Team:Hong Kong HKUST/Project

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  <a href="https://2013.igem.org/Main_Page"><img id="iGEM_Logo" src="https://static.igem.org/mediawiki/2013/4/46/Igem_qgem_logo.png"></a>
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<a href="http://www.ust.hk/eng/index.htm"><img id="hkust_Logo" src="https://static.igem.org/mediawiki/2013/5/55/Hkust_logo.gif"></a>
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<a href=https://2013.igem.org/Team:Hong_Kong_HKUST><center><div id="kepala"><img src="https://static.igem.org/mediawiki/igem.org/c/c7/BANNER1_%281%29.png" style="height:121px;width:100%;"></div></center></a>
<a href=https://2013.igem.org/Team:Hong_Kong_HKUST><center><div id="kepala"><img src="https://static.igem.org/mediawiki/igem.org/c/c7/BANNER1_%281%29.png" style="height:121px;width:100%;"></div></center></a>
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<li><a href="https://2013.igem.org/Team:Hong_Kong_HKUST/advisors">Advisors</a></li>
<li><a href="https://2013.igem.org/Team:Hong_Kong_HKUST/advisors">Advisors</a></li>
<li><a href="https://2013.igem.org/Team:Hong_Kong_HKUST/instructors">Instructors</a></li>
<li><a href="https://2013.igem.org/Team:Hong_Kong_HKUST/instructors">Instructors</a></li>
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<li><a href="https://2013.igem.org/Team:Hong_Kong_HKUST/attribution">Attribution</a></li>
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<li><a href="https://2013.igem.org/Team:Hong_Kong_HKUST/acknowledge">Acknowledgement</a></li>
</ul>
</ul>
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<ul>
<ul>
<li><a href="https://2013.igem.org/Team:Hong_Kong_HKUST/abstract">Abstract</a></li>
<li><a href="https://2013.igem.org/Team:Hong_Kong_HKUST/abstract">Abstract</a></li>
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<li><a href="https://2013.igem.org/Team:Hong_Kong_HKUST/modelling">Modelling</a></li>
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<li><a href="https://2013.igem.org/Team:Hong_Kong_HKUST/modules">Modules Description</a></li>
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<li><a href="https://2013.igem.org/Team:Hong_Kong_HKUST/characterization">Characterization</a></li>
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<li><a href="https://2013.igem.org/Team:Hong_Kong_HKUST/data">Data Page</a></li>
<li><a href="https://2013.igem.org/Team:Hong_Kong_HKUST/Parts">Parts</a></li>
<li><a href="https://2013.igem.org/Team:Hong_Kong_HKUST/Parts">Parts</a></li>
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<li><a href="https://2013.igem.org/Team:Hong_Kong_HKUST/datapage">Data Page</a></li>
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<li><a href="https://2013.igem.org/Team:Hong_Kong_HKUST/characterization">Characterization</a></li>
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<li><a href="https://2013.igem.org/Team:Hong_Kong_HKUST/results">Results</a></li>
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<li><a href="https://2013.igem.org/Team:Hong_Kong_HKUST/results">Result</a></li>
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<li><a href="https://2013.igem.org/Team:Hong_Kong_HKUST/future">Future Work</a></li>
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<li><a href="https://2013.igem.org/Team:Hong_Kong_HKUST/Wetlab">Wetlab</a>
<li><a href="https://2013.igem.org/Team:Hong_Kong_HKUST/Wetlab">Wetlab</a>
<ul>
<ul>
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<li><a href="https://2013.igem.org/Team:Hong_Kong_HKUST/notebook">notebook</a></li>
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<li><a href="https://2013.igem.org/Team:Hong_Kong_HKUST/notebook">Notebook</a></li>
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<li><a href="https://2013.igem.org/Team:Hong_Kong_HKUST/protocols">protocols</a></li>
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<li><a href="https://2013.igem.org/Team:Hong_Kong_HKUST/protocols">Protocols</a></li>
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<li><a href="https://2013.igem.org/Team:Hong_Kong_HKUST/safety">safety</a></li>
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<li><a href="https://2013.igem.org/Team:Hong_Kong_HKUST/safety">Safety</a></li>
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</ul>
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<li><a href="https://2013.igem.org/Team:Hong_Kong_HKUST/hp">Human Practice</a>
<li><a href="https://2013.igem.org/Team:Hong_Kong_HKUST/hp">Human Practice</a>
<ul>
<ul>
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<li><a href="https://2013.igem.org/Team:Hong_Kong_HKUST/hp/cp">Country Profile</a></li>
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<li><a href="https://2013.igem.org/Team:Hong_Kong_HKUST/hp/blog">Blog</a></li>
<li><a href="https://2013.igem.org/Team:Hong_Kong_HKUST/hp/interview">Interviews</a></li>
<li><a href="https://2013.igem.org/Team:Hong_Kong_HKUST/hp/interview">Interviews</a></li>
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<li><a href="https://2013.igem.org/Team:Hong_Kong_HKUST/hp/presentation">Presentation</a></li>
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<li><a href="https://2013.igem.org/Team:Hong_Kong_HKUST/hp/article/genet">Article</a></li>
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<li><a href="https://2013.igem.org/Team:Hong_Kong_HKUST/hp/article">Articles</a></li>
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<li><a href="https://2013.igem.org/Team:Hong_Kong_HKUST/hp/video">Videos</a></li>
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<li><a href="https://2013.igem.org/Team:Hong_Kong_HKUST/hp/presentation">Presentations</a></li>
</ul>
</ul>
</li>
</li>
</ul>
</ul>
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</div>
</div>
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<br><br><br><br><br><br><br>
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<div id="slide1"><h3 class="title"><center>FAT BUSTER - Artificial Futile Cycle</center></h3></div>
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<div id="contain">
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<div id="more" class="ijo"><center><h3>Abstract</h3></center>
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<div id="abs"><a href="https://2013.igem.org/Team:Hong_Kong_HKUST/abstract"><img src="https://static.igem.org/mediawiki/2013/0/04/Abstracts.png" style="width:95%;"></a></div>
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<br><br><br><div id="slide" class="center"><center><h3 style="font-size:24px;">FAT BUSTER</h3><p style="font-size:19px;">Artificial Futile Cycle</p><p>While low-fat diet and regular exercise are popular approaches to fight obesity, one easy alternative is simply to increase energy metabolism. <br><br>
 
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In terms of fat storage, conversion of carbohydrates or protein into fat uses ten times more calories of energy than simply storing fat in a fat cell. This brought us attention to one method of burning calories - increase energy expenditure by converting fat into glucose. However, mammals cannot convert fatty acids into carbohydrate due to lack of glyoxylate enzymes, while plants and bacteria can. We envision to introduce glyoxylate enzymes into mammalian cells and create an artificial futile cycle.<br><br>
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<div id="more" class="pink"><center><h3>Modules Description</h3></center>
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<div id="mod"><a href="https://2013.igem.org/Team:Hong_Kong_HKUST/modules"><img src="https://static.igem.org/mediawiki/2013/c/c4/Mods.png" style="width:110%;height:50px;"></a></div>
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</div>
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While the consequence of introducing nonnative cycle unknown, Dean et al. at UCLA recently has introduced glyoxylate shunt into mammalian liver cell to investigate fatty acid metabolism (2009). They observed that although fatty acids could not be converted into glucose in normal mammalian cells, human hepatocytes expressing the glyoxylate shunt have increased fatty acid oxidation and mice expressing the shunt were resistance to diet-induced obesity.<br><br>
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<div id="more" class="ijo"><center><h3>Data Page</h3></center>
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<div id="dp"><a href="https://2013.igem.org/Team:Hong_Kong_HKUST/data"><img src="https://static.igem.org/mediawiki/2013/d/db/Datapage.png" style="width:85%;"></a></div>
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In addition to introducing a constitutive glyoxylate shunt, our team plans to elaborate the UCLA study by introducing inducible system that allows tunable fatty acid uptake by sensing fatty acid concentrations. This inducible system prevents the risk of fatty acid deficiency, while greater fatty acid uptake at high circulating concentrations can be facilitated. Fatty acids uptake will be quantified to compare the activities in wild type cells and cells expressing constitutive and inducible glyoxylate shunt.<br><br>
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<div id="more" class="pink"><center><h3>Parts</h3></center>
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<div id="par"><a href="https://2013.igem.org/Team:Hong_Kong_HKUST/Parts"><img src="https://static.igem.org/mediawiki/2013/9/99/Part.png" style="width:113%;height:60%;"></a></div>
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</div>
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We believe the introduction of an inducible glyoxylate shunt will serve as an artificial futile cycle in human liver cell that increases energy expenditure responding to high circulating fatty acid levels. This will help obesity patients increase expenditure of calories and alleviate health complications, including cardiovascular disease, diabetes, and cancers.</p></center></div>
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<div id="more" class="ijo"><center><h3>Result</h3></center>
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<div id="more"><h3>To know more about our project, you can view this video beside!</h3></div>
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<div id="re"><a href="https://2013.igem.org/Team:Hong_Kong_HKUST/results"><img src="https://static.igem.org/mediawiki/2013/1/17/Results.png" style="width:95%;"></a></div>
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<div id="vidproj"><iframe width="560" height="315" src="//www.youtube.com/embed/OqSTkwxIdVk?rel=0" frameborder="0" allowfullscreen></iframe></div>
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<div id="moddesc">
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<b>In our project includes four modules: cell vaibility & fatty acid
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quantification, fatty acid sensing mechanism, protein trafficking and
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glyoxylate shunt. These four modules are essential to introduce
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inducible our glyoxylate shunt into human liver cell. Hover & click into the images below to learn more about each modules!</b>
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</div>
</div>
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<div id="more" class="pink"><center><h3>Future Work</h3></center>
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<div id="ftr"><a href="https://2013.igem.org/Team:Hong_Kong_HKUST/future"><img src="https://static.igem.org/mediawiki/2013/a/af/Future.png" style="width:70%;"></a></div>
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</div>
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<div id="more2" class="ijo"><center><h3>Characterization</h3></center>
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<div id="char"><a href="https://2013.igem.org/Team:Hong_Kong_HKUST/characterization"><img src="https://static.igem.org/mediawiki/2013/d/d2/Char.png" style="width:80%;"></a></div>
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<div id="projinteract"></div>
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<div id="vidproj"><iframe width="560" height="320" src="//www.youtube.com/embed/oFWilKz1zl8?rel=0" frameborder="0" allowfullscreen></iframe></div>
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<div id="interview"><h3>Cell Viability & Fatty Acid Quantification</h3><p><b><i>Responsible for:</i></b><br>Measuring cell viability at different fatty acid concentration & measure fatty acid uptake rate</i><br><b><i>Parts submitted:</b> - </i></p></div>
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<div id="presentation"><h3>Fatty Acid Sensing Mechanism</h3><p><b><i>Responsible for:</b></i><br>Introduce inducible system that allows tunable fatty acid uptake by sensing fatty acid concentration<br><b><i>Parts submitted:</b> - </i></p></div>
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<div id="slide"><p id="isi">While a low-fat diet and regular exercise are popular approaches to fight obesity, one easy alternative is simply to increase energy metabolism. <br><br>
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<div id="article"><h3>Protein Trafficking</h3><p><b><i>Responsible for:</b></i><br>Target ACE proteins into mitochondria<br><b><i>Parts submitted:</b> </i></p></div>
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<div id="article2"><h3>Glyoxylate Shunt</h3><p><b><i>Responsible for:</b></i><br>Introduce glyoxylate enzymes responsible for the shunt<br><b><i>Parts submitted:</b> </i></p></div>
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In terms of fat storage, conversion of carbohydrates or protein into fat uses ten times more calories than simply storing fat in a fat cell. This brought our attention to one method of burning calories - increase energy expenditure by converting fat into glucose. However, mammals cannot convert fatty acids into carbohydrate due to lacking glyoxylate enzymes, while plants and bacteria can. We intend to introduce glyoxylate enzymes into mammalian cells and create an artificial futile cycle.<br><br>
 +
 
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While the consequences of introducing such a nonnative cycle are not fully known, Dean et al. (2009) at UCLA recently introduced glyoxylate shunt into mammalian liver cells to investigate fatty acid metabolism. They observed that although fatty acids could not be converted into glucose in normal mammalian cells, human hepatocytes expressing the glyoxylate shunt have increased fatty acid oxidation and mice expressing the shunt were resistance to diet-induced obesity.<br><br>
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In addition to introducing a constitutive glyoxylate shunt, our team plans to elaborate the UCLA study by introducing an inducible system that allows tunable fatty acid uptake by sensing fatty acid concentrations. This inducible system prevents the risk of fatty acid deficiency, while greater fatty acid uptake at high circulating concentrations can be facilitated. Fatty acid uptake will be quantified to compare the activities in wild type cells, cells expressing the shunt constitutively, and cells expressing the shunt in an inducible manner.<br><br>
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So, to sum up, we envision developing an inducible glyoxylate shunt that will serve to generate an artificial futile cycle in human liver cells. We hope our work will point to a future where obesity patients can increase expenditure of calories and thus alleviate health complications, including cardiovascular disease, diabetes, and cancers.</p></div>
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Latest revision as of 22:51, 27 September 2013








FAT BUSTER - Artificial Futile Cycle

Abstract

Modules Description

Data Page

Parts

Result

Future Work

Characterization

While a low-fat diet and regular exercise are popular approaches to fight obesity, one easy alternative is simply to increase energy metabolism.

In terms of fat storage, conversion of carbohydrates or protein into fat uses ten times more calories than simply storing fat in a fat cell. This brought our attention to one method of burning calories - increase energy expenditure by converting fat into glucose. However, mammals cannot convert fatty acids into carbohydrate due to lacking glyoxylate enzymes, while plants and bacteria can. We intend to introduce glyoxylate enzymes into mammalian cells and create an artificial futile cycle.

While the consequences of introducing such a nonnative cycle are not fully known, Dean et al. (2009) at UCLA recently introduced glyoxylate shunt into mammalian liver cells to investigate fatty acid metabolism. They observed that although fatty acids could not be converted into glucose in normal mammalian cells, human hepatocytes expressing the glyoxylate shunt have increased fatty acid oxidation and mice expressing the shunt were resistance to diet-induced obesity.

In addition to introducing a constitutive glyoxylate shunt, our team plans to elaborate the UCLA study by introducing an inducible system that allows tunable fatty acid uptake by sensing fatty acid concentrations. This inducible system prevents the risk of fatty acid deficiency, while greater fatty acid uptake at high circulating concentrations can be facilitated. Fatty acid uptake will be quantified to compare the activities in wild type cells, cells expressing the shunt constitutively, and cells expressing the shunt in an inducible manner.

So, to sum up, we envision developing an inducible glyoxylate shunt that will serve to generate an artificial futile cycle in human liver cells. We hope our work will point to a future where obesity patients can increase expenditure of calories and thus alleviate health complications, including cardiovascular disease, diabetes, and cancers.

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