Surgery'' demonstrated a statistically significant reduction in both serum triglyceride and total cholesterol levels following a standard two-week, six treatment Zerona administration.<ref>{{cite journal |first1=Robert F. |last1=Jackson |first2=Greg C. |last2=Roche |first3=Kevin |last3=Wisler |year=2010 |title=Reduction in Cholesterol and Triglyceride Serum 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>⏎
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==Zerona Canada marketing controversy==
In January 2014 a broadcast story on Zerona Canada marketing fraud allegations was aired by the Canadian [[investigative journalism|investigative]] [[newsmagazine]] [[television program]] [[16:9 (TV series)|''16x9'']].<ref>{{cite web|author1=Alan Carter|author2=Krysia Collyer (Producer)|title=Full Story: Fat Zapping|url=http://globalnews.ca/video/1091434/full-story-fat-zapping|publisher=[[Global Television Network]]|date=January 18, 2014}}</ref>

== References ==
{{reflist|2}}

==External links==
* [http://www.erchonia.com/ Erchonia Corp., Official Website]

[[Category:Laser medicine]]
[[Category:Management of obesity]]