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<pubDate>Fri, 24 May 2013 22:23:07 GMT</pubDate>
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			<category>Articles</category>
			<link>http://www.pharmacytechnician.org/en/art/616/</link>
			<title>Study Ties Gene in Fat Cells to Type 2 Diabetes</title>
			<description>&lt;div&gt;
	&lt;span &gt;&lt;span &gt;&lt;img align=&quot;right&quot; alt=&quot;Jorge Moscat, PhD, Chair of UC Cancer and Cell Biology Department, hopes that understanding the role PKC-zeta plays in Type 2 Diabetes and tumor growth will lead to new drugs that can help prevent both diseases.&quot; height=&quot;143&quot; src=&quot;/attachments/wysiwyg/47260/JorgeMoscatPhD.jpg&quot; width=&quot;215&quot; /&gt;A new &lt;a href=&quot;http://www.cell.com/cell-metabolism/abstract/S1550-4131%2810%2900156-7&quot; target=&quot;_blank&quot;&gt;study&lt;/a&gt; by researchers at the &lt;a href=&quot;http://www.uc.edu/&quot; target=&quot;_blank&quot;&gt;University of Cincinnati&lt;/a&gt; (UC) suggests that a specific gene in found in the fat cells could play a major role in the development of Type 2 Diabetes.&lt;/span&gt;&lt;/span&gt;&lt;/div&gt;
&lt;div&gt;
	&lt;span &gt;&lt;span &gt;&lt;br&gt;
	According to the UC study, led by Dr. Jorge Moscat, Ph.D., chair of the University of Cincinnati cancer cell and biology department, fat cells are regulated by a gene known as protein kinase C-zeta (&lt;a href=&quot;http://en.wikipedia.org/wiki/Protein_kinase_M_zeta/Protein_kinase_C_zeta&quot; target=&quot;_blank&quot;&gt;PKC-zeta&lt;/a&gt;). Obesity, however, can cause the fat cells to become inflamed, which causes PKC-zeta to release a substance called IL-6. IL-6 travels to the liver, eventually causing the insulin resistance that leads to Type 2 Diabetes. &amp;nbsp;&lt;/span&gt;&lt;/span&gt;&lt;/div&gt;
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	&lt;span &gt;&lt;span &gt;Moscat says this research is unique in that &lt;a href=&quot;http://www.sciencedaily.com/releases/2007/11/071106133106.htm&quot; target=&quot;_blank&quot;&gt;earlier studies&lt;/a&gt; had said a different gene called &lt;a href=&quot;http://en.wikipedia.org/wiki/C-Jun_N-terminal_kinases&quot; target=&quot;_blank&quot;&gt;JNK1&lt;/a&gt;, known to regulate immune cells, also regulated fat cells and therefore was behind the inflammation in fat cells that could ultimately lead to Type 2 Diabetes.&lt;/span&gt;&lt;/span&gt;&lt;/div&gt;
&lt;div&gt;
	&lt;span &gt;&lt;span &gt;&lt;br&gt;
	&amp;quot;This finding is quite novel because current drug development efforts target immune cells to eliminate this hyperinflammation. Our research suggests obesity-related glucose intolerance has nothing to do with the immune system. It may be more effective to target adipocytes (fat cells),&amp;rdquo; said Moscat in a UC &lt;a href=&quot;http://healthnews.uc.edu/news/?/10819/&quot; target=&quot;_blank&quot;&gt;press release&lt;/a&gt;.&lt;br&gt;
	&lt;br&gt;
	Type 2 Diabetes affects more than 23 million Americans, according to the &lt;a href=&quot;http://diabetes.niddk.nih.gov/dm/pubs/statistics/index.htm#allages&quot;&gt;CDC&lt;/a&gt;. According to Moscat, drug developers are currently working on treatments for Type 2 Diabetes that target JNK1, so these treatments could affect the both fat cells and immune cells. However, if PKC-zeta is what is really causing fat cells to become inflamed, drug developers will be able to produce pharmaceuticals that can treat Type 2 Diabetes without compromising the immune system.&lt;/span&gt;&lt;/span&gt;&lt;/div&gt;
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	&lt;span &gt;&lt;span &gt;Moscat and his colleagues are currently working with the University of Cincinnati&amp;rsquo;s Drug Discovery Department to develop compounds that regulate PKC-zeta for further research. In addition to treating Type 2 Diabetes, Moscat hopes that this research can help explain the role PKC-zeta plays in tumor growth and help researchers develop new drugs to prevent certain cancers.&lt;/span&gt;&lt;/span&gt;&lt;/div&gt;
&lt;div&gt;
	&lt;span &gt;&lt;span &gt;&lt;br&gt;
	&amp;ldquo;We believe a similar mechanism of action is at play in malignant tumor development,&amp;rdquo; Moscat said. &amp;ldquo;Now we are trying to understand how PKC-zeta regulates IL-6 to better determine how we can manipulate the protein to help prevent diabetes and cancer.&amp;rdquo;&lt;br&gt;
	&lt;br&gt;
	The study is available online in the July issue of &lt;a href=&quot;http://www.cell.com/cell-metabolism/abstract/S1550-4131%2810%2900156-7&quot; target=&quot;_blank&quot;&gt;&lt;em&gt;Cell Metabolism&lt;/em&gt;&lt;/a&gt;.&lt;br&gt;
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		&lt;span &gt;&lt;span &gt;Copyright &lt;span color:=&quot;&quot; new=&quot;&quot; roman=&quot;&quot; serif=&quot;&quot; times=&quot;&quot;&gt;&amp;copy; 2010&lt;/span&gt; NPTA. All rights reserved.&lt;/span&gt;&lt;/span&gt;&lt;/div&gt;
&lt;/div&gt;
 
&lt;br&gt;&lt;br&gt;9-Jul-10 10:00 AM
</description>
			<itunes:subtitle>Study Ties Gene in Fat Cells to Type 2 Diabetes</itunes:subtitle>
			<itunes:summary>
	A new study by researchers at the University of Cincinnati (UC) suggests that a specific gene in found in the fat cells could play a major role in the development of Type 2 Diabetes.
 
	 
	According to the UC study, led by Dr. Jorge Moscat, Ph.D., chair of the University of Cincinnati cancer cell and biology department, fat cells are regulated by a gene known as protein kinase C-zeta (PKC-zeta). Obesity, however, can cause the fat cells to become inflamed, which causes PKC-zeta to release a substance called IL-6. IL-6 travels to the liver, eventually causing the insulin resistance that leads to Type 2 Diabetes.  
 
	 
	
 
	Moscat says this research is unique in that earlier studies had said a different gene called JNK1, known to regulate immune cells, also regulated fat cells and therefore was behind the inflammation in fat cells that could ultimately lead to Type 2 Diabetes.
 
	 
	&quot;This finding is quite novel because current drug development efforts target immune cells to eliminate this hyperinflammation. Our research suggests obesity-related glucose intolerance has nothing to do with the immune system. It may be more effective to target adipocytes (fat cells),&quot; said Moscat in a UC press release. 
	 
	Type 2 Diabetes affects more than 23 million Americans, according to the CDC. According to Moscat, drug developers are currently working on treatments for Type 2 Diabetes that target JNK1, so these treatments could affect the both fat cells and immune cells. However, if PKC-zeta is what is really causing fat cells to become inflamed, drug developers will be able to produce pharmaceuticals that can treat Type 2 Diabetes without compromising the immune system.
 
	 
	
 
	Moscat and his colleagues are currently working with the University of Cincinnati's Drug Discovery Department to develop compounds that regulate PKC-zeta for further research. In addition to treating Type 2 Diabetes, Moscat hopes that this research can help explain the role PKC-zeta plays in tumor growth and help researchers develop new drugs to prevent certain cancers.
 
	 
	&quot;We believe a similar mechanism of action is at play in malignant tumor development,&quot; Moscat said. &quot;Now we are trying to understand how PKC-zeta regulates IL-6 to better determine how we can manipulate the protein to help prevent diabetes and cancer.&quot; 
	 
	The study is available online in the July issue of Cell Metabolism. 
	 
	
 
	 
		Copyright &amp;copy; 2010 NPTA. All rights reserved.

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			<guid isPermaLink="false">http://www.pharmacytechnician.org/en/art/616/</guid>
			<author>Kristina Michel - noemail@pharmacytechnician.org</author>
			<pubDate>Fri, 09 Jul 2010 15:00:00 GMT</pubDate>
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